Peripheral motor neurons. Intraspinal recurrent inhibitory and facilitatory influences (Renshaw cells, gamma loop)
Renshaw cells are inhibitory interneurons located in the anterior horns of the spinal cord, somewhat dorsal and medial than motor neurons. These are small cells. The diameter of the Renshaw cell body is 10-20 microns, the dendrites are 100-150 microns long, and the axons of these cells are long.
Principle of operation
A single muscle contraction lasts quite a long time. But it should be taken into account that when a muscle containing a huge number of muscle fibers is tense, their simultaneous excitation never occurs. The activity of different muscle fibers alternates to some extent, due to this the muscle becomes less tired. Therefore, to maintain continuous muscle tension, a high frequency of discharge of the motor nerve cell is not needed. For this purpose, a pulse frequency not exceeding ten pulses per second is sufficient. Motor neurons have mechanisms that stabilize their discharge at exactly this frequency and prevent the occurrence of impulses of too high a frequency, which could lead to disruption of muscle activity. Such a stabilizing mechanism is, firstly, the development in the soma of the motor neuron of a long-term trace hyperpolarization after the generation of an impulse. Its duration reaches approximately 100 ms, and during its development the new synaptic action will be weakened. This mechanism itself should help stabilize the motor neuron discharge rate at a level of about 10 impulses per second. In addition to the internal stabilization mechanism, the motor neuron also has a second, external mechanism that works in the same direction. This external mechanism is represented by a short chain of negative feedback through which the motor neuron inhibits itself, but in the case when it sends a discharge to the axon.
The general scheme of the activity of such a chain is as follows. Renshaw cells terminate reentrant axonal collaterals that, within the gray matter, give off alpha motor neurons that innervate the motor muscles, and therefore they always “know” how strongly the neuron is excited. Renshaw cells, in turn, terminate on motor neurons with inhibitory synapses. There is no trace hyperpolarization in Renshaw cells, and therefore they can generate a whole train of impulses at a very high frequency of up to 1500 impulses per second at one synaptic potential. Each of these impulses, arriving at the motor neurons, causes an inhibitory reaction in them, which is summed up as long as the discharge of the Renshaw cell lasts. Therefore, the total duration of inhibition after a single impulse in the axon collateral reaches approximately 100 ms. Recurrent inhibition combines with subsequent hyperpolarization and further contributes to maintaining the motor neuron discharge at a low frequency. Renshaw cells receive input from more than one motor neuron and themselves send axons to many motor neurons. Since in the process of evolution such effective overlapping mechanisms for stabilizing the discharge of a motor neuron arose, it is obvious that the latter mechanism is essential for the normal implementation of a motor act.
Renshaw cells use glycine as a neurotransmitter, an inhibitory neurotransmitter that acts on alpha motor neurons.
The frequency of impulses sent by a Renshaw cell is, over a wide range, directly proportional to the frequency of impulses sent by its associated motor neuron, and the frequency of impulses of a motor neuron is inversely proportional to the frequency of impulses sent by a Renshaw cell. Renshaw cells act as "limiters" or "regulators" of the alpha motor neuron system, and thus help prevent tetanus and muscle damage. Thanks to their activity, the impulse of motor neurons is maintained in the optimal range necessary for controlled muscle contraction.
A neuron of the motor zone of the cerebral cortex, the axon of which is involved in the formation of the corticospinal or corticobulbar tracts.
An efferent neuron of the anterior horns of the spinal cord, the axon of which innervates the contractile elements of intrafusal fibers.
An efferent neuron of the anterior horns of the spinal cord, the axon of which innervates the extrafusal fibers of skeletal muscles.
The inhibitory neuron of the cerebellar cortex inhibits the activity of both the nuclei of the cerebellum itself and the vestibular nuclei of the medulla oblongata.
Inhibitory interneuron of the spinal cord, which takes part in the organization of recurrent inhibition.
REFLEX..... IS MANIFESTED IN:
A. Ashner-Danini. B Hering-Breuer.
B. Viscero-visceral. G. Viscero-dermal.
Changes in the activity of internal organs when their interoreceptors are irritated.
Changes in the activity of internal organs due to irritation of certain areas of the skin.
Changes in sweating and skin sensitivity due to irritation of internal organs.
Decrease in heartbeat when pressing on the eyeballs.
Inhibition of inhalation when the lungs are stretched.
TYPE OF NERVE FIBER.... HAS FUNCTIONAL FEATURES
A. Type A. B. Type B. C. Type C.
Postganglionic autonomic fibers and afferent fibers from some receptors of heat, pressure, pain have the lowest excitation velocity (0.503 m/sec).
Preganglionic autonomic fibers with excitation velocity (3-18 m/sec.).
Axons of motor neurons innervating skeletal muscles and afferent fibers from muscle receptors, which have the highest conduction speed - 120 m/sec.
Determine whether the statements are true or false and the relationship between them:
ON ONE NEURON ONLY EITHER IPSP OR EPSP CAN BE SUMMED, BECAUSE ACCORDING TO DALE'S PRINCIPLE, ONE NEURON USES ONLY ONE TYPE OF MEDIATOR IN ALL ITS TERMINALS
1. ВВВ 2. ННН 3. НВН 4. ВНН 5. ВВН
EITHER EXCITATION OR INHIBITION CAN PROPADE ALONG THE Axon OF A NEURON, BECAUSE WHEN EPSP AND IPSP ARE SUMMED, THE TOTAL TOTAL CAN BE EITHER POSITIVE OR NEGATIVE
1. ВВВ 2. ННН 3.. НВН 4. ВНН 5 ВВН
THE SECHENOV EXPERIMENT IS CARRIED OUT ON THE SPINAL FROG BECAUSE IN THE SECHENOV EXPERIMENT THE TIME OF THE SPINAL REFLEX IS MEASURED
SECHENOV'S EXPERIMENT IS CARRIED OUT ON THE THALAMIC FROG. BECAUSE TO SUPPRESS THE SPINAL REFLEX, IT IS NECESSARY TO PLACE A SALT CRYSTAL ON THE VISUAL THUMBS
INHIBITION OF THE SPINAL REFLEX IN SECHENOV’S EXPERIMENT IS CAUSED BY IRRITATION OF THE OPTICAL THABLES WITH A SALT CRYSTAL, BECAUSE SODIUM AND CHLORINE IONS CAUSE HYPERPOLARIZATION OF NEURONS
1. ВНН 2. НВН 3. ВВН 4. ВВВ 5. ННН
PRESYNAPTIC INHIBITION IS VERY EFFECTIVE IN PROCESSING INFORMATION COMING TO A NEURON, BECAUSE IN THIS EXCITATION CAN BE SUPPRESSED SELECTIVELY AT ONE SYNAPTIC INPUT
RECEPTORS SENSITIVE TO SEROTONIN ARE CALLED SEROTONINergic, BECAUSE SEROTONIN HAS BOTH EXCITATING AND INHIBITORY INFLUENCES
1. НВН 2., ННН 3. ВНН 4. ВВВ 5. ВВН
TO DEMONSTRATE THE ROLE OF INHIBITION, A FROG IS INTRODUCED WITH STRYCHNINE BECAUSE STRYCHNINE ACTIVATES INHIBITORY SYNAPSES
1. VNN 2. NNN 3. ВВН 4. ВВВ 5. НВН
TO DEMONSTRATE INHIBITION, A FROG IS INTRODUCED WITH STRYCHNINE BECAUSE STRYCHNINE BLOCKS INHIBITORY SYNAPSES
TO DEMONSTRATE THE ROLE OF INHIBITION, THE FROG IS INTRODUCED WITH STRYCHNINE, BECAUSE AFTER THE INTRODUCTION OF STRYCHNINE, THE FROG OBSERVES DIFFUSE IRRADIATION OF EXCITATION
1. НВН 2. ННН 3. ВВН 4. ВВВ 5. ВНН
A NEURON CAN BE IN A STATE OF EITHER EXCITATION OR INHIBITION, BECAUSE ONE NEURON CAN SUMMARY EITHER EXCITATTORY OR INHIBITORY POSTSYNAPTIC POTENTIALS
1. НВН 2. ННН 3. ВВН 4. ВНН 5. ВВВ
THE EFFERENT PARASYMPATHETIC PATHWAY HAS A TWO-NEURAL STRUCTURE BECAUSE THE CENTERS OF THE PARASYMPATHETIC DIVISION OF THE AUTONOMIC NERVOUS SYSTEM ARE LOCALIZED IN THE BRAIN AND SPINAL CORD.
1. НВН 2. ННН 3. ВВВ 4. ВНН 5. ВВН
THE EFFERENT SYMPATHETIC PATHWAY HAS A TWO-NEURAL STRUCTURE BECAUSE THE CENTERS OF THE SYMPATHETIC DIVISION OF THE AUTONOMIC NERVOUS SYSTEM ARE LOCALIZED IN THE BRAIN AND SPINAL CORD
1. НВН 2. ННН 3. ВВН 4. ВНН 5. ВВВ
PREGANGLIONARY SYMPATHETIC FIBERS ARE SHORTER THAN POSTGANGLIONARY, BECAUSE PREGANGLIONARY SYMPATHETIC NERVE FIBERS ARE TYPE B, AND POSTGANGLIONARY ARE TYPE C
1. НВН 2. ННН 3. ВВН 4. ВНН 5 ВВВ
PREGANGLIONARY SYMPATHETIC FIBERS ARE LONGER THAN POSTGANGLIONARY, BECAUSE PREGANGLIONARY NERVE FIBERS OF THE SYMPATHETIC DIVISION OF THE AUTONOMIC NERVOUS SYSTEM ARE TYPE B:
1. ВВВ 2. НВН 3. ВВН 4. ВНН 5. ННН
INTRAMURAL EFFERENT NEURONS OF THE HEART ARE A COMMON END PATHWAY FOR THE PARASYMPATHETIC AND METASYMPATHETIC DIVISIONS OF THE ANS, BECAUSE THEY TRANSMIT EXCITATION FROM BOTH THE PREGANLIONAR VAGUS FIBERS AND FROM THE INTRAMURAL INTERNEURONS:
1. НВН 2. ННН 3. ВВН 4. ВНН 5. ВВВ
THE METASYMPATHETIC NERVOUS SYSTEM REGULATES THE VISCERAL ORGANS FASTER THAN THE SYMPATHETIC AND PARASYMPATHETIC, BECAUSE METASYMPATHETIC REFLEXES ARE LOCAL PERIPHERAL
1. ВВВ 2. ННН 3. ВВН 4. ВНН 5. НВН
METASYMPATHETIC REGULATION MECHANISMS RELEASE THE CNS FROM EXCESSIVE INFORMATION, BECAUSE METASYMPATHETIC REFLEXES ARE LOCKED OUTSIDE THE CNS - IN THE INTRAMURAL GANGLIA
THE OBJECT OF INNERVATION OF THE SYMPATHETIC DIVISION OF THE AUTONOMIC NERVOUS SYSTEM IS THE WHOLE ORGANISM, BECAUSE THE SYMPATHETIC NERVE FIBERS FORM PLEXUS AROUND ALL VESSELS BRINGING BLOOD TO ORGANS AND TISSUE
1. НВН 2. ННН 3. ВВВ 4. ВНН 5. ВВН
WITH THE SIMULTANEOUS STOP OF IRRITATION OF THE SYMPATHETIC AND PARASYMPATHETIC NERVE FIBERS GOING TO THE HEART, THE EFFECT OF THE SYMPATHETIC NERVE LASTS LONGER BECAUSE THE ACTIVITY OF ACETYLCHOLINESTERASE IS HIGHER THAN THE ACTIVITY OF MONOAMINE OXIDASE
1. НВН 2. ННН 3 ВВВ 4. ВНН 5. ВВН
IN THE TISSUE OF INTERNAL ORGANS, THE MEDIATOR OF POSTGANGLIAR NERVE FIBERS CAN BE NORADRENALINE, ACETYLCHOLINE, HISTAMINE, BECAUSE THE ACTION OF POSTGANGLIONAR NERVE FIBERS IS REALIZED THROUGH ADRENO-, CHOLINO-, HISTAMINOREC. PTORY:
1. ВВВ 2. ННН 3. ВВН 4. ВНН 5 НВН
NORADRENALINE CAN CAUSE BOTH CONTRACTION AND DILATION OF ARTERIOLES BECAUSE THE EFFECT OF NORADRENALINE DEPENDS ON THE TYPE OF RECEPTORS (ALPHA AND BETA) WITH WHICH IT INTERACTS
1. НВН 2. ННН 3. ВВН 4. ВНН 5. ВВВ
MANY FUNCTIONS OF INTERNAL ORGANS (E.G. MOTOR) ARE PRESERVED AFTER CROSSING THE SYMPATHETIC AND PARASYMPATHETIC PATHWAYS BECAUSE THERE IS A METASYMPATHETIC SYSTEM INCLUDING GENERAL NEURONS IN THE WALLS OF THESE ORGANS TORA
1. НВН 2. ВВВ 3. ВВН 4. ВНН 5. ННН
PHYSIOLOGY OF BLOOD CIRCULATION
PHYSIOLOGY OF CARDIAC ACTIVITY
Choose one correct answer:
MINUTE VOLUME OF CARDIAC OUTPUT AT REST
1.5 - 2 liters;
3 - 3.5 liters;
4.5 - 5 liters.
25 -30 liters
3 - 3.5 liters;
4.5 - 5 liters;
8 - 10 liters.
THE MINUTE VOLUME OF CARDIAC OUTPUT DURING HEAVY PHYSICAL WORK IS EQUAL:
The left one is closed, the right one is open.
FLAP VALVES DURING A GENERAL PAUSE:
More than 120 -130 mm Hg.
More than 25 - 30 mm Hg.
More than 70 - 80 mm Hg.
IN THE LEFT VENTRICLE THE AORTIC VALVE OPENS AT PRESSURE:
Time of expulsion of blood from the ventricles;
Time from the beginning of ventricular relaxation to the closure of the semilunar valves;
Atrial contraction time;
PROTODIASTOLIC PERIOD IS:
Intracellular regulation;
SYNCHRONOUS CONTRACTION OF CARDIOMYOCYTES IS PROVIDED BY:
Intraorgan peripheral reflex;
Intercellular interaction;
Intracellular regulation.
STRENGTHENING THE CONTRACTION OF THE LEFT VENTRICLE DURING STRETCHING OF THE WALLS OF THE RIGHT ATRIUM IS PROVIDED BY:
Intracardiac peripheral reflex;
Intercellular interaction.
STRENGTHENING MYOCARDIAL CONTRACTIONS WITH AN INCREASE IN THE INITIAL LENGTH OF MUSCLE FIBERS IS PROVIDED BY:
Decreases;
Does not change;
First it increases, then it decreases;
Increasing.
DURING IRRITATION OF THE VAGUS NERVE, THE PERMEABILITY OF THE HEART MUSCLE MEMBRANE FOR POTASSIUM IONS:
Myocardial excitability;
Contraction forces;
Myocardial conductivity.
BATHMOTROPIC EFFECT ON HEART ACTIVITY IS A CHANGE:
Conductivity;
Forces of contractions;
Excitability;
INOTROPIC EFFECT ON HEART ACTIVITY IS A CHANGE:
Forces of contractions;
Excitability;
Myocardial conductivity.
DROMOTROPIC EFFECT ON HEART ACTIVITY IS A CHANGE:
Conductivity;
Forces of contractions;
Contraction frequencies;
Excitability.
CHRONOTROPIC EFFECT ON HEART ACTIVITY IS A CHANGE:
Positive inotropic, negative chronotropic;
Positive inotropic, positive chronotropic;
Negative inotropic, negative chronotropic;
Negative inotropic, positive chronotropic.
SYMPATHETIC NERVES HAVE EFFECTS ON THE HEART MUSCLE:
Acetylcholine;
Adrenalin;
Norepinephrine.
THE ENDINGS OF THE SYMPATHETIC NERVE IN THE HEART RELEASE:
Adrenalin;
Acetylcholine;
Serotonin.
THE TERMINATIONS OF THE VAGUS NERVE ARE RELEASED:
Depolarization of myocytes;
Hyperpolarization of myocytes
Activation of sodium channels;
Blockade of sodium channels.
WHEN APPLICATION OF HIGH CONCENTRATION ACETYLCHOLINE TO THE CARDIAC MUSCLE THE following will occur:
Increase in heart rate towards the end of exhalation;
Increased breathing due to arrhythmia;
Decrease in heart rate towards the end of exhalation.
RESPIRATORY ARRHYTHMIA OF THE HEART IS MANIFESTED IN:
Medulla oblongata;
THE CENTER OF SYMPATHETIC INNERVATION OF THE HEART IS LOCATED IN:
Medulla oblongata;
Upper cervical segments of the spinal cord;
Upper thoracic segments of the spinal cord.
THE CENTER OF PARASYMPATHETIC INNERVATION OF THE HEART IS LOCATED IN:
Extracardial and intracardial;
Extracardiac;
Intracardiac.
THE HEART HAS INNERVATION:
Heart rate when pressure changes in the arterial system;
The strength of heart contractions when the initial length of muscle fibers changes;
The strength of heart contractions when pressure changes in the arterial system or when the frequency of stimulation changes;
Resistance without changing diastolic filling.
THE HOMEOMETRIC MECHANISM OF REGULATION OF HEART WORK IS CHANGED IN:
Forces of heart contractions when pressure changes in the arterial system;
The strength of heart contractions with an increase in the initial length of muscle fibers;
Heart rates with changes in the initial length of muscle fibers.
THE HETEROMETRIC MECHANISM OF REGULATION OF HEART WORK IS CHANGED IN:
Changes in heart contractions when the initial length of muscle fibers changes;
Decreased heart rate when pressing on the eyeballs;
Reflex cardiac arrest due to irritation of mesenteric receptors.
THE LOAR REFLEX IS:
Changes in the force of heart contraction when the initial length of the muscle fiber changes;
Reflex cardiac arrest with a blow to the epigastric region;
THE DANINI-ASCHNER REFLEX IS:
Changes in the strength of heart contractions when the initial length of muscle fibers changes;
In changes in the force of heart contraction with changes in pressure in the arterial system;
Decreased heart rate when pressing on the eyeballs.
THE ANREPA EFFECT IS:
CAN HEART RATE CHANGE CONDITIONALLY-REFLEX?
THE ROLE OF THE HYPOTHALAMUS IN THE REGULATION OF HEART FUNCTION IS:
Conditioned reflex change in frequency;
Changes in contraction frequency when holding the breath;
Adaptation of heart function to real conditions.
Right hand - left foot;
Left leg - left hand;
Right hand - left hand.
ELECTRODES FOR ECG REGISTRATION IN 1 STANDARD LEAD ARE LOCATED AS follows:
Right hand - left hand;
Right hand - left foot;
Left hand - left foot.
ELECTRODES FOR ECG REGISTRATION IN STANDARD LEAD II ARE LOCATED AS follows:
Right hand - left hand, right foot;
Right hand - left foot, left hand;
Left hand - left leg, right leg.
ELECTRODES FOR ECG REGISTRATION IN THE I ENHANCED LEAD AVR ARE LOCATED AS follows:
Left hand - left foot;
Right hand - left foot;
Right hand - left foot.
ELECTRODES FOR ECG REGISTRATION IN STANDARD LEAD III ARE LOCATED AS follows:
Standard leads;
Wilson chest leads.
SINGLE-POLE ARE:
Excitation in the ventricles;
Repolarization in the ventricles;
Atrial excitation.
THE P WAVE ON THE ELECTROCARDIOGRAM REFLECTS:
Atrial excitation;
Excitation in the ventricles;
Repolarization in the ventricles.
THE QRS COMPLEX ON AN ELECTROCARDIOGRAM REFLECTS:
Excitation in the ventricles;
Atrial excitation;
Repolarization in the ventricles.
THE T WAVE ON THE ELECTROCARDIOGRAM REFLECTS:
Ventricular diastole;
Atrial systole;
General pause of the heart.
TP INTERVAL ON THE ELECTROCARDIOGRAM CORRESPONDING TO:
The nature of the occurrence and spread of excitation throughout the myocardium;
Cardiac output;
The strength of heart contractions.
BY ELECTROCARDIOGRAM YOU CAN JUDGE ABOUT:
Registration of total activity of cardiomyocytes;
Registration of the movement of the electrical axis of the heart in 3 projections.
THE ESSENCE OF THE VECTOR ELECTROCARDIOGRAPHY METHOD IS:
I HEART SOUND ARISES:
During the phase of rapid ventricular filling
When the flap valves slam shut
When the semilunar valves close
II HEART SOUND ARISES:
During the phase of rapid ventricular filling;
When the flap valves slam;
When the semilunar valves close.
III HEART SOUND IS RECORDED ON THE PHONOCARDIOGRAM:
During the phase of rapid ventricular filling;
When the flap valves slam;
With contraction of the atria and additional blood flow into the ventricles.
IV HEART SOUND IS RECORDED ON THE PHONOCARDIOGRAM:
In the second intercostal space to the right of the sternum;
To the right of the sternum at the base of the xiphoid process.
THE MITRAL VALVE IS BETTER TO AUDITIZE:
In the fifth intercostal space on the left, 1.5 cm medially from the midclavicular line;
TRIPLE VALVE IS BETTER TO AUDIT:
To the right of the sternum at the base of the xiphoid process;
From the second intercostal space. to the right of the sternum.
PULMONARY VALVE IS BETTER TO AUDITIZE:
To the right of the sternum at the base of the xiphoid process;
In the second intercostal space to the left of the sternum;
In the second intercostal space to the right of the sternum.
THE AORTIC VALVE IS BETTER TO AUDITIZE:
Measuring blood pressure in different phases of the cardiac cycle;
Measuring tissue resistance to electric current;
Measuring fluctuations in the volume of a body part depending on its filling with blood.
THE ESSENCE OF THE METHOD OF PLETHYSMOGRAPHY IS:
Phonocardiography;
Sphygmography;
Phase analysis of cardiac activity;
Ballistocardiography.
THE METHOD ALLOWS TO INVESTIGATE THE CONTRACTIVE FUNCTION OF THE MYOCARDIUM:
WHAT PRESSURE DEVELOPES IN THE ATRIA DURING SYSTOL?
WHICH VESSEL IS THE BLOOD SPREADED FROM THE RIGHT VENTRICLE?
superior vena cava;
Pulmonary artery;
Inferior vena cava;
Portal vein.
0.1-0.12 sec.
0.06-0.08 sec.
HOW LONG DOES 2ND HEART SOUND LAST?
Isotonic;
Isometrically;
HOW DOES THE HEART MUSCLE CONTRACT DURING THE TENSION PHASE?
0.12-0.18 sec.
WHAT IS THE DURATION OF ONE CARDIAC CYCLE?
Atrial systole;
At the end of the isometric tension phase;
Slow expulsion phase;
Diastole;
Rapid expulsion phase.
AT WHAT PHASE OF CONTRACTION DO THE SEMILUNA VALVES OF THE HEART OPEN?
WHAT IS THE BLOOD PRESSURE IN THE AORTA AT THE BEGINNING OF VENTRICULAR SYSTOLE?
WHAT POSITION ARE THE HEART VALVES LOCATED DURING THE GENERAL PAUSE?
The semilunar and leaflet valves are closed;
The semilunar and leaflet valves are open;
The lunates are closed, the valves are open;
Lunates are open, valves are closed.
WHAT VALUES DOES THE PRESSURE REACH IN THE RIGHT VENTRICLE DURING ITS SYSTOL?
WHAT VALUES DOES THE PRESSURE REACH IN THE LEFT VENTRICLE DURING ITS SYSTOLE AT THE HEIGHT OF THE EXILITION PHASE?
DOES BLOOD FROM THE HEART ENTER THE VENA CAVAS DURING ATRIAL SYSTOLE?
WHAT IS THE DURATION OF THE RAPID EXPELATION PHASE?
HOW LONG DOES THE FIRST HEART SOUND LAST?
0.1-0.12 sec.
0.06-09.08 sec.
Contractility and tonicity;
Automaticity and contractility;
Automaticity, excitability, conductivity, contractility,
Tonicity.
0.06-0.08 m/sec.
0.25-0.33 m/sec.
4.5 – 5.0 m/sec.
INDICATE THE SPEED OF EXCITATION PROPAGATION IN THE HISS BEAM:
INDICATE THE DELAY TIME IN THE ATRIOVENTRICULAR NODE:
WHICH IONS FLOW INTO THE CELL DETERMINES THE DEVELOPMENT OF THE PLATEAU PHASE OF CARDIOMYOCYTE AP?
WHAT FORMATION IS THE FIRST ORDER RHYTHMDRIVERS OF THE HEART?
Atrioventricular node;
Sinoatrial node;
Purkinje fibers;
Bundle of His.
A gradual increase in the PQ interval to 0-0.21 seconds followed by loss of the QRS complex;
There is a contraction of the atria in their own rhythm, and the ventricles in their own;
Loss of the QRS complex, without prior prolongation of the PQ interval.
WHAT IS AN INCOMPLETE SECOND DEGREE BLOCK EXPRESSED ON AN ECG?
Depolarization phase;
Rapid repolarization phase;
Slow repolarization;
Plateau phase;
TO WHICH AP PHASE DOES THE ST SEGMENT ON THE ECG CORRESPOND?
WILL THE VENTRICLES BE EXCITED IN COMPLETE TRANSVERSE HEART BLOCK?
WITH WHAT FREQUENCY CAN PULSES OCCUR IN THE ATRIOVENTRICULAR NODE?
40-50 per min.
70-80 per min.
30-40 per minute
10-20 per minute
WILL THE RIGHT VENTRICLE CONTRACT WHEN THE RIGHT BAND OF HISS IS BLOCKED?
WHAT LEADS ARE CALLED UNIPOLAR (SINGLE-POLE)?
Standard limb leads;
Chest leads;
Reinforced limb leads;
Chest and reinforced from the limbs.
Yes, to a threshold stimulus;
Yes, to a subthreshold stimulus;
Yes, to a suprathreshold stimulus.
CAN HEART TISSUE RESPOND TO ADDITIONAL IRRITATIONS DURING THE RELATIVE REFRACTORY PHASE?
To the atrioventricular node;
To the bundle of His;
To the sinoatrial node.
WHICH SECTION OF THE HEART DOES THE RIGHT VAGUS APPLY TO?
To the atrioventricular node;
To the bundle of His;
To the sinoatrial node.
WHICH COMPARTMENT OF THE HEART DOES THE LEFT VAGUS APPROPRIATE TO?
WHAT IS THE DURATION OF RELATIVE HEART REFRACTORY?
WHERE ARE THE BODIES OF THE FIRST PARASYMPATHETIC NEURONS INNERVATING THE HEART?
In the thoracic spinal cord;
In the cervical spinal cord;
In the medulla oblongata;
In the hypothalamus.
Negative dromotropic effect;
Negative bathmotropic effect.
WHAT IS A REDUCED EXCITABILITY OF THE HEART CALLED DURING STRONG VAGUS IRRITATION?
WHAT EXPLAINS THE PHENOMENON OF BOWDICH'S LADDER?
An increase in intracellular Ca ++ concentration;
An increase in intracellular K+ concentration;
An increase in intracellular Na+ concentration.
Negative inotropic effect;
Negative chronotropic effect;
WHAT IS THE DECREASE IN THE FORCE OF HEART CONTRACTIONS DURING IRRITATION OF THE VAGUS NERVE CALLED?
Negative inotropic effect;
Negative chronotropic effect;
Negative bathmotropic effect;
Negative dromotropic effect.
WHAT IS THE DECREASE IN HEART CONDUCTIVITY DUE TO IRRITATION OF THE VAGUS NERVE CALLED?
Predominant in both atria;
Predominant in the ventricles;
Evenly throughout all parts of the heart.
WILL THE CARDIAC MUSCLE RESPONSE WITH AN EXTRAORDINARY CONTRACTION TO THE ADDITIONAL IRRITATION DURING THE SHORTENING PERIOD?
WHAT IS THE SLOW OF HEART RATE DURING VAGUS IRRITATION CALLED?
Negative inotropic effect;
Negative chronotropic effect;
Negative bathmotropic effect;
Negative dromotropic effect.
Left atrium;
Right atrium;
Ventricles;
Atria and ventricles.
WHICH PARTS OF THE HEART ARE INNERVED BY SYMPATHETIC NERVES?
WHAT IS THE DURATION OF ABSOLUTE HEART REFRACTORY?
IS THERE A FUNCTIONAL CONNECTION BETWEEN ATYPICAL AND NERVE CELLS IN THE HEART?
HOW DOES THE FORCE OF VENTRICULAR CONTRACTION CHANGE WITH INCREASED RESISTANCE IN THE ARTERIAL SYSTEM?
Remains the same;
Increasing;
Decreasing.
CAN HEART TISSUE RESPOND TO IRRITATIONS DURING THE ABSOLUTE REFRACTORY PHASE?
CAN THE DURATION OF THE ABSOLUTE REFRACTORY PHASE CHANGE?
WHAT CHANGES IN HEART FUNCTION CAN BE OBSERVED AFTER CROSSING THE NERVES COMING FROM THE AORTIC ARCH AND CAROTID SINUS?
Reducing frequency;
No changes.
Aortic arch and carotid sinus;
Receptors of the eyeballs;
Reflexogenic zones of the stomach, intestines and peritoneum.
WHICH REFLEXOGENIC ZONE IS IRRITATED BY THE LOAR REFLEX?
Raise;
They don't change.
HOW DO CATECHOLAMINES INFLUENCE THE PERMEABILITY OF THE MEMBRANE FOR ENDOGENOUS CALCIUM?
Acetylcholine;
Serotonin;
Catecholamines;
Vasopressin;
Aldosterone.
WHAT IS ADENYLATE CYCLASE, INVOLVED IN THE REGULATION OF CARDIAC ACTIVITY, ACTIVATED?
Excess calcium, catecholamines;
Excess potassium, acetylcholine;
Excess sodium;
Excess calcium.
WHAT CHEMICALS INCREASE THE TONE OF THE VAGUS NERVES?
Potassium and chlorine;
Sodium and calcium;
FOR WHICH IONS DOES THE PERMEABILITY OF MEMBRANES CHANGE WHEN THEY ARE EXPOSED BY CATECHOLAMINES?
Between the atria and ventricles, proves the leading role of the atria in automation;
WHERE IS THE FIRST STANNIUS LIGATURE APPLIED, WHAT DOES IT PROVE?
Between the atria and ventricles proves the leading role of the atria in automation;
Between the venous sinus and the atria, proves the leading role of the venous sinus;
To the apex of the heart to prove the presence of myocardial excitability.
WHERE IS THE SECOND STANNIUS LIGATURE APPLIED, WHAT DOES IT PROVE?
Only when causing severe irritation;
Only when applying additional irritations during a general pause;
When applying strong irritations during diastole and pause.
WHEN DO EXTRASYSTOLES OCCUR DURING ADDITIONAL IRRITATION?
Atrioventricular;
Atrial;
Sinus.
WHAT EXTRASYSTOLES DO NOT HAVE A COMPENSATORY PAUSE?
There is a positive foreign and chronotropic effect;
There is a negative foreign and chronotropic effect;
Positive dromo- and negative bathmotropic influences are noted.
HOW WILL CARDIAC ACTIVITY CHANGE WHEN THE HEART IS EXPOSED TO ACETYLCHOLINE?
Increased and weakened contractions, stopping in the diastole phase;
Decrease and weakening of contractions, stopping in the systole phase;
Decrease and weakening of contractions, stopping in the diastole phase.
WHAT ARE THE CHANGES IN THE AMPLITUDE AND FREQUENCY OF HEART CONTRACTIONS AND IN WHAT PHASE DOES CARDIAC START OCCUR DUE TO EXCESS POTASSIUM IONS?
Will go down;
Will rise;
Will not change.
HOW DOES THE TONE OF THE VAGUS CENTERS CHANGE WHEN THE SINUS NERVE IS IRRITATED?
Excitability;
Conductivity;
Contractility;
Excitability and conductivity;
All of the above.
WHAT PROPERTIES OF THE HEART MUSCLE DOES ELECTROCARDIOGRAPHY ALLOW YOU TO STUDY IN DETAIL?
Increase in frequency and amplitude, stopping in the systole phase;
Strengthening and weakening of contractions, stopping in the diastole phase;
Strengthening and weakening of contractions, stopping in the systole phase.
WHAT ARE THE CHANGES IN HEART RATE AND AMPLITUDE AND IN WHAT PHASE DOES THE HEART STOP WITH EXCESS CALCIUM?
In the left atrium;
In the left ventricle;
In the right atrium;
In the right ventricle.
THE GREAT CIRCLE OF BLOOD CIRCULATION BEGINS.....
In the left atrium;
In the left ventricle;
In the right atrium;
In the right ventricle.
THE LARGE CIRCLE OF BLOOD CIRCULATION ENDS.....
In the left atrium;
In the left ventricle;
In the right atrium;
In the right ventricle.
THE SMALL CIRCULATION BEGINS.....
The time of one systole and one diastole of the ventricles and atria;
Ventricular systole, diastole and pause;
One heartbeat and blood ejection;
The time it takes the heart to pump all the blood through the circulation.
THE CYCLE OF THE HEART IS....
WITH A CYCLE DURATION OF 0.8 SECONDS, ATRIAL SYSTOLE DURATION:
WITH A CYCLE DURATION OF 0.8 SECONDS, THE DURATION OF ATRIAL DIASTOLE:
WITH A CYCLE DURATION OF 0.8 SECONDS, THE DURATION OF LEFT VENTRICLE SYSTOLE:
WITH A CYCLE DURATION OF 0.8 SECONDS, THE DURATION OF SYSTOLE OF THE RIGHT VENTRICLE:
WITH A CYCLE DURATION OF 0.8 SECONDS, THE DURATION OF LEFT VENTRICLE DIASTOLE:
DURATION OF RIGHT VENTRICLE DIASTOLE:
IN ONE SYSTOLE AT REST, THE RIGHT VENTRICLE EXPUTS:
250 ml of blood;
70 ml. blood;
30 ml of blood;
25 ml of blood.
250 ml of blood;
70 ml. blood;
30 ml of blood;
25 ml of blood;
IN ONE SYSTOLE AT REST, THE LEFT VENTRICLE EXPUTS:
250 ml of blood;
70 ml. blood;
30 ml of blood;
25 ml of blood;
IN ONE SYSTOLE AT REST THE LEFT ATRIUM EXPUTS....
250 ml of blood;
70 ml. blood;
30 ml of blood;
25 ml. blood;
8% of the blood volume in the ventricle.
IN ONE SYSTOLE AT REST, THE RIGHT ATRIUM EXPUTS:
50-60 per minute;
75 per second;
60-80 per minute;
80-100 per minute.
RESTING HEART RATE IN ADULTS...
60-80 per minute;
220 per minute;
140-150 per minute;
180 per minute.
MAXIMUM HEART RATE AT WHICH NO HEMODYNAMIC DISORDERS ARE OBSERVED:
140-160 per minute;
60-80 per minute;
120-140 per minute;
40-50 per minute.
FETAL HEART RATE:
100-110 per minute;
160-180 per minute;
80-90 per minute;
120-140 per minute.
HEART RATE IN A NEWBORN:
80-90 per minute;
60-80 per minute;
110-120 s minute;
140-160 per minute.
HEART RATE IN A 1 YEAR OLD CHILD:
Increased heart rate;
TACHYCARDIA IS.....
Decrease in heart rate;
Increased heart rate;
Increased heart rate;
Increasing the speed of excitation through the myocardium.
BRADYCARDIA IS...
The amount of blood ejected by two ventricles in one systole;
The amount of blood ejected by the left atrium in one systole;
The amount of blood ejected by each ventricle in one systole;
The amount of blood ejected by the atria during one systole.
SYSTOLIC VOLUME IS...
The amount of blood returning to the heart per minute;
The amount of blood filling the ventricles per minute;
The amount of blood ejected by each atrium per minute;
The amount of blood ejected by each ventricle per minute.
MINUTE VOLUME IS....
In the left atrium;
At the mouth of the inferior vena cava
Between the mouth of the superior vena cava and the right ear;
In the atrioventricular septum.
SINOATRIAL NODE IS LOCATED:
Conduction system of the heart;
Second order pacemaker;
A group of typical muscle cells of the heart that set its rhythm;
A group of atypical myocardial cells that set the rhythm of the heart.
PACEMAKER OF THE HEART IS....
The ability of heart cells to self-excite;
An increase in the degree of automation of sections of the conduction system with distance from the sinoatrial node;
Decreasing degree of automaticity with distance from the sinoatrial node;
Average degree of automation of all pacemaker cells.
AUTOMATION GRADIENT IS..
Sinoatrial node;
Atrioventricular node;
Conduction system of the heart;
Bundle of His.
THE FIRST ORDER RHYTHM DRIVERS IS:
Sinoatrial node;
Atrioventricular node;
Conduction system of the heart;
Bundle of His.
THE SECOND ORDER RHYTHM DRIVERS IS:
Sinoatrial node;
Atrioventricular node;
Conduction system of the heart;
Bundle of His.
THE THIRD ORDER RHYTHM DRIVERS IS:
Right atrium;
Lower third of the ventricles;
All sections are automatic;
Purkinje fibers.
THE SECTION OF THE CONDUCTING SYSTEM DOES NOT HAVE ITS OWN AUTOMATION IN THE AREA:
0.9-1.0 cm/sec.
0.9-1.0 m/sec.
EXCITATION ACROSS THE MYOCARDIUM SPREADS AT THE SPEED OF:
0.02-0.05 s/sec
EXCITATION SPREADS AT SPEED ALONG THE HIS BUNCH.....
0.02-0.05 m/sec.
0.08-1 m/sec.
IN THE ATRIOVENTRICULAR NODE EXCITATION SPREADS AT SPEED.....
Rest of the heart;
Ensuring synchronous contraction of the ventricles;
Ensuring the heart is fully filled with blood;
Coordination of contractions of the atria and ventricles.
THE DELAY OF EXCITATION IN THE ATRIOVENTRICULAR NODE HAS THE FOLLOWING PHYSIOLOGICAL SIGNIFICANCE:
ABSOLUTE REFRACTORY OF THE CARDIAC MUSCLE IS......
The time during which the heart muscle responds only to suprathreshold stimuli;
The time during which the heart muscle does not respond to any stimuli;
The time during which the heart muscle is relaxed;
The time when the heart muscle responds only to subthreshold stimuli.
RELATIVE REFRACTORY OF THE CARDIAC MUSCLE IS....
DURATION OF THE PERIOD OF ABSOLUTE MYOCARDIAL REFRACTORY:
DURATION OF THE PERIOD OF RELATIVE MYOCARDIAL REFRACTORY:
FRANK-STARLING'S LAW CHARACTERIZES ............. MYOCARDIAL:
Conductivity;
Contractility;
Excitability;
Automation.
The less the heart stretches during diastole, the stronger its contraction during systole;
Increased elongation of the heart during diastole leads to increased contraction during systole;
The higher the blood pressure in the aorta, the greater the force of contraction of the ventricular myocardium.
THE FRANK-STARLING LAW IS THAT. WHAT:
Does not change;
Decreases;
Increases;
WHEN IRRITATION OF THE VAGUS NERVE, MYOCARDIAL EXCITABILITY.....
Does not change;
Decreases;
Increases;
First it rises, then it falls.
WHEN THE SYMPATHETIC NERVE IS IRRITATED, THE MYOCARDIAL EXCITABILITY.....
Does not change;
Decreases;
Increases;
First it rises, then it falls;
First it falls, then it rises.
WHEN THE VAGUS NERVE IS IRRITATED, MYOCARDIAL CONDUCTIVITY.....
Does not change;
Decreases;
Increases;
First it rises, then it falls;
First it falls, then it rises.
WHEN THE SYMPATHETIC NERVE IS IRRITATED, MYOCARDIAL CONDUCTIVITY.....
Does not change;
Decreases;
Increases;
First it rises, then it falls;
First it falls, then it rises.
WHEN THE VAGUS NERVE IS IRRITATED, MYOCARDIAL CONTRACTILITY.....
Does not change;
Decreases;
Increases;
First it rises, then it falls;
First it falls, then it rises.
WHEN THE SYMPATHETIC NERVE IS IRRITATED, MYOCARDIAL CONTRACTILITY.....
Does not change;
Decreases;
Increases;
First it rises, then it falls;
First it falls, then it rises.
WHEN THE VAGUS NERVE IS IRRITATED, THE FREQUENCY OF MYOCARDIAL CONTRACTIONS.....
Does not change;
Decreases;
Increases;
First it rises, then it falls;
First it falls, then it rises.
WHEN THE SYMPATHETIC NERVE IS IRRITATED, THE FREQUENCY OF MYOCARDIAL CONTRACTIONS.....
High, sonorous, drawn-out;
Short, sonorous, low;
High, drawn-out, dull;
Low, drawn-out, dull.
SOUND CHARACTERISTICS OF THE FIRST HEART SOUND:
High, sonorous, short;
Short, sonorous, low;
High, drawn-out, dull;
Low, drawn-out, dull.
SOUND CHARACTERISTICS OF THE SECOND HEART SOUND:
Closure of the semilunar valve, closure of the atrioventricular valves, vibration of the aortic wall;
Vibrations during myocardial contraction, opening of the mitral valve, closing of the atrioventricular valves, vascular noise;
Vibrations of the walls of the heart during myocardial contraction, closure of atrioventricular valves, opening of semilunar valves, vascular murmur;
Closing of the semilunar valves, opening of the atrioventricular valves, vibration of the heart walls during myocardial relaxation, vascular murmur.
THE CAUSE OF THE FIRST HEART SOUND ARE SOUND PHENOMENA ARISING FROM:
Closure of the semilunar valve, closure of the atrioventricular valves, vibration of the aortic wall;
Vibration during myocardial contraction, opening of the mitral valve, closing of the atrioventricular valves, vascular noise;
Vibration during myocardial contraction, closure of atrioventricular valves, opening of semilunar valves, vascular noise;
Vibration during myocardial relaxation, closure of semilunar valves, opening of atrioventricular valves, vascular noise.
THE FOLLOWING SOUND COMPONENTS ARE THE CAUSE OF THE SECOND HEART SOUND:
Atrial systole.
Release of blood from the ventricles.
The impact of blood on the aortic valves.
Filling of the ventricles with blood during diastole.
REASON FOR A THIRD HEART SOUND:
Filling of the ventricles with blood during diastole;
Ventricular systole;
Atrial systole;
Relaxation of the atria.
REASON FOR A FOURTH HEART SOUND:
Pumping function;
Regulation of vascular blood flow;
Hematopoietic function.
THE FUNCTION OF THE HEART IS... .
Reduced vascular resistance;
Due to the periodic repetition of systole and diastole;
Thanks to blood flow to the heart.
THE PUMPING FUNCTION OF THE HEART IS CARRIED OUT... .
General systole;
Atrial systole;
Ventricular systoles.
EACH INDIVIDUAL CYCLE OF CARDIAC ACTIVITY STARTS WITH
Ventricular systole;
Ventricular diastole;
Compensatory pause.
WITH THE END OF ATRIAL SYSTOLE, IT BEGINS... .
Compensatory pause;
General pause;
Ventricular diastole.
THE END OF VENTRICULAR SYSTOL IS FOLLOWED BY... .
Breathing movements;
Anatomical structure of veins;
The presence of a heart valve apparatus.
ONE-WAY BLOOD FLOW IN THE DIRECTION “ATRIUM - VENTRICLES - AORTA” IS PROVIDED... .
Release of blood into the ventricles and veins;
Unidirectional flow of blood from the atria to the ventricles;
Its back and forth movement into the ventricles and back.
BLOOD MOVEMENT DURING ATRIAL CONTRACTION IS CHARACTERIZED... .
Valvular apparatus of veins;
Flap valves;
The sequence of contraction of the atrium muscles, which ensures compression of the mouth of the vena cava in the first place.
WHAT CAUSES ONE-WAY BLOOD MOVEMENT IN ATRIAL SYSTOLE?
Korotkov method;
Intracardiac sounding method;
Riva-Rocci method.
WHAT IS THE BASIC METHOD FOR DETERMINING PRESSURE IN THE CAVITIES OF THE HEART?
25-30 mm. rt. Art.
70-80 mm. rt. Art.
5 - 8 mm. rt. Art.
0 mm. rt. Art.
AT THE HEIGHT OF SYSTOL, BLOOD PRESSURE IN THE ATRIMS REACHES.
25-30 mm. rt. Art.
70-80 mm. rt. Art.
5 - 8 mm. rt. Art.
0 mm. rt. Art.
DURING DIASTOLE, BLOOD PRESSURE IN THE ATRIMS DECREASES TO... .
25-30 mm. rt. Art.
70-80 mm. rt. Art.
120-130 mm Hg.
AT SYSTOLIC HEIGHT, BLOOD PRESSURE IN THE LEFT VENTRICLE REACHES
EXPELATION OF BLOOD FROM THE LEFT VENTRICLE BEGINS AT A BLOOD PRESSURE IN THE AORTA EQUAL TO... MM. RT. ST.
AT THE HEIGHT OF SYSTOL, BLOOD PRESSURE IN THE RIGHT VENTRICLE REACHES... .
70-80 mm. rt. Art.
120-130 mm. rt. Art.
25-30 mm. rt. Art.
EXPELATION OF BLOOD FROM THE RIGHT VENTRICLE BEGINS AT A BLOOD PRESSURE IN THE PULMONARY ARTERY EQUAL TO... MM. RT. ST.
WHAT EFFECT OF THE ACTIVITY OF THE SEMILUNARY VALVES IS PROVIDED BY THE PAPILLARY MUSCLES WITH TENDON FILMS?
Retention of the leaflet valves during ventricular systole and thereby preventing the return of blood to the aorta;
Full flow of blood into the ventricle during diastole;
Retention of the leaflet valves during ventricular systole and thereby preventing the return of blood to the aorta;
Retains the leaflet valves during ventricular systole and thereby prevents blood from returning to the atrium.
WHAT EFFECT OF LEAF VALVES ACTIVITY IS PROVIDED BY PAPILLARY MUSCLES WITH TENDON FILMS?
Possibility of ejection of blood from the right ventricle into the aorta;
Obstruction of blood flow from the aorta to the left ventricle during ventricular diastole;
Possibility of ejection of blood from the right ventricle into the pulmonary trunk.
THE AORTIC SEMILUNA VALVE PROVIDES... .
Differences in blood pressure between the ventricle and the aorta;
CLOSURE OF THE AORTIC SEMILUNA VALVE OCCURS DUE TO... .
Differences in blood pressure in the ventricle and in the pulmonary trunk;
Activity of special structures of the left ventricle;
The volume of blood entering the ventricle during atrial systole.
CLOSING OF THE SEMILUNA VALVE OF THE PULMONARY ARTERY OCCURS DUE TO... .
The left one is closed, the right one is open;
SEMILUNARY VALVES DURING A GENERAL PAUSE... .
The left one is closed, the right one is open;
SEMILUNA VALVES DURING VENTRICULAR DIASTOLE... .
Stenosis;
Insufficiency;
DISRUPTION OF THE FUNCTIONAL ACTIVITY OF THE HEART VALVE IN THE FORM OF INCOMPLETE CLOSURE OF THE SYSTEM IS CALLED... .
Stenosis;
Insufficiency;
DISRUPTION OF THE FUNCTIONAL ACTIVITY OF THE HEART VALVE IN THE FORM OF NARROWING OF THE VALVE ORIFICE OF THE ACASTUS IS CALLED... .
IN A RESTING STATE, THE VENTRICLES ARE RELEASED...% OF THE VOLUME OF BLOOD CONTAINED IN THEM.
AT MAXIMUM SYSTOL,...% OF THE VOLUME OF BLOOD CONTAINED IN THEM IS RELEASED FROM THE VENTRICLES.
THE RESERVE VOLUME OF BLOOD OF THE VENTRICLE IS...:
The amount of blood that the heart can additionally eject at maximum systole;
The volume of blood remaining in the ventricle after normal systole;
The volume of blood remaining in the heart after systole;
The volume of blood remaining in the ventricle after systole;
The volume of blood remaining in the ventricle after maximum systole.
THE RESIDUAL VOLUME OF THE VENTRICLE IS CALLED... .
The maximum systolic volume of blood that can be ejected by the ventricle due to the maximum volume of atrial systole;
Ventricular reserve volume;
The maximum systolic volume of blood that can be ejected by the ventricle due to the maximum expulsion of the normal and reserve volumes.
WHAT IS MAXIMUM SYSTOL?
3 - 3.5 liters;
8 - 10 liters;
4.5 - 5 liters;
25 - 30 liters.
THE MINUTE VOLUME OF CARDIAC OUTPUT DURING HEAVY PHYSICAL WORK IS EQUAL... .
Exclusively due to heart rate;
Only due to an increase in systolic ejection;
Due to an increase in heart rate and systolic ejection;
Due to respiratory arrhythmia.
INCREASE IN IOC OCCURS:
Lomonosov;
THE MOST ACCURATE AND PHYSIOLOGICAL METHOD FOR DETERMINING IOC IS PROPOSED:
Heart rate, respiratory rate, amount of exhaled CO2;
Arteriovenous oxygen difference and the amount of oxygen absorbed in 1 minute;
TO DETERMINE MOC USING THE FIC METHOD YOU NEED TO KNOW... .
From the kinetic energy of the blood ejected by the ventricles;
Contraction of skeletal muscles, promoting blood flow to the heart;
From contractions of vascular smooth muscles.
WHAT IS THE RESIDUAL FORCE OF CARDIAC CONTRACTING FORMED FROM, PROMOTING THE FLOW OF BLOOD TO THE HEART?
Not applicable;
Refers to active;
Refers to passive.
MUSCLE PUMP... FACTORS OF FILLING THE HEART WITH BLOOD.
Kinetic energy of blood released by the ventricles;
Contractions of skeletal muscles, promoting the flow of blood to the heart due to the presence of valves in the veins;
Contractions of the skeletal muscles of the lower extremities and automatic contractions of the walls of small veins.
WHAT SHOULD BE UNDERSTANDED BY MUSCLE PUMP
Smooth muscles of the intestines and parenchymal organs;
Smooth muscle of the vascular wall;
Skeletal muscles of the lower extremities.
WHICH MUSCLE MAKES THE BIGGEST CONTRIBUTION TO THE SO-CALLED MUSCLE PUMP?
Does not apply to..;
Refers to active;
Refers to passive.
RESPIRATORY PUMP... FACTORS OF FILLING THE HEART WITH BLOOD.
During exhalation, the pressure on the mediastinal organs decreases, which facilitates blood flow to the heart;
During inhalation, the pressure experienced by the mediastinal organs increases, which leads, in particular, to compression of the vena cava and an increase in blood flow to the heart;
Expansion of the lung during inhalation promotes the movement of blood through the microvasculature of the pulmonary circulation;
During inhalation, the pressure in the vena cava and atria decreases, which promotes blood flow to the heart.
WHAT IS THE ESSENCE OF A BREATHING PUMP?
Displacement of the atrioventricular septum during systole into the ventricular cavity;
Compression of the elastic component of the myocardium during ventricular systole and its expansion during diastole;
Active expansion of the coronary arteries, filled with blood during diastole;
Factors 2 and 3;
All of the above factors.
THE ACTIVITY OF THE HEART PUMP IS PROVIDED... .
Mechanical;
Sound;
Electrical;
Mechanical and sound;
Mechanical, sound, electrical.
EXTERNAL MANIFESTATIONS OF THE HEART ACTIVITY INCLUDE... MANIFESTATIONS.
Vectorcardiogram;
Heart beat;
Apex impulse;
Cardiac and apical impulse.
MECHANICAL MANIFESTATIONS OF HEART ACTIVITY NORMALLY INCLUDE... .
Palpation and visual;
Vectorcardiography;
Electrocardiography.
THE PRESENCE OF AN APEXIC IMPLICUS IS DETERMINED USING:
Palpation;
Apexcardiography;
Electrocardiography.
REGISTRATION OF THE HEART IMPACT IS PRODUCED USING:
Apex impulse;
APEX CARDIOGRAPHY IS A GRAPHIC RECORDING
Oscillations of the chest that occur during the activity of the heart;
Apex impulse;
Vibrations of the body that occur during the activity of the heart.
BALLISTOCARDIOGRAPHY IS A GRAPHIC REGISTRATION... .
Phonocardiography and auscultation;
Percussion and electrocardiography;
Auscultation and ballistocardiography.
METHODS FOR STUDYING SOUND MANIFESTATIONS OF HEART ACTIVITY INCLUDE... .
Auscultation;
Phonocardiography;
Ballistocardiography.
A SUBJECTIVE METHOD FOR REGISTRATION OF SOUND PHENOMENA OF HEART ACTIVITY IS:
Auscultation;
Phonocardiography;
Ballistocardiography.
AN OBJECTIVE METHOD FOR REGISTRATION OF SOUND PHENOMENA OF HEART ACTIVITY IS:
Sound phenomena that occur during the cardiac cycle;
Sound phenomena recorded during heart contractions;
All of the above.
WHAT ARE HEART TOnes?
Match up;
Mostly not the same;
The same in newborns.
PLACES OF PROJECTION OF THE HEART VALVES ON THE FRONT SURFACE OF THE CHEST... WITH THE PLACE OF THEIR BEST AUSING.
To the right of the sternum at the base of the xiphoid process;
In the second intercostal space to the right of the sternum.
THE MITRAL VALVE IS BETTER AUDITABLE
At the base of the xiphoid process;
In the fifth intercostal space on the left, 1.5 cm medial from the midclavicular line;
In the second intercostal space to the right of the sternum.
THREE LEAF VALVE IS BETTER TO AUDIT... .
To the right of the sternum at the base of the xiphoid process;
In the second intercostal space to the left of the sternum;
In the second intercostal space to the right of the sternum.
THE PULMONARY ARTERY VALVE IS BETTER AUDIBLE... .
To the right of the sternum at the base of the xiphoid process;
In the second intercostal space to the left of the sternum;
In the second intercostal space to the right of the sternum.
THE AORTIC VALVE IS BETTER AUDIBLE... .
Contractility and tonicity;
Tonicity, excitability, conductivity;
Tonicity, automaticity and contractility;
Automaticity, excitability, conductivity, contractility.
INDICATE THE MAIN PROPERTIES OF THE CARDIAC MUSCLE:
Provide contractile function of the myocardium;
Form the conduction system of the heart;
They form the valve apparatus of the heart.
ATYPICAL CONTRACTIVE ELEMENTS OF THE MYOCARDIAL:
Atrioventricular node - sinoatrial node - Hiss bundle - Hiss legs - typical cardiomyocytes;
Sinoatrial node - atrioventricular node - Hiss bundle - Hiss legs - Purkinje fibers - typical cardiomyocytes;
Sinoatrial node - Hiss bundle - atrioventricular node - Hiss legs - typical cardiomyocytes.
WHAT IS THE NORMAL SEQUENCE OF EXCITATION THROUGH THE HEART CONDUCTION SYSTEM?
At the mouth of the vena cava;
WHERE IS THE FIRST ORDER RHYTHM DRIVERS LOCATED?
At the mouth of the vena cava;
On the right atrioventricular septum;
In the interventricular septum.
WHERE IS THE SECOND ORDER RHYTHM DRIVER LOCATED?
At the mouth of the vena cava;
On the right atrioventricular septum;
In the interventricular septum.
WHERE IS THE THIRD ORDER RHYTHM DRIVERS LOCATED?
SPONTANEOUS PULSES IN THE SINOATRIAL NODE NORMALLY OCCUR WITH A FREQUENCY... IMPULS/MIN.
IMPULSES IN THE SINOATRIAL NODE ARISE... .
Under the influence of the cerebral hemispheres;
Under the influence of efferent impulses of the cardiac center of the medulla oblongata;
Spontaneously.
SPONTANEOUS IMPULSES IN THE ATRIOVENTRICULAR NODE APPEAR AT A FREQUENCY... IMPULS/MIN.
NORMALLY, PULSATION FROM THE ATRIOVENTRICULAR NODE IS DETERMINED BY THE FREQUENCY OF EXCITATION... .
First order pacemaker;
Second order pacemaker;
Third order pacemaker.
SPONTANEOUS PULSES IN THE HISS BEAM APPEAR WITH A FREQUENCY... IMPULS/MIN.
THE SAME FOR CARDIOMYOCYTE AND SKELETAL MUSCLE FIBER IS... .
The presence of intercellular contacts – nexuses;
Automatic ability;
The resting potential is determined almost entirely by the concentration gradient of potassium ions.
Extrasystole;
Implementation of pacemaker property;
Compensatory pause;
The emergence of an action potential.
WHEN A TYPICAL CARDIOMYOCYTE IS EXPOSED IN A RESTING STATE TO AN ADEQUATE STIMULAR WITH A FORCE OF ONE THRESHOLD,... .
THE ACTION POTENTIAL OF A TYPICAL CARDIOMYOCYTE IS AN AVERAGE.
THE AMOUNT OF ACTION POTENTIAL OF A TYPICAL CARDIOMYOCYTE ...... THE AMOUNT OF ACTION POTENTIAL OF A SKELETAL MUSCLE MYOCYTE.
Compliant;
400-600 ms.
300-400 ms.
150-200 ms.
110-130 ms.
THE DURATION OF THE ACTION POTENTIAL OF A TYPICAL CARDIOMYOCYTE IS ON AVERAGE.
Duration, shape, sequence of ionic currents;
Duration, sequence of ion currents;
Sequence of ion currents.
THE ACTION POTENTIAL OF A TYPICAL CARDIOMYOCYTE IS DIFFERENT FROM THE ACTION POTENTIAL OF A SKELETAL MUSCLE MYOCYTE... .
THE PHASE OF RAPID DEPOLARIZATION OF A CARDIOMYOCYTE IS DETERMINED BY THE FLOW OF IONS... INTO THE CELL.
THE INITIAL PART OF THE REPOLARIZATION PHASE OF THE CARDIOMYOCYTE AP IS ASSOCIATED WITH AN INCREASE IN THE CURRENT OF IONS... FROM THE CELL.
THE PLATEAU PHASE OF CARDIOMYOCYTE PD IS DETERMINED BY IONIC CURRENTS... .
Sodium and calcium from the cell, chlorine - into the cell;
Sodium and calcium into the cell, potassium out of the cell;
Calcium into the cell, potassium out of the cell.
WHICH IONS FROM THE CELL FLOW DUE TO THE DEVELOPMENT OF THE RAPID REPOLARIZATION PHASE?
SLOW DIASTOLIC DEPOLARIZATION IS CHARACTERISTIC TO CELLS:.
Pacemakers of the heart;
Cardiomyocytes;
Skeletal muscle fibers.
2.3-2.4 ms..
0.27-0.28 sec..
0.023-0.024 sec.
WHAT IS THE DURATION OF ABSOLUTE REFRACTORY OF TYPICAL CARDIOMYOCYTES?
Displacement of the ECG curve from the isoline;
Isoline section;
Artifact.
WHAT DO YOU MEAN BY ECG WAVE?
A set of teeth.
WHAT DO YOU MEAN BY ECG SEGMENT?
The isoline section between the end of one tooth and the beginning of the next;
The tooth and the isoline section following it;
A set of teeth.
WHAT DOES ECG INTERVAL MEAN?
The isoline section between the end of one tooth and the beginning of the next;
The tooth and the isoline section following it;
A collection of teeth and intervals.
WHAT SHOULD BE UNDERSTANDED BY COMPLEX ON AN ECG?
Wilson;
Einthoven;
Korotkov.
THE DIAGRAM OF MODERN STANDARD DOUBLE-POLE LEADINGS WAS PROPOSED IN 1913... .
UNIPOLAR ENHANCED ABSOLUTION OF THE RIGHT ARM IS DEDICATED AS... .
UNIPOLAR REINFORCED ABSOLUTION OF THE LEFT ARM IS DEDICATED AS... .
UNIPOLAR ENHANCED ABLEDDER OF THE LEFT LEG IS DESIGNATED AS... .
WHAT IS WILSON'S FIRST CHORACIC UNIPOLAR ADVANCE DESIGNATED?
WHERE IS THE ELECTRODE PLACED TO RECORD LEAD V1?
In the 4th intercostal space along the right edge of the sternum;
In the 4th intercostal space along the left edge of the sternum;
At the level of the 5th rib along the left parasternal line.
WHERE IS THE ELECTRODE PLACED TO RECORD LEAD V2?
1. In the 4th intercostal space along the right edge of the sternum;
2. In the 4th intercostal space along the left edge of the sternum;
3. At the level of the 5th rib along the left parasternal line.
WHERE IS THE ELECTRODE PLACED TO RECORD LEAD V3?
WHERE IS THE ELECTRODE PLACED TO RECORD LEAD V4?
In the 5th intercostal space along the left anterior axillary line;
In the 5th intercostal space along the left midclavicular line;
In the 5th intercostal space along the midaxillary line.
WHERE IS THE ELECTRODE PLACED TO RECORD LEAD V5?
In the 5th intercostal space along the left anterior axillary line;
In the 5th intercostal space along the left midclavicular line;
B. 5th intercostal space along the midaxillary line.
WHERE DOES THE ELECTRODE PLACE TO RECORD LEAD V6?
0.1 - 0.2 sec.
0.12 – 0.18 sec.
0.06 - 0.09 sec.
THE DURATION OF THE PQ INTERVAL ON THE ELECTROCARDIOGRAM IS NORMALLY EQUAL TO...
0.1 - 0.2 sec.
0.12 - 0.18 sec.
0.06 - 0.1 sec.
THE NORMAL DURATION OF THE QRS COMPLEX ON THE ELECTROCARDIOGRAM IS... .
WHAT IS THE RELATIONSHIP OF THE VOLTAGE OF THE P AND R WAVES IN LEAD II IN A HEALTHY PERSON?
TO WHAT PHASE OF CARDIOMYOCYTE PD DOES THE ST SEGMENT ON THE ECG CORRESPOND?
Depolarization phase;
Rapid repolarization phase;
Slow repolarization phase;
Plateau phase;
The phase of supernormal excitability.
Blockade;
Extrasystole;
Remission;
Arrhythmia.
DISRUPTION OF HEART RHYTHM IS CALLED
Endocardial, myocardial and pericardial;
Ventricular and atrial;
Transmural and non-transmural.
HOW ARE EXTRASYSTOLES CLASSIFIED BY THE LOCATION OF THE ECTOPIC FOCUS OF EXCITATION?
Change in the shape of the P wave or fusion with the ventricular complex;
Reduced R wave voltage.
HOW WILL A UNILATERAL VENTRICULAR EXTRASYSTOLIA AFFECT THE ECG FORM?
Sharp distortion of the ventricular complex;
Change in the direction of the P wave or fusion with the ventricular complex;
Reduced R wave voltage.
WHAT IS AN ECG SIGN OF EXTRASYSTOLE ARISING FROM THE ATRIOVENTRICULAR NODE?
WILL THERE BE A COMPENSATORY PAUSE DURING SINUS EXTRASYSTOLE?
WILL THERE BE A COMPENSATORY PAUSE DURING ATRIOVENTRICULAR EXTRASYSTOLE?
DISRUPTION OF EXCITATION THROUGH THE CONDUCTION SYSTEM OF THE HEART IS CALLED:
Blockade;
Extrasystole;
In remission.
Stable rhythm of ventricular complex loss with normal PQ;
WHAT IS A SIGN OF 1st DEGREE BLOCK ON ECG?
Increasing duration of PQ with loss of the ventricular complex at maximum PQ;
Sinus rhythm with stable PQ equal to 0.2-0.3;
Stable rhythm of ventricular complex loss with normal PQ.
Contractions of the atria and ventricles in their own modes
WHAT IS A SIGN OF SECOND DEGREE BLOCK ON ECG?
A few days later;
After 5-10 cardiac cycles;
After 1-4 heart contractions.
HOW OFTEN DOES THE QRS COMPLEX OCCUR IN 2ND DEGREE BLOCK?
Increasing PQ duration with loss of the ventricular complex after one contraction;
Sinus rhythm with stable PQ equal to 0.2-0.3;
Stable rhythm of loss of one or more ventricular complexes with normal PQ;
Contractions of the atria and ventricles in their own modes.
WHAT IS A SIGN OF 3rd DEGREE BLOCK ON ECG?
Every fifth cardiac systole is absent;
For every 4 atrial systole there is 1 ventricular systole;
Every fourth atrial systole is absent.
WHAT IS THE III DEGREE HEART BLOCK INDICATED BY A PARTICULAR PATIENT'S PROPORTION OF 4:1?
Increasing duration of PQ with loss of the ventricular complex at maximum PQ;
Sinus rhythm with stable PQ equal to 0.2-0.3;
stable rhythm of ventricular complex loss with normal PQ;
Excitation of the atria and ventricles in their own modes.
WHAT IS A SIGN OF COMPLETE HEART BLOCK ON ECG?
Will not change;
Will be violated;
Heart rate will increase.
HOW WILL THE HEART RHYTH CHANGE DURING 1ST DEGREE BLOCK?
Will not change;
Will be violated;
Heart rate will increase.
HOW WILL THE HEART RHYTH CHANGE DURING 2nd DEGREE BLOCK?
Does not change;
Increasing.
Decreases
Changes according to the body's needs
CARDIAC ACTIVITY... DURING THE DAY.
Saving energy costs and adapting to external and internal environmental conditions;
Constant readiness for intense physical activity;
Always ready to sleep.
WHAT IS THE PURPOSE OF CARDIAC VARIABILITY?
Molecular, cellular, systemic;
Humoral, nervous, tissue;
Cellular, organ, systemic.
WHAT ARE THE LEVELS OF CARDIAC REGULATION?
Intracellular regulation;
intracardiac peripheral reflex;
Intercellular interaction.
SYNCHRONOUS CONTRACTION OF CARDIOMYOCYTES IS PROVIDED... .
Intracardiac peripheral reflex;
Intracellular regulation
Intercellular interaction
STRENGTHENING THE CONTRACTION OF THE LEFT VENTRICLE DURING STRETCHING OF THE WALLS OF THE RIGHT VENTRICLE IS PROVIDED BY:
Intracardiac peripheral reflex;
Intracellular self-regulation;
Intercellular interaction.
STRENGTHENING MYOCARDIAL CONTRACTIONS WITH AN INCREASE IN THE INITIAL LENGTH OF MUSCLE FIBERS (FRANK-STARLING LAW) IS PROVIDED BY:
Minimal stretching of the heart muscle;
Stretching the muscle not exceeding its physiological capabilities (30% more than the original length);
Stretching the muscle by 50-60% of its original length.
THE FRANK-STARLING LAW APPEARS WHEN... .
Accumulation of potassium ions near myofibrils;
Accumulation of calcium ions near myofibrils;
Deficiency of calcium ions in the sarcoplasmic reticulum.
WHAT IS THE MECHANISM OF THE PHENOMENON OF THE BOWDICH LADDER AND THE ANREPA EFFECT?
Does not affect;
Excitability decreases;
Excitability increases;
HOW DOES WEAK IRRITATION OF THE VAGUS NERVE AFFECT MYOCARDIAL EXCITABILITY?
Does not affect;
Excitability decreases;
Excitability increases;
Excitability first increases and then decreases.
HOW DOES STRONG IRRITATION OF THE VAGUS NERVE AFFECT MYOCARDIAL EXCITABILITY?
Left vagus;
Right vagus;
Sympathetic nerve.
TROPHIC CARDIAC NERVE ACCORDING TO PAVLOV IS... .
Not expressed at all;
Strongly expressed;
Plays a minor role.
IN THE REGULATION OF CARDIAC ACTIVITY TONE OF N. VAGUS
Tachycardia will occur;
Bradycardia will occur.
HOW IS THE INTRODUCTION OF ATROPINE OR CARDIAC DENERVATION FROM THE INFLUENCE OF N. VAGUS AFFECTED CARDIAC ACTIVITY?
Excitability increases;
Does not affect;
Excitability decreases;
Excitability first increases and then decreases.
HOW DOES SYMPATHETIC NERVE IRRITATION AFFECT MYOCARDIAL EXCITABILITY?
Does not affect;
Contractility decreases;
Contractility increases.
HOW DOES IRRITATION OF THE VAGUS NERVE AFFECT MYOCARDIAL CONTRACTILITY?
Contractility first increases and then decreases;
Contractility first decreases and then increases;
Contractility decreases;
Contractility increases.
HOW DOES IRRITATION OF THE SYMPATHETIC NERVE AFFECT MYOCARDIAL CONTRACTILITY?
Acetylcholine;
Adrenalin;
Norepinephrine.
THE TERMINATIONS OF THE SYMPATHETIC NERVE INNERVATING THE HEART ARE RELEASED... .
Acetylcholine;
Adrenalin;
Serotonin.
THE TERMINATIONS OF THE VAGUS NERVE ARE RELEASED... .
Hyperpolarization of myocytes
Depolarization of myocytes
Activation of sodium channels
WHEN APPLICATION OF ACETYLCHOLINE ON THE CARDIAC MUSCLE WILL OCCUR
Will not change;
Will increase;
Will decrease.
WHEN APPLICATION OF NORADRENALINE ON THE CARDIAC MUSCLE, THE PERMEABILITY OF CARDIOMYOCYTE MEMBRANES FOR CALCIUM IONS... .
Decrease in heart rate;
Increased strength and frequency of contractions.
Decreased strength and frequency of contractions
HOW DOES HYPERKALEMIA AFFECT THE HEART?
Only ordering;
Increased strength and frequency of contractions;
Decreased strength and frequency of contractions.
HOW DOES HYPOKALEMIA AFFECT THE HEART?
Cerebral cortex;
Reticular formation of the brainstem;
Aortic arch, sinocarotid zone;
Brain vessels.
THE TONE OF THE CENTERS REGULATING CARDIAC ACTIVITY IS MAINLY DUE TO IMPULSATION COMING FROM... .
Predominant in the left atrium;
Evenly across all departments;
Mainly in the atria;
Mainly in the ventricles.
HOW ARE THE SYMPATHETIC NERVES DISTRIBUTED IN DIFFERENT SECTIONS OF THE HEART?
Pavlov's nerve;
Glossopharyngeal;
Sympatheticus.
THE ACTIVITY OF THE HEART AT REST IS GREATLY INFLUENCED BY... .
To increase heart rate;
To reduce heart rate;
To complete heart block.
A REDUCTION IN THE TONE OF THE CENTER OF PARASYMPATHETIC INNERVATION OF THE HEART WILL LEAD... .
Reducing frequency;
Increased heart rate.
WHAT CHANGES IN HEART FUNCTION CAN BE OBSERVED AFTER CROSSING THE NERVES COMING FROM THE AORTIC ARCH AND CAROTID SINUS?
Will rise;
Will go down.
HOW WILL THE TONE OF THE CENTERS OF THE VAGUS NERVE CHANGE WHEN IRRITATION OF HERING'S NERVE?
To the parasympathetic;
It is a branch of the sympathetic nerve;
To somatic;
It has properties of both the sympathetic and parasympathetic nerve.
WHICH PART OF THE NERVOUS SYSTEM DOES THE REINFORCING NERVE OF THE HEART BELONG TO?
Conditioned reflex change in frequency;
Change in contraction frequency when holding your breath;
Integrative adaptation of heart function to real conditions.
THE ROLE OF THE HYPOTHALAMUS IN THE REGULATION OF HEART WORK IS:
Catecholamines reduce the permeability of cell membranes to Ca++ ions;
Do not change the permeability of cell membranes to Ca++ ions;
Increases the permeability of cell membranes to Ca++ ions.
HOW DO CATECHOLAMINES INFLUENCE THE PERMEABILITY OF MEMBRANES FOR ENDOGENOUS Ca++?
In the diastole phase;
In the systole phase.
IN WHAT PHASE DOES HEART STOP OCCUR DUE TO EXCESS POTASSIUM IONS?
In the systole phase;
In the diastole phase.
IN WHAT PHASE DOES THE HEART STOP DUE TO EXCESS CALCIUM?
Determine whether the statements are true or false and the relationship between them:
THE AORTIC SEMILUNARA VALVE OPENS DURING RAPID EXPULATION BECAUSE DURING THIS PERIOD, THE PRESSURE IN THE LEFT VENTRICLE EXCEEDS THE PRESSURE IN THE AORTA
The activity of different muscle fibers alternates to some extent, due to this the muscle becomes less tired. Therefore, to maintain continuous muscle tension, a high frequency of discharge of the motor nerve cell is not needed. For this purpose, a pulse frequency not exceeding ten pulses per second is sufficient. Motor neurons have mechanisms that stabilize their discharge at exactly this frequency and prevent the occurrence of impulses of too high a frequency, which could lead to disruption of muscle activity. Such a stabilizing mechanism is, firstly, the development in the soma of the motor neuron of a long-term trace hyperpolarization after the generation of an impulse. Its duration reaches approximately 100 ms, and during its development the new synaptic action will be weakened. This mechanism itself should help stabilize the motor neuron discharge rate at a level of about 10 impulses per second. In addition to the internal stabilization mechanism, the motor neuron also has a second, external mechanism that works in the same direction. This external mechanism is represented by a short chain of negative feedback through which the motor neuron inhibits itself, but in the case when it sends a discharge to the axon.
The general scheme of the activity of such a chain is as follows. Renshaw cells terminate reentrant axonal collaterals that, within the gray matter, give off alpha motor neurons that innervate the motor muscles, and therefore they always “know” how strongly the neuron is excited. Renshaw cells in turn terminate on motor neurons at inhibitory synapses. There is no trace hyperpolarization in Renshaw cells, and therefore they can generate a whole train of impulses at a very high frequency at a single synaptic potential - up to 1500 impulses per second. Each of these impulses, arriving at the motor neurons, causes an inhibitory reaction in them, which is summed up as long as the discharge of the Renshaw cell lasts. Therefore, the total duration of inhibition after a single impulse in the axon collateral reaches approximately 100 ms. Recurrent inhibition combines with subsequent hyperpolarization and further contributes to maintaining the motor neuron discharge at a low frequency. Renshaw cells receive input from more than one motor neuron and themselves send axons to many motor neurons. Since in the process of evolution such effective overlapping mechanisms for stabilizing the discharge of a motor neuron arose, it is obvious that the latter mechanism is essential for the normal implementation of a motor act.
Functions
- One of the most important functions of Renshaw cells, common to all types of motor neurons, is stabilizing the frequency of their work while maintaining a posture or holding a load. That is, the CDs smooth out the oscillations at the output of the MN. When the input flow to the MN increases, the MNs pulse more strongly, the operating frequency of the CR increases, and they slow down the MN.
This function was proposed by Hesse et al. in 1975. This idea is very natural, because MN with CD is a typical system with negative feedback. In the 70s of the 20th century, such systems were intensively discussed by cyberneticists.
- RCs play an important role in managing the MN pool, which consists of MNs of different types. For example, when a person gradually strains the muscles of his arm, according to the principle of magnitude, slow motor units are first turned on, then the frequency of the impulses increases to 50 Hz, then the FR (fatigue-resistant; fast) MN comes into play, but at the same time the frequency of the S-MN (slow) not growing. Once FR-MNs are turned on, it means the influx of impulses to this MN pool has increased. The frequency of S-MNs does not increase, since FR-MNs excite CRs, which stabilize the frequency of S-MNs. This is necessary to protect neurons from “overload”, that is, so that the neuron does not work for a long time at a high frequency, as they die from this.
Thus, another function of CR is the protection of slow MNs from death. The high sensitivity of S-MN to return braking was shown by Granit in 1957. And in 1960, he suggested that return inhibition stabilizes the discharge frequency of S-MN. While only S-MNs were working, that is, the frequency did not exceed 50 Hz, they did not activate any noticeable number of CRs, and with an increase in the influx of impulses, the frequency of these MNs increased.
- In 1971, Hultborn and Yankovskaya showed that CRs inhibit the reciprocal inhibition interneuron.
Even with very strong excitation of the MN of the synergist (muscle), it is impossible to strongly inhibit the MN of the antagonist. The higher the frequency of impulses along fibers 1a, the stronger the inhibition of the antagonist MNs should be, but at the same time, the synergist MNs work more strongly, and therefore the Renshaw cells excited by them. CRs inhibit the inhibitory interneuron so that the antagonist muscle does not become too inhibited and can quickly respond to an excitatory impulse. This is necessary so that the sequence of work of the antagonist muscles is observed, so that their reaction is quick. When the antagonist muscle begins to work, a similar reciprocal inhibition occurs for the synergist muscle MN.
- Another function of the CD is desynchronization of the MN of one pool. Its mechanism is poorly understood.
- One of the additional functions of the CR is that in fast, sudden movements, for example, the shaking off reflex, slow MEs can interfere with its implementation; for this, their activity must be suppressed, that is, they must be slowed down.
- Another function of the CD. Fiffe (1991) showed that CRs form synapses on MN dendrites, in contrast to reciprocal inhibition, where they form synapses on MN bodies. These synapses make it possible to selectively inhibit some inputs to the cell, without inhibiting other inputs to the MN.
All of the above functions of the CR were within one MN pool, but there are a number of hypotheses about their functions at the level of coordination of the work of pools of different muscles.
- CRs provide collaterals of their axons to the MNs of the synergist muscles of one joint and to the MNs of the flexors (or extensors) of different joints of the limb. Thus, CRs connect MN pools of different muscles into a single MN pool.
- Another idea is that motor commands coming from the cerebral cortex may excite the MN and CR needed for movement, which inhibit the MN of muscles that should not be involved in this movement. Thus, it is assumed that the CR is part of the mechanism for controlling voluntary movements!
There are several other functions of Renshaw cells. For example, Rill showed in 1970 that CRs can inhibit other CRs, with agonist CRs inhibiting antagonist CRs more strongly. CR can inhibit neurons of the ventral spinocerebellar tract and other neurons of the ascending tracts. Most of the results described were obtained on the MN of the cat's hind paw. It turned out that the effectiveness of recurrent inhibition in other joints is different.
Violations
There are a number of substances that inhibit the activity of Renshaw cells. The most famous of them are strychnine and toxin Clostridium tetani(the causative agent of tetanus).
Strychnine specifically affects the ability of Renshaw cells to control the functioning of alpha motor neurons. It is an antagonist of the neurotransmitter glycine and blocks its receptors on alpha motor neurons and other neurons. As a result, alpha motor neurons are not inhibited, resulting in uncontrolled muscle contractions (cramps). Strychnine can be fatal due to its effects on the respiratory muscles, including the diaphragm, by blocking the ability to make breathing movements.
Renshaw cells are also a target for the toxin Clostridium tetani, a spore-forming anaerobic bacterium that lives in soil. When S.tetani enters the body through damage to the skin and its toxin enters the spinal cord through the bloodstream, the release of glycine is disrupted and the transmission of inhibitory influence from Renshaw cells to alpha motor neurons is blocked. As a result, alpha motor neurons become overactive and the muscles begin to engage in tetanic contractions. The cramps involve large muscle groups and in severe cases can last almost continuously. Death can occur at the height of convulsions from asphyxia due to spasm of the laryngeal muscles in combination with a decrease in pulmonary ventilation due to tension in the intercostal muscles and diaphragm. In addition, the cause of death can be direct damage to the respiratory and vascular-motor centers of the brain stem.
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Literature
- V. V. Shulgovsky “Fundamentals of Neurophysiology” textbook for university students, 2nd edition M. AspectPress, 2005.
- “Human Physiology” edited by V. M. Pokrovsky, G. F. Korotko, 2nd edition ed. "Medicine"
- Savelyev A.V. Modeling of Renshaw cell systems // In the collection: “Modeling of non-equilibrium systems”. Krasnoyarsk: INM SB RAS, 2003. pp. 143-145.
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Excerpt characterizing the Renshaw Cage
-Have you not read the letter? – Sonya asked.“I didn’t read it, but she said that everything was over, and that he was already an officer...
“Thank God,” said Sonya, crossing herself. “But maybe she deceived you.” Let's go to maman.
Petya walked silently around the room.
“If I were Nikolushka, I would kill even more of these French,” he said, “they are so vile!” I would beat them so much that they would make a bunch of them,” Petya continued.
- Shut up, Petya, what a fool you are!...
“I’m not a fool, but those who cry over trifles are fools,” said Petya.
– Do you remember him? – after a minute of silence Natasha suddenly asked. Sonya smiled: “Do I remember Nicolas?”
“No, Sonya, do you remember him so well that you remember him well, that you remember everything,” Natasha said with a diligent gesture, apparently wanting to attach the most serious meaning to her words. “And I remember Nikolenka, I remember,” she said. - I don’t remember Boris. I don't remember at all...
- How? Don't remember Boris? – Sonya asked in surprise.
“It’s not that I don’t remember, I know what he’s like, but I don’t remember it as well as Nikolenka.” Him, I close my eyes and remember, but Boris is not there (she closed her eyes), so, no - nothing!
“Ah, Natasha,” said Sonya, looking enthusiastically and seriously at her friend, as if she considered her unworthy to hear what she had to say, and as if she were saying this to someone else with whom one should not joke. “I once fell in love with your brother, and no matter what happens to him, to me, I will never stop loving him throughout my life.”
Natasha looked at Sonya in surprise and with curious eyes and was silent. She felt that what Sonya said was true, that there was such love as Sonya spoke about; but Natasha had never experienced anything like this. She believed it could be, but she didn't understand.
-Will you write to him? – she asked.
Sonya thought about it. The question of how to write to Nicolas and whether to write and how to write was a question that tormented her. Now that he was already an officer and a wounded hero, was it good of her to remind him of herself and, as it were, of the obligation that he had assumed in relation to her.
- Don't know; I think if he writes, I’ll write too,” she said, blushing.
“And you won’t be ashamed to write to him?”
Sonya smiled.
- No.
“And I’ll be ashamed to write to Boris, I won’t write.”
- Why are you ashamed? Yes, I don’t know. Embarrassing, embarrassing.
“And I know why she will be ashamed,” said Petya, offended by Natasha’s first remark, “because she was in love with this fat man with glasses (that’s how Petya called his namesake, the new Count Bezukhy); Now she’s in love with this singer (Petya was talking about the Italian, Natasha’s singing teacher): so she’s ashamed.
“Petya, you’re stupid,” Natasha said.
“No more stupid than you, mother,” said nine-year-old Petya, as if he were an old foreman.
The Countess was prepared by hints from Anna Mikhailovna during dinner. Having gone to her room, she, sitting on an armchair, did not take her eyes off the miniature portrait of her son embedded in the snuffbox, and tears welled up in her eyes. Anna Mikhailovna, with the letter, tiptoed up to the countess's room and stopped.
“Don’t come in,” she said to the old count who was following her, “later,” and closed the door behind her.
The Count put his ear to the lock and began to listen.
At first he heard the sounds of indifferent speeches, then one sound of Anna Mikhailovna's voice, making a long speech, then a cry, then silence, then again both voices spoke together with joyful intonations, and then steps, and Anna Mikhailovna opened the door for him. On Anna Mikhailovna's face was the proud expression of an operator who had completed a difficult amputation and was introducing the audience so that they could appreciate his art.
“C”est fait! [The job is done!],” she said to the count, pointing with a solemn gesture at the countess, who was holding a snuffbox with a portrait in one hand, a letter in the other, and pressed her lips to one or the other.
Seeing the count, she stretched out her arms to him, hugged his bald head and through the bald head again looked at the letter and portrait and again, in order to press them to her lips, she slightly pushed the bald head away. Vera, Natasha, Sonya and Petya entered the room and the reading began. The letter briefly described the campaign and two battles in which Nikolushka participated, promotion to officer, and said that he kisses the hands of maman and papa, asking for their blessing, and kisses Vera, Natasha, Petya. In addition, he bows to Mr. Sheling, and Mr. Shos and the nanny, and, in addition, asks to kiss dear Sonya, whom he still loves and about whom he still remembers. Hearing this, Sonya blushed so that tears came to her eyes. And, unable to withstand the glances directed at her, she ran into the hall, ran up, spun around and, inflating her dress with a balloon, flushed and smiling, sat down on the floor. The Countess was crying.
-What are you crying about, maman? - Vera said. “We should rejoice at everything he writes, not cry.”
This was completely fair, but the count, the countess, and Natasha all looked at her reproachfully. “And who did she look like!” thought the Countess.
Nikolushka's letter was read hundreds of times, and those who were considered worthy of listening to it had to come to the countess, who would not let him out of her hands. Tutors, nannies, Mitenka, and some acquaintances came, and the countess re-read the letter every time with new pleasure and each time, from this letter, she discovered new virtues in her Nikolushka. How strange, extraordinary, and joyful it was for her that her son was the son who had barely noticeably moved with tiny limbs inside her 20 years ago, the son for whom she had quarreled with the pampered count, the son who had learned to say before: “ pear,” and then “woman,” that this son is now there, in a foreign land, in a foreign environment, a courageous warrior, alone, without help or guidance, doing some kind of manly work there. All the world's centuries-old experience, indicating that children imperceptibly from the cradle become husbands, did not exist for the countess. The maturation of her son in every season of manhood was as extraordinary for her as if there had never been millions of millions of people who matured in exactly the same way. Just as she couldn’t believe 20 years ago that that little creature that lived somewhere under her heart would scream and begin to suck her breast and start talking, so now she couldn’t believe that this same creature could be that strong, a brave man, an example of the sons and men he was now, judging by this letter.
- What a calm, how cute he describes! - she said, reading the descriptive part of the letter. - And what a soul! Nothing about myself... nothing! About some Denisov, and he himself is probably braver than them all. He writes nothing about his suffering. What a heart! How do I recognize him! And how I remembered everyone! I haven't forgotten anyone. I always, always said, even when he was like this, I always said...
For more than a week they prepared, wrote brouillons and copied letters to Nikolushka from the whole house; under the supervision of the countess and the care of the count, the necessary items and money were collected to outfit and equip the newly promoted officer. Anna Mikhailovna, a practical woman, managed to arrange protection for herself and her son in the army, even for correspondence. She had occasion to send her letters to Grand Duke Konstantin Pavlovich, who commanded the guard. The Rostovs assumed that the Russian guard abroad had a completely definite address, and that if the letter reached the Grand Duke, who commanded the guard, then there was no reason why it should not reach the Pavlograd regiment, which should be nearby; and therefore it was decided to send letters and money through the Grand Duke’s courier to Boris, and Boris should have already delivered them to Nikolushka. The letters were from the old count, from the countess, from Petya, from Vera, from Natasha, from Sonya and, finally, 6,000 money for uniforms and various things that the count sent to his son.
On November 12, the Kutuzov military army, camped near Olmutz, was preparing for the next day to review the two emperors - Russian and Austrian. The guard, which had just arrived from Russia, spent the night 15 versts from Olmutz and the next day, right for the review, at 10 o’clock in the morning, entered the Olmutz field.
On this day, Nikolai Rostov received a note from Boris informing him that the Izmailovsky regiment was spending the night 15 miles short of Olmutz, and that he was waiting for him to give him a letter and money. Rostov especially needed money now that, having returned from the campaign, the troops stopped near Olmutz, and well-supplied sutlers and Austrian Jews, offering all kinds of temptations, filled the camp. The Pavlograd residents had feasts after feasts, celebrations of awards received for the campaign and trips to Olmutz to visit Caroline of Hungary, who had recently arrived there, who opened a tavern there with female servants. Rostov recently celebrated its production of cornets, bought Bedouin, Denisov's horse, and was in debt to his comrades and sutlers. Having received Boris's note, Rostov and his friend went to Olmutz, had lunch there, drank a bottle of wine and went alone to the guards camp to look for his childhood comrade. Rostov had not yet had time to get dressed. He was wearing a shabby cadet's jacket with a soldier's cross, the same leggings lined with worn leather, and an officer's saber with a lanyard; the horse he rode on was a Don horse, bought on a campaign from a Cossack; the hussar's crumpled cap was pulled back and to one side in a jaunty manner. Approaching the camp of the Izmailovsky regiment, he thought about how he would amaze Boris and all his fellow guardsmen with his shelled combat hussar appearance.
The guard went through the entire campaign as if on a festivities, flaunting their cleanliness and discipline. The crossings were short, the backpacks were carried on carts, and the Austrian authorities prepared excellent dinners for the officers at all crossings. The regiments entered and left the cities with music, and throughout the campaign (of which the guards were proud), by order of the Grand Duke, people walked in step, and the officers walked in their places. Boris walked and stood with Berg, now the company commander, throughout the campaign. Berg, having received a company during the campaign, managed to earn the trust of his superiors with his diligence and accuracy and arranged his economic affairs very profitably; During the campaign, Boris made many acquaintances with people who could be useful to him, and through a letter of recommendation he brought from Pierre, he met Prince Andrei Bolkonsky, through whom he hoped to get a place on the headquarters of the commander-in-chief. Berg and Boris, cleanly and neatly dressed, having rested after the last day's march, sat in the clean apartment assigned to them in front of the round table and played chess. Berg held a smoking pipe between his knees. Boris, with his characteristic accuracy, placed the checkers in a pyramid with his white thin hands, waiting for Berg to make a move, and looked at his partner’s face, apparently thinking about the game, as he always thought only about what he was doing.
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(motoneurons) are large multipolar cells. Each motor neuron innervates from a few to thousands of muscle fibers to form a motor unit. There are medial, central and lateral groups (nuclei) of motor neurons. The medial group of neurons innervates the muscles of the trunk, the central group innervates the muscles of the pelvic and shoulder girdle, and the lateral group innervates the muscles of the limbs. Neurons are functionally divided into large alpha motor neurons, small alpha motor neurons and gamma motor neurons. Large alpha motor neurons transmit impulses to extrafusal muscle fibers, causing rapid phasic contractions. Alpha motor neurons maintain skeletal muscle tone. Gamma motor neurons send axons to the intrafusal muscle fibers of the neuromuscular spindle. Each alpha motor neuron receives direct excitatory inputs from cortical motor neurons and from sensory neurons innervating the muscle spindles. Exciting influences also come to alpha and gamma motor neurons from the motor nuclei of the brain stem and interneurons of the spinal cord - both through direct pathways and with switches.
The anterior horn of the spinal cord contains a large number of small neurons called Renshaw cells, which are closely associated with motor neurons. Once the anterior motor neuron axon leaves the cell body, its collaterals go to the adjacent Renshaw cells. These are inhibitory cells that conduct inhibitory signals to surrounding motor neurons. Thus, stimulation of each motor neuron leads to inhibition of adjacent motor neurons. This effect, called lateral inhibition, is extremely important. The motor system uses lateral inhibition to focus, i.e. "sharpening" its signals, just as this principle is used by the sensory system to ensure that the primary signal is carried in the desired direction without attenuation, while simultaneously suppressing the tendency of signals to spread laterally.
Gamma motor neurons activate intrafusal muscle fibers, thereby increasing the sensitivity of muscle receptors, i.e., muscle spindles to muscle stretching. The consequence of this is an increase in the flow of impulses coming from muscle spindles to alpha motor neurons (including through interneurons), which leads to excitation of alpha motor neurons and the muscle fibers innervated by them. This mechanism of alpha motor neuron activation is called the gamma loop.
IN anterior horns of the spinal cord there are a large number of small neurons called Renshaw cells, closely associated with motor neurons. Once the anterior motor neuron axon leaves the cell body, its collaterals go to the adjacent Renshaw cells. These are inhibitory cells that conduct inhibitory signals to surrounding motor neurons. Thus, stimulation of each motor neuron leads to inhibition of adjacent motor neurons.
This Effect, called lateral inhibition, is extremely important. The motor system uses lateral inhibition to focus, i.e. "sharpening" its signals, just as this principle is used by the sensory system to ensure that the primary signal is carried in the desired direction without attenuation, while simultaneously suppressing the tendency of signals to spread laterally.
Multiple intersegmental connections of the spinal cord. Propriospinal fibers More than half of the ascending and descending nerve fibers of the spinal cord are propriospinal fibers. They pass from one segment of the spinal cord to another. In addition, when sensory fibers enter the spinal cord along its dorsal roots, they branch, and the branches run up and down along the spinal cord; some of them conduct signals to only one or two segments, while others conduct signals to many segments.
These ascending and descending propriospinal fibers provide pathways for the multisegmental reflexes outlined later in this chapter, including reflexes that coordinate simultaneous movements of the forelimbs and hindlimbs.
Muscle sensory receptors
For proper regulation of muscle function not only stimulation of the muscle by motor neurons of the anterior horns of the spinal cord is required. Constant information is also needed, based on the principle of feedback between the muscle and the spinal cord, about the functional state of each muscle at a given moment: the length of the muscle, its tension, the rate of change in its length and tension at each moment.
This information provide two special types of receptors present in muscles and their tendons: (1) muscle spindles, which are distributed along the entire length of the muscle belly and send information to the nervous system about the length of the muscle or its rate of change); (2) Golgi tendon organs, which are located in muscle tendons and transmit information about tendon tension or rate of change.
Signals from these two types of receptors completely or almost completely designed to regulate the contractile function of “their” muscle. They operate almost on a subconscious level, but at the same time transmit a huge amount of information not only to the spinal cord, but also to the cerebellum and even to the cerebral cortex, helping each of these parts of the nervous system regulate muscle contractions.
