Download Regulation of circulation

Specific circulatory systemregulation of the heart and vessel
activities
Romana Šlamberová, MD PhD
Department of Normal, Pathological and
Clinical Physiology
Introduction


Slides from the lecture.
Respecting the copyrights it was not
possible to publish pictures showed at the
lecture at our website.
© 2006, Romana Slamberova, MD PhD
Distribution of blood
circulation

Total volume of blood in all vessels
(intravascular volume):



man: 5.4 l (77 ml / kg)
woman: 4.5 l (65 ml / kg)
Distribution:



Heart 7%
Pulmonary circulation 9%
Systemic circulation 84%




from that veins 75%
large arteries 15%
small arteries 3%
capilaries: 7%
Resistance of blood circulation



Total peripheral resistance:  of all paralel
restistance in the body
Actual resistance is given based on the lumen of
vessels and viscosity of blood
Percentage portion of resistance in different types of
vessels:





large arteries 19%
small arteries 47%
capillaries 27%
veins 7%
Resistance depends not only on type of vessel, but
also on the actual situation of blood need in organs
Regulation of blood circulation
Mechanisms of regulation:
 Local




Humoral (chemical) – O2, CO2, H+
Nervous
Enzymatic and hormonal
General


Fast = short-term (regulate blood pressure)
Slow = long-term (regulate blood volume) – several
days
Local chemical regulatory
mechanisms



The most obvious in the heart and the brain
Goal: autonomic regulation of resistance by
organ based on its metabolic needs
Principal: accumulation of products of
metabolism (CO2, H+, lactacid ) or
consumption of substances necessary for
proper function (O2) directly affects smooth
muscles of vessels and induce vasodilatation
Local nervous regulatory
mechanisms



The most obvious in the skin and mucous
Goal: central regulation of blood distribution
Principal: Autonomic nervous system

Sympaticus



Vasoconstriction – activation of α receptors in vesselsnoradrenalin (glands, GIT, skin, mucous, kidneys, other inner organs)
Vasodilatation – activation of β receptors in vessels – adrenalin
(heart, brain, skeletal muscles)
Parasympaticus - Acetylcholin


Vasoconstriction – heart
Vasodilatation – salivatory glands, GIT, external genitals
Local enzymatic and hormonal
regulatory mechanisms

Kinin ↑ = vasodilatation




Cells of GIT glands contain kallikrein – changes kininogen to
kinin → kallidin → bradykinin (vasodilatation)
Kinins are any of various structurally related polypeptides,
such as bradykinin and kallikrein, that act locally to induce
vasodilation and contraction of smooth muscle.
A role in inflammation, blood pressure control, coagulation
and pain.
Hormones of adrenal medula: adrenalin
(vasodilatation), noradrenalin (vasoconstriction)
General fast (short-term)
regulatory mechanisms (1)

Nervous autonomic reflexes

Baroreflex






glomus caroticum, glomus aorticum
Afferentation: IX and X spinal nerve
Centre: medulla oblongata, nucleus tractus solitarii
Efferentation: X spinal nerve, sympatetic fibres
Effector: heart (atriums), vessels
Effect: After acute increase of blood pressure –
activation of receptors – decrease of blood pressure
(vasodilatation, decrease of effect of sympaticus)
General fast (short-term)
regulatory mechanisms (2)

Receptors in the heart


Reflex of atrial receptors – mechano- and volumoreceptors
– activated by increased blood flow through the heart
 A receptors – sensitive to ↑ of wall tension after systole of
atriums
 B receptors – sensitive to ↑ of wall tension after systole of
ventricles
Ventricular receptors – mechano- and chemical receptors activated in pathological cases
 Hypoxia of myocardium → decrease of heart rate
(Bezold-Jarisch reflex) → protection of myocardium of
larger damage
General fast (short-term)
regulatory mechanisms (3)

Humoral mechanisms



Adrenalin – β receptors →
vasodilatation → ↓ peripheral
resistance → blood from skin
and GIT to skeletal muscles,
heart and brain → ↑ minute
heart volume
Noradrenalin – α receptors
→ vasoconstriction → ↑ blood
pressure
Renin-angiotensin –
activated by ↓ pressure in vas
afferens
General slow (long-term)
regulatory mechanisms
Regulatory mechanisms of water and electrolytes
exchanges

Regulation of total blood volume by kidneys


Increase of ADH (vasopressin)


When ↑ blood pressure → ↑ of filtration pressure in glomeruli → ↑
production of urine → ↓ volume of circulating blood → ↓ blood
pressure
↑ ADH → ↑ of the permeability of collecting ductus for the water →
water is reabsorbed → ↑ volume of circulating blood → ↑ blood
pressure
Increase of Aldosterone

↑ aldosterone → ↑ reabsorbtion Na+ and water → ↓ volume of urine
→ ↑ volume of circulating blood → ↑ blood pressure
Intracardial regulatory
mechanisms (1)


Frank-Starling’s law =
initial length of the fibers is
determined by the degree
of diastolic filling of the
heart, and the pressure
developed in the ventricle is
proportionate to the total
tension developed.
The developed tension
increases as the diastolic
volume increases until it
reaches a maximum, then
tends to decrease.
Ganong: Review of Medical Physiology
Intracardial regulatory
mechanisms (2)

Ionotropic effect of heart rhythm

↑ heart frequency → ↑ amount of Ca2+ that
goes into heart cells → ↑ Ca2+ available for
tubules of sarkoplasmatic reticulum → ↑ Ca2+
that is freed by each contraction → ↑ strength
of contraction
Extracardial regulatory
mechanisms

Cardiomotoric centers



Inhibition – ncl. Ambiguus (beginning of n. vagus in
medulla oblongata)
Excitation - Th1-3 beginning of sympathetic fibres
Vasomotoric centers



In brain stem (medulla oblongata, Pons Varoli)
In the hypothalamus (controls activity of vasomotoric
centers in brain stem)
Brain cortex – control both the hypothalamus and the
brain stem
Stunning
Postischemic stunning - paralyzed
myocardium
Short-time ischemia of cardiac muscle provokes defects of contraction of
cardiac muscle.

Reversible dysfunction of contraction.

Persists also after reperfusion of ischemic myocardium, cardiac cells were
not permanently damaged and coronary flow was totally renewed.

There is no necrosis.
There is:

defect of calcium homoeostasis – antagonistic effect of calcium ameliorates
reparation of conctractions after ischemic stress - :








reduces transfer of calcium to the cells just during ischemia
lower reduction of ATP
reducing of volume of lesion
reducing of reperfusionallesion.
increasing of free oxygene radicals
increased transfer of extracellular Ca++ to the cells (always pathology!!)
antioxidants reduce (N-Acetylcystein, Oxypurinol)
Hibernation
Hibernating myocardium





some hours persisting defect of contraction function
reduced coronary flow
living cardiac cells
Adaptive response to low flow, hypoxia does not induces cellular death and
metabolism and clinical symptom s of ischemia.
After revival of coronary flow the function is regenerating.
Stunning x Hibernation x Si1ent ischemia
Coronary flow
normal or almost normal
significantly reduced

Differential diagnosis

To measure contraction function and regional blood flow.