NEURAL MECHANISM OF HEART’ REGULATION.
The cardiac system is self-regulating. It is nearly impossible tconsciously increase or decrease contraction rate due tits involuntary operation. The large number of influential factors affecting cardiac performance combine in a complex manner, thus providing the ability tadapt quickly and efficiently tthe needs of the body. This is accomplished by twpathways. The intrinsic pathway represents the alterations occurring within the myocardial cells which dor dnot depend on a change in the initial myocardial fiber length. The extrinsic pathway occurs primarily through neural and humoral adaptations. These discrete interrelated biological interactions indicate that regulating any certain physiological control pathway is not easy.
( I ) Nervous regulation:
The heart rate is regulated by twcenter present in the medulla oblongata: Cardiac.Activation.Center which is connected with the sympathetic nervous system and Cardiac.Inhibition.Center which is connected with the vagus nerve i.e. parasympathetic nervous system. The twcenters receive impulses from the following sites:
(1) Afferent impulses from the higher centers:
A) Cerebral cortex: Cerebral cortex affects HR as in the following conditions:
* Conditioned reflexes; in certain conditions; seeing, hearing or smelling lead t( in HR e.g. seeing the examiner or hearing about the exam leads t( HR.
* Voluntary; yoga players can increase or decrease their HR voluntarily.
* Emotions: Most types of emotions ( fear, anger anxiety etc) leads t( HR. Sudden unexpected news leads t(HR or may stop the heart.
(B) Hypothalamus:
– Stimulation of anterior nuclei (which control the parasympathetic activity) leads t( HR as in quite sleep, and severe emotions ( sudden unexpected news).
– Stimulation of posterior nuclei (which control the sympathetic activity) leads t( HR as in mild emotions and stress, and muscular exercise.
(2) Afferent impulses from the circulatory system:
(A) Afferent from the venous side (Rt. Side of the heart):
1. Bainbridge reflex: ( venous pressure caused by ( venous return (VR) in the right atrium leads t(HR. ( VR stimulates stretch receptors present in the wall of the tight atrium. These receptors send impulses along vagus nerve tthe medulla causing stimulation of CAC and inhibition of CIC. CAC sends efferent impulses through sympathetic fibers tthe SAN causing ( HR.
Some authors believe that the increase in HR results from stretch of the SAN leading t( rate of discharge from it. So, it is a local effect and not a true nervous reflex.
Significance: The increased HR pumps the excess VR tthe arterial side and prevents stagnation of blood in veins.
2. Mc Dowel’s reflex: ( VR (or ( pressure in right atrium) as in haemorrhage leads treflex ( HR and V.C of arterioles.
Significance: During haemorrhage the increased HR and VC help traise ABP and maintain circulation tthe vital organs (brain, heart kidneys and liver).
(B) Afferent impulses from arterial side (carotid sinus and aortic arch):
Mary’s law: The HR is inversely proportional tthe arterial blood pressure provided that other factors affecting HR remain constant.
( ABP (( HR , ( ABP (( HR
Mechanism: ( ABP stimulates baroreceptors present in carotid sinus and Aortic arch from which afferent impulses pass through sinus nerve and aortic nerve. These impulses cause stimulation of CIC leading t( HR. ( ABP as in haemorrhage reduce the inhibitory impulses from the baroreceptors leading t( HR.
Significance: These reflex buffers the excessive changes in ABP. In case of ( ABP, the decreased HR helps t( ABP tnormal. In case of ( ABP (during haemorrhage) the increased HR helps traise the ABP again tnormal.
(3) Afferent from the respiratory system:
Respiratory sinus arrhythmia: During inspiration, the HR ( while during expiration the HR (. It is commonly seen in infants:
Mechanism: During inspiration the HR increases due to:
1. The respiratory center radiates impulses tthe CAC causing its stimulation.
2. Lung inflation stimulates stretch receptors in the alveoli which send impulses (through the vagus nerve) that stimulate CAC leading t( HR.
3. Bainbridge reflex, during inspiration the VR ( (due to( negativity of the intra-pleural pressure), this leads t( pressure in right which causes ( in HR.
During expiration the HR decreases due tdecreased activity of respiratory center, elastic recoil of the lung, and ( VR.
(4) Afferent from the other parts of the body:
1. From the muscles: Alam Smirk reflex: Contraction of any voluntary muscle leads t( HR. Muscle contraction stimulates proprioceptors in the muscles and joints These receptors send impulses which stimulate CAC ( ( HR, tsupply the active muscle with excess blood.
2. From the skin and viscera: Mild or moderate pain from the skin leads t( HR (due tstimulation of CAC). Severe pain from the skin (e.g. massive burn) or any pain from the viscera leads t( HR (due tstimulation of CIC).
3. From The trigger zones: Pain from the trigger zones (sensitive areas) e.g. larynx, epigastrium, pericardium and tests produces sever decrease in HR and even stop the heart. These areas are richly supplied by parasympathetic fibers.
4. From they eye: Oculo-cardiac reflex: Pressure over the eyeball produces reflex ( HR.
( II ) Physical regulation:
In hyperthermia e.g. fever, the rise in body temperature by 1OC increases the HR by 10 beats / min, due tdirect stimulation of SAN and stimulation of CAC by impulses coming from the heat regulating center in the hypothalamus.
In hypothermia, the HR decreases by 10 beats / min for each 1OC decrease in body temperature.
( III ) Chemical regulation:
1- ( O2 (Hypoxia): Mild or moderate hypoxia ( ( HR due tstimulation of CAC, both directly and indirectly (through the chemoreceptors present in carotid body and aortic body). Severe hypoxia ( ( HR, then the heart stops due tdamage of the medullary centers and SAN.
2- ( CO2 and als( H+ ( acidosis ): causes initial ( in HR due tstimulation of CIC followed by ( in HR due tdirect stimulation of CAC and paralysis of CIC.
3- Blood hormones:
a. Adrenaline: Small dose of adrenaline ( HR due tdirect stimulation of SAN. Large does of adrenaline ( HR because it produces VC and ( ABP (Mary’s law).
b. Noradrenaline: Small or large dose of noradrenaline ( HR because of the generalized V.C which leads t( ABP (Mary’s law).
c. Thyroxin: ( HR due tdirect stimulation of SAN. and ( sensitivity of SAN tthe circulating adrenaline. Thyroxin als( the general metabolism of the body which leads t( Body temperature ( ( HR.
4- Other chemicals:
a. Chemicals ( HR:
* Sympathomimetic drugs e.g. ephedrine and amphetamine.
* Parasympatholytic drugs e.g. atropine which inhibits the vagal effect on the heart.
* Histamine ( marked capillary VD ( ( ABP ( (HR ( Mary’s law).
b. Chemicals ( HR:
* Parasympathomimetic drugs e.g. acetylcholine and pilocarpine.
* Bile salts cause direct inhibition of SAN and stimulation of CIC.
* Morphine stimulates CIC.
* Toxins e.g. typhoid and diphtheria toxins.
Innervation of the heart
The activity of the heart is regulated by twcenters present in the medulla oblongata.
1) Cardiac Inhibitory centre: C.I.C. It is a part of the dorsal nucleus of vagus, the axons of their neurons leave the medulla as preganglionic fibers. They relay in terminal ganglia present in the heart.
2) Cardiac accelerator centre: CAC. It lies near the inhibitory center, the axon of their neurons descend in the white matter of the spinal cord and synapse in lateral horn cells (L.H.C) of upper 5 thoracic segment. Preganglionic fibers arise from L.H.C and relay in the three cervical sympathetic ganglia. Postganglionic fibers pass from these ganglia tsupply the whole heart.
Nerve supply tthe heart:
I. Parasympathetic innervation: (vagus nerve)
Preganglionic fibers of vagus arise from the neurons of C.I.C. They reach the heart as preganglionic fibers and relay in terminal ganglia present in the substance of the atrial muscle particularly the nodal tissues. Postganglionic fibers supply SA node, A-V node and main stem of A-V bundle (but not its branches), atrial muscle, and coronary blood vessels. Vagus nerve does not supply the ventricles, branches of A-V bundle and Purkinje fibers.
Function of vagus nerve: (Parasympathetic supply tthe heart)
1) It inhibits all cardiac properties; contractility, rhythmicity, excitability, and conductivity.
2) Constriction of coronary blood vessels.
Vagus escape phenomenon: Stimulation of vagus slow HR, strong stimulation of vagus stops the heart completely. If the strong stimulus is maintained, the ventricles begin tbeat by its own rhythm “Idio-ventricular rhythm” (25 – 40 / min). This phenomenon is called vagus escape. It means escape of the ventricle from the inhibitory effect of vagus. It is a proof that the vagus does not supply the ventricles.
Physiological significance of absent vagal supply tthe ventricles:
In case of idio-ventricular rhythm, the ventricular rhythm is (25-40 beats/min) which is inadequate tmaintain sufficient circulation. If vagus supplies the ventricle, it will further ( the rate which is not desirable.
Vagus tone: During rest vagus nerve continuously discharge inhibitory impulses tthe heart t( the high rhythm of S-A node ( from 110-120 beat / min( 70 beat/ min), this is called “Vagus tone”.
Mechanism of vagus tone:
It is a reflex mechanism in which the stimulus is the resting A.B.P. Receptors: baroreceptors or pressure receptors present in carotid sinus and Aortic arch. Afferents: through sinus nerve which is a branch of Glossopharyngeal nerve (IX.C) and Aortic nerve which is a branch of vagus nerve (X.C). Centre : C.I.C. Efferent: vagus nerve which ( the high rhythm of S-A node.
Proof: Cutting of both vagi in animal result in ( in HR. ( from 70 t120). Stimulation of the cut end of vagus ( ( in HR.
Vagus tone ( : In man more than women, in athletes more thaon athletes, and in adult more than children.
Physiological significance of vagus tone: Vagus tone ( HR from 120 – t70 beat / min. This ( in HR will be a reserve tbe used at times of need as in muscular exercise.
II. Sympathetic supply tthe heart:
It begins at C.A.C in the medulla oblongata near C.I.C. The axons of their neuron descend in the white matter of the spinal cord, and relay at L.H.C of upper 5 thoracic segment. Preganglionic fibers of L.H.C pass in sympathetic chain and ascend upwards trelay in the three cervical sympathetic ganglia (superior, middle and inferior cervical sympathetic ganglia. Postganglionic fibers pass from the ganglia tthe heart where they supply all the structures of the heart including the ventricles.
Function of sympathetic supply tthe heart:
1- It increases all cardiac properties; contractility, rhythmicity, excitability, and conductivity.
2- Vasodilatation of coronary vessels.
Cardiac Output (COP)
During rest and exercise
Cardiac Output (COP); in the volume of blood pumped by each ventricle per minute. It equals 5-
Stroke volume (S.V); in the volume of blood pumped by each ventricle per beat. It equals the difference between end diastolic volume (EDV) and end systolic volume (ESV). COP = SV X HR.
End diastolic volume (EDV); is the volume of blood in the ventricle at the end of diastole, it is about 130 ml.
End systolic volume (ESV); in the volume of blood in the ventricle at the end of systole, it is about 60 ml.
So, SV = EDV – ESV = 130 – 60 = 70 ml
Cardiac index (C.I): in the volume of blood pumped by each ventricle per min per square meter surface area i.e. COP/ body surface area. It equals
Ejection fraction (EF): in the % ratiof the SV tthe EDV.
EF = X 100, Normally it is about 65%. It is increased when the ventricular contractility ( and decreased when the ventricular contractility ( ( as in heart failure).
Factors affecting cardiac output (COP)
(I) Venous return , VR (or preload):
Under normal condition the VR and the COP are identical. When the VR ( (e.g. during muscular exercise) the COP(. When the VR ( (e.g. during haemorrhage), COP ( tthe same extent.
Factors affecting VR:
1) Pressure gradient: Pressure in the peripheral venules:
2) Respiratory movements:
A) During inspiration VR ( :
During normal inspiration: The intra-thoracic pressure becomes more negative (–6 mm Hg) while the intra-abdominal pressure becomes positive (due tdescend of diaphragm). These twfactors ( VR.
In forced inspiration: the intra-thoracic pressure becomes more negative (–30 mm Hg), this leads tmarked ( in VR.
B) During expiration VR ( :
During normal expiration: The intra-thoracic pressure becomes less negative (–3 mm Hg), So, the VR is lesser than during inspiration.
In forced expiration: the intra-thoracic pressure becomes positive (+ 50 mmHg). This leads tstagnation of blood in the extra-thoracic veins. So, the VR ( markedly.
3) Muscle contraction and muscle tone:
During contraction the veins and capillaries are compressed between the muscle fibers, and sthe venous blood is squeezed towards the heart leading t( VR and COP. During relaxation blood does not return back because the veins contain valves which allow blood tpass only towards the heart.
Continuous contraction and relaxation of the muscle pump blood towards the heart and against gravity. So, voluntary muscles act as a “peripheral hearts”. In absence of muscle contraction, VR is helped by muscle tone.
4) Diameter of blood vessels:
a) Diameter of arterioles: If arterioles are dilated, the blood flows easily from arteries tveins increasing the VR e.g. during muscular exercise. If the arterioles are constricted the VR (.
b) Diameter of capillaries: Normally about 10% only of the capillaries are opened and the other 90% are closed, this is known as capillary tone. If the capillaries are widely dilated, they will accommodate the whole blood volume. So, VR and COP are markedly decreased, ABP als( leading tshock and death may occur as in sever burn.
c) Diameter of veins: Venous tone ( slight constriction ) prevents full distension of the veins with blood and, shelps tmaintain VR. Loss of venous tone causes stagnation of most of the blood in the veins leading t( VR and ( COP.
5) Arterial pulsation:
In most cases, veins run parallel tthe arteries. Arterial pulsation are mechanically conducted tthe veins. This helps tdrive blood towards the heart owing tthe presence of valves in the veins.
6) Valves of veins:
Veins of the lower limbs contain valves which are very important because they allow blood tpass only in one direction i.e towards the heart.
They divide the column of blood intsegments which prevent distension of the vein by the blood. If these valves are destroyed, this leads t”varicose veins” where the veins become tortuous and filled with blood.
7) Gravity:
In the recumbent position, gravity has neffect on VR. In the erect position gravity ( VR from parts above the level of the heart (head and neck), and ( VR from parts below the level of the heart (lower limbs and abdomen).
8) Blood volume:
( blood volume leads t( VR and ( COP as during muscular exercise. The increased blood volume during exercise results from contraction of the blood reservoirs (spleen and liver). ( blood volume leads t( VR and COP as during haemorrhage.
9) Atrial systole:
Atrial systole helps VR because it evacuates 30% of the blood intthe ventricles. VR replace the evacuated blood.
10) Ventricular systole:
It forms a force from behind. It causes increase pressure in the arteries, then in capillaries and lastly in veins, thus helping VR.
(II) Arterial blood pressure (after load):
When the ABP increases suddenly, the heart is unable tpump all the blood against this high resistance. Residual blood remains in the heart is added tthe next diastolic volume. The next diastolic volume ( , sthe strength of ventricular contraction ( (Starling’s law) tovercome this high resistance. So, the heart adjust itself tovercome this high ABP, and so, COP remains constant.
When the elevated blood pressure is maintained, the work of the heart is increased tovercome this high resistance. This leads tventricular hypertrophy, then heart failure where the heart is enable tpump the whole blood, sCOP (.
(III) Heart rate:
Changes in HR with constant VR:
1) Physiological variations of HR (50 – 100 beat / min): has neffect on COP. COP = HR x SV = 70 beats /min x 70 ml /beat = 5 liter/min.
If HR ( (e.g. 100 beats / min) the diastolic periods will decrease leading tdecrease SV (50 ml/beat). COP = HR x SV = 100 x 50 = 5 liter/min.
If HR ( (e.g. 50 beats/min) the diastolic periods will increase leading tincrease SV (100 ml/beat). COP = HR x SV = 50 x 100 = 5 liter/min.
2) Physiological (excessive) variations of HR:
Excessive ( in HR (as in paroxysmal tachycardia 200/min). In this case the diastolic period is toshort leading tmarked ( in SV and ( in COP.
COP = HR x SV = 200 x 20 = 4000 ml/min.
Excessive ( in HR (as in heart block, 25–40 beat 200/min). In this case the diastolic period becomes more prolonged and more filling occurs but up ta certain limit, after which stagnation of blood occurs outside the heart . COP = HR x SV = 30 x 120 = 3600 ml/min.
Changes in HR with change in VR (e.g. during M. exercise):
During muscular exercise both the HR and the VR (hence the SV) are increased leading tmarked ( in COP. COP = HR x SV = 200 x 200 = 40.000 ml/min.
(IV) Strength of ventricular contraction:
SV and COP are directly proportional tthe strength of the ventricular contraction. The strength of ventricular contraction is affected by:
a) Diastolic volume: Within limit, ( diastolic volume leads t( ventricular contraction (Starling’s law).
b) Coronary blood supply: Decrease coronary blood supply leads t( strength of ventricular contraction and ( in COP. If coronary arteries are suddenly closed (coronary thrombosis) death will occur.
Regulation Of COP:
The Cop is regulated tmeet the body needs under different condition. This occurs by:
I) Intrinsic system (auto-regulation):
The heart is an automatic pump which is normally capable of pumping whatever the amount of blood that flows intthe atrium ( even without (HR ).
* Iormal persons up t15 liters / min ( i.e. 3 times COP).
* In athletes up t20 liters / min ( i.e. 4 times the COP).
Autregulation controls the COP by adjusting the SV only and includes:
A) Heterometric auto-regulation: (Starling’s law)
( VR (( end diastolic volume (EDV) of the ventricle ( ( initial length of the muscle fibers (hetero-metric) ( according tStarting’s law the strength of ventricular contraction ( ( ( SV tpump the excess VR.
SV = EDV (markedly (() – ESV (normal or slightly ()
Heterometric auto-regulation is observed when a person lie down, a relatively large volume of blood shifts from the Veins of the lower limbs tthe heart. The EDV and SV are increased for few heats then returns back tnormal.
B) Homeo-metric auto-regulation:
If the increase in VR persists, the end diastolic volume (EDV) returns tnormal within few seconds. Then the excess VR is pumped by the strong ventricular contraction which causes ( in the end systolic volume (ESV). So, the SV remains elevated.
SV = EDV (normal) – ESV (decreased).
The increase in the strength of ventricular contraction without change in the EDV (homeo-metric) is due to:
1. The ( in diastolic volume in the hetero-metric state improves the condition of the cardiac muscle ( (ATP, ( Ca++, ( viscosity) which extend tthe next homeo-metric state.
2. Release of myocardial catecholamine.
II) Extrinsic regulation:
The extrinsic ( Nervous and chemical) regulation controls the COP by adjusting both SV and HR.
A) Nervous regulation:
* Sympathetic stimulation ( COP by:
1. ( HR.
2. ( Strength of ventricular contraction. This leads t( ESV and ( SV.
3. Rapid relaxation of the ventricles which acts as a suction force leading t( ventricular filling i.e. ( EDV.
4. V.C which decreases the capacity of the circulatory system ( ( mean circulatory pressure (MCP) ( (pressure gradient ( (VR.
* Parasympathetic stimulation decreases the ( COP because it decreases the HR.
B) Chemical regulation:
* Chemical ( COP:
1. Catecholamines (adrenaline, noradrenaline and isoprenaline) and Sympathomimetic drugs (ephedrine, amphetamine); they ( COP because they ( HR and (SV.
2. Thyroxin; (HR (discussed before) and (VR (because of the peripheral VD) ((SV((COP.
Work of the heart during rest and exercise
The work done by the cardiac muscle is composed of twparts:
1) Pumping blood against resistance (potential work):
It represents the major part of the work of the heart. It is used tpump the blood (COP) form the ventricles tthe peripheral arteries against the resistance of ABP. So, it depends on twfactors; COP and ABP.
Potential work = COP x mean ABP
* Work of the left ventricle: = 5 L x 100 mm Hg x 13.6 (density of mercury) = 6800 gm. Meter / min = 6.8 Kg. Meter / min.
* Work of the Rt. ventricle:
The COP of the Rt. ventricle = COP of the left ventricle.
The mean pulmonary BP ( 17 mm Hg ) = 1/6 the mean arterial BP (
So, the work of the Rt. ventricle = 1/6 the work of the left ventricle.
* Work of the whole heart:
= Work of left ventricle + work of Rt. ventricle.
= 6.8 + 1/6 x 6.8 = About 8 Kg. Meter / min = 480 Kg. Meter/ hour.
2) Giving velocity tthe ejected blood (kinetic work):
During rest the kinetic work represent about 2% of the total work of the heart ( 0.14 Kg. met / min). so, it is usually neglected.
During muscular exercise it increases markedly ( up t20% of the total work ) due tincrease in the blood velocity.
Mechanical Efficiency of the heart
during rest and exercise
The energy used by the heart is partially transformed intmechanical work and the other part is liberated as heat. So, ME of the heart is the percentage ratiof the work done tthe total energy expenditure.
ME of the heart equals 20 % during rest, 30% during muscular exercise, 40% in athletes during exercise and 3 % in heart failure.
ME of the heart can be increased either by:
a) Increasing the work done OR.
b) Decreasing the energy expenditure.
Since the work of the heart = COP x BP. So, the work of the heart ( and consequently the ME ) can be increased either by:
I) Loading reflex, caused by ( VR ( preload ):
( VR ( ( COP ( ( work of the heart ( ( ME.
Also, ( VR ( ( HR ( Bainbridge reflex ) and ( sympathetic stimulation ( ( O2 consumption ( ( energy expenditure.
So, the net result is a mild ( in ME. This means that the heart can increase its work ( tpump the excess VR ) but with much O2 consumption.
II) Unloading reflex, caused by ( BP ( after load ):
( ABP ( ( work of the heart ( ( M.E.
Also, ( ABP ( ( HR (Mary’s law) and ( vagus stimulation ( ( O2 consumption ( ( energy expenditure.
So, the net result is a marked ( in ME. This means that the heart can ( its work tovercome the high peripheral resistance ((ABP) without increase in O2 consumption or energy expenditure (i.e. economically).
Cardiac reserve
The cardiac reserve is the difference between the cardiac work done during rest and that done during sever muscular exercise. The heart can ( its work during severe muscular exercise by about 10 times or more. The work of the heart increases during muscular exercise due to:
1. ( COP.
2. ( Arterial BP.
3. ( Velocity of blood flow (( the work by about 20%).
Mechanism of cardiac reserve:
The heart can perform an extra work by the following 3 mechanisms:
1) HR reserve; by acceleration:
HR( from 70 beat/min 200 beat / min ( i.e. 3 times) so, the COP ( 3 times ( provided that the VR is adequate ) so, the work of the heart ( 3 times.
2) SV reserve; by dilatation (( EDV) and alsby ( ESV:
* SV( from 70 cc /beat 200 cc / beat ( i.e.3 times ). So, the COP ( 3 times and alsthe work of the heart ( 3 times. SV increases due to:
* Dilatation of the ventricle ( (EDV ) which is due t( VR. This leads t( strength of ventricular contraction ( Starling’s law) (( SV.
* Sympathetic stimulation which increases more the strength of ventricular contraction ( ( ESV (( SV.
COP = HR ( (3 times) x SV (( 3 times) = ( 9 times.
3) Hypertrophy of the cardiac muscle:
Hypertrophy is the increase in the size of the cardiac muscle which occurs very slowly as a result of prolonged strain on the heart as in:
* Physiological hypertrophy which occurs in athletes of weight lifting and long distance runners.
* Pathological hypertrophy which occurs in patients with hypertension, aortic stenosis or aortic regurgitation.
– Hypertrophy ( the strength of ventricular contraction ( ( ESV ( ( SV.
– Also, hypertrophy is accompanied by dilatation and ( EDV ( ( contraction (Starling’s law) (( SV.
Limits of the cardiac reserve:
The cardiac reserve mechanisms have certain limits, beyond which the work decreases. These limits are:
1) Excessive acceleration (above 200 beat / min), shortens the diastolic period (( diastolic filling ((SV((COP.
2) Excessive dilatation, leads t( strength of the ventricular contraction because the limit of Starlings law is exceeded, sSV ( and COP(.
3) Excessive hypertrophy causes insufficient blood supply tthe hypertrophied cardiac muscle (relative ischaemia). So, the strength of the contraction ( leading t( SV and ( COP.
1. Humoral regulation
a) Effects of catecholamines are transmitted by alpha- and beta-adrenal receptors.
Adrenalin and noradrenalin stimulate heat activity and cause positive regulatory effects:
– Positive inotropic effect – increasing strength of heart contractions;
– Positive chrono-tropic effect – increasing heartbeat rate;
– Positive dromo-tropic effect – increasing heart conductibility;
– Positive bathmo-tropic effect – increasing excitability of heart muscle.
Nor-epinephrine increases permeability of cardiac fiber membrane tNa+ and Ca2+.
b) Effects of acetylcholine leads tincrease of K+ permeability through cell membrane in conductive system, which leads thyper-polarization and cause such effects tthe heart activity:
– Negative inotropic effect – decreasing strength of heart contractions;
– Negative chrono-tropic effect – decreasing heartbeat rate;
-Negative dromo-tropic effect – decreasing heart conductibility;
– Negative bathmo-tropic effect – decreasing excitability of heart muscle.
c) Effects of ions:
-Ca2+ causes spastic contraction of heart. Decreasing Ca2+ causes cardiac flaccidity.
Excessive concentration of K+ causes decreasing heart rate. Impulse’ transmission through AV bundle is blocked. If K+ level was previously decreased, increasing Concentration of K+ capable normalize cardiac rhythm. Na+ competes Ca2+ in contractile process. Sincreasing Na+ may depress cardiac contraction.
d) Effects of thyroid hormones.
Thyroid hormones increase transmission process in ribosome and nucleus of cells. Intracellular enzymes are stimulated due tincreasing protein synthesis. Alsincreases glucose absorption and uptake of glucose by cells, increases glycolisis and gluconeogenesis. In blood plasma increases contents of free fatty acids. All these effects of thyroid hormones lead tincrease activity of mitochondria in heart cells and ATP formation in it. So, both activity of heart muscle and conduction of impulses are stimulated.
e) Effects of adrenocortical hormones.
Aldosterone causes increasing Na+ and Cl- in blood and decreases K+. This is actually for producing action potential in the heart. Cortisol stimulates gluconeogenesis and increase blood glucose level. Aminacids blood level and free fatty acids concentration in blood increases also. Utilization of free fatty acids for energy increases. These mechanisms actual in stress reaction. Sheart activity is stimulated.
f) Hormones of islets of Langerhans effects.
Insulin promotes facilitated diffusion of glucose intcells by activation glucokinase that phosphorilates glucose and traps it in the cell, promotes glucose utilization, causes active transport of aminacids intcells, promote translation of mRNA in ribosome tform new proteins. Alsinsulin promotes glucose utilization in cardiac muscle, because of utilization fatty acids for energy. Clucagone stimulate gluconeogenesis, mobilizes fatty acids from adipose tissue, promotes utilization free fatty acids foe energy and promotes gluconeogenesis from glycerol. Sboth hormones can increase strength of heartbeat.
g) Endocrine function of heart. Myocardium, especially in heart auricles capable tsecretion of regulatory substances as atria Na-ureic peptide, which increases loss of Na+ in increase of systemic pressure, or digitalis-like substances, which can stimulate heart activity.
