Humoral and intra cardiac

mechanisms of heart ‘
regulation.
 Humoral regulation of heart
 Effects of thyroid hormones
 Thyroid hormones increase transmission process in
ribosome and nucleus of cells. Intracellular enzymes are
stimulated due to increasing protein synthesis. Also
increases 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 to increase
activity of mitochondria in heart cells and ATP formation
in it. So, both activity of heart muscle and conduction of
impulses are stimulated.
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.
 Amino acids 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. So heart
activity is stimulated.
 Hormones of Langerhans’ islets
effects
 Insulin promotes facilitated diffusion of glucose into cells
by activation glucokinase that phosphorilates glucose
and traps it in the cell, promotes glucose utilization,
causes active transport of amino acids into cells,
promote translation of mRNA in ribosome to form new
proteins. Also insulin 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. So both hormones can increase strength of
heartbeat.
 Endocrine function of heart
 Myocardium, especially in heart auricles
capable to secretion 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.
 Intrinsic regulation
 Intrinsic regulation is performed in response
changes of blood volume, flowing into the heart.
It is known as Frank Starling low. Within
physiological limits heart pumps all blood that
comes to it without allowing excessive damming
of blood in veins.
 Cardiac contraction is directly proportional to
initial length of its fibers. In end-diastolic volume
over 180 ml excessive stretching heart fibers
occurs and strength of next cardiac contraction
decreases.
 Anrep's effect
 Increase of blood flow in aorta and so
coronary arteries leads to excessive
stretching surrounding myocardial cells.
 According to Frank Starling low cardiac
contraction is directly proportional to initial
length of its fibers. So increase of
coronary blood flow leads to stimulation
heartbeat.
 Boudichi phenomenon
 In evaluation heart beat rate increase of
every next heart contraction is observed.
 It caused by rising of Ca2+ influx into
myocardial cells without perfect outflow,
because of shortening of cardio cycle
duration.
 Effects of nn. vagi
 Effects of nn. vagus on
the heart activity.
Parasympathetic
stimulation causes
decrease in heart rate
and contractility, causing
blood flow to decrease.
 It is known as negative
inotropic, dromotropic,
bathmotropic and
chronotropic effect.
 Effects of acetylcholin
 Effects of acetylcholin leads to increase of K+
permeability through cell membrane in conductive
system, which leads to hyper-polarisation and cause
such effects to the 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.
 Location of receptors in the heart
 Heart muscle contains, both chemical
and stretch receptors in coronary
vessels, all heart cameras and
pericardium. Stretch receptors are
irritated by changing blood pressure
in heart cameras and vessels.
 Chemo sensitive cells, which are
stimulated by decrease O2, increase
of CO2, H+ and biological active
substances also, are called as
chemoreceptors.
 Reflexes from atria
 When atria pressure increase due to increasing blood
volume, atria stretched. Signals pass to afferent arterioles in
kidneys to cause vasodilatation and glomerullar capillary
pressure, thereby increasing glomerullar filtration. Signals
also pass to hypothalamus to decrease antidiuretic hormone
secretion and so fluid reabsorbtion. It causes decreasing
both blood volume and arterial pressure to normal.
 Other reflex reaction is known as atria and pulmonary artery
reflex. When atria pressure increase due to increasing blood
volume, atria stretched. Low-pressure receptors, similar to
baroreceptors, in atria and pulmonary arteries stretched and
stimulated. Signals pass to vasomotor center and inhibit
vasculomotor area. Arterial pressure decreases to normal.
 Reflex reactions from receptors of
pericardium, endocardium and
coronary vessels
 Reflex reactions from receptors of pericardium,
endocardium and coronary vessels lead to
stimulation n. vagus. It leads to parasympathetic
stimulation of the heart.
 Parasympathetic stimulation causes decrease in
heart rate and contractility, causing blood flow to
decrease. It is known as negative inotropic,
dromotropic, bathmotropic and chronotropic
effect.
 Baroreceptor reflexes
 Increasing arterial pressure stretched and stimulated
baroreceptors in carotid sinus and aortic arc. Signals
pass through glossopharyngeal and vagal nerve to
tractus solitarius in medulla. Secondary signals from
tractus solitarius inhibit vasoconstrictor center and excite
vagal center.
 Peripheral vasodilatation and decrease both heart rate
and contractility occur. Arterial pressure decreases to
normal. When arterial pressure decreases, whole process
occurs, causing opposite result.
 Irritation of visceroreceptors

 Irritation of visceroreceptors results in stimulation

of vagal nuclei, which cause decreasing blood
pressure and heartbeat. Parasympathetic
stimulation causes decrease in heart rate and
contractility, causing blood flow to decrease. It is
known as negative inotropic, dromotropic,
bathmotropic and chronotropic effect.
 This mechanism is important for doctor in
performing diagnostic procedures, when probes
from apparatuses are attached into visceral
organs. This may cause excessive irritation of
visceral receptors.
 Mechanisms of heart auto
regulation
 Greater rate of metabolism or less blood flow causes
decreasing O2 supply and other nutrients. Therefore rate
of formation vasodilator substances (CO2, lactic acid,
adenosine, histamine, K+ and H+) rises. When decreasing
both blood flow and oxygen supply smooth muscle in
precapillary sphincter dilate, and blood flow increases.
 Moderate increasing temperature increases contractile
strength of heart. Prolonged increase of temperature
exhausts metabolic system of heart and causes cardiac
weakness. Anoxia increases heart rate. Moderate increase
CO2 stimulates heart rate. Greater increase CO2 decreases
heart rate.
Atria and pulmonary artery reflex

 When arterial pressure increases due to

increasing blood volume, atria stretched. Low-
pressure receptors, similar to baroreceptors, in
atria and pulmonary arteries stretched and
stimulated. Signals pass to vasomotor center
and inhibit vasculomotor area. Arterial pressure
decreases to normal.
 Excessive stretching of lung tissue causes
excitation of n. vagus. It leads to
parasympathetic stimulation of the heart.
Parasympathetic stimulation causes decrease in
heart rate and contractility, causing blood flow to
decrease.
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