Download Regulation

Special circulation - fetal
Fetal circulation
birth
Changes in pressure closure of foramen ovale
• Umbilical artery ligation  2x increase of peripheral resistance
 increase of blood pressure in left heart and systemic
circulation
• Lung inflation + vasodilatation  5x decrease of resistance 
decrease of blood pressure in right heart
Changes in pO2  closure of ductus arteriosus
• pO2 from 20 to 100 mm Hg  vasoconstriction  closure 1-8
days later + fibrotization after 1-4 months
Vascular spasm  closure of ductus venosus
Change HbF into HbA
Relative blood distribution
Specific circulation – coronary
blood flow
Specific circulation – brain and
blood-brain barrier
Specific circulation – portal
systems
Specific circulation –
countercurrent mechanism
Specific circulation – liver and
intestine

Hepatic sinuses

Blood supply to
enterocytes
The goals of regulation

To increase blood flow where necessary
(working muscle, digestion, gland secretion etc)

To regulate temperature
skin vasodilatation/vasoconstriction resulting in heat
spare/loss

To maintain constant blood flow where
necessary and/or functional
(brain, heart, … kidney, lungs)
principles
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heart (cardiomotor)
inotropy,
bathmotropy,
chronotropy,
dromotropy
blood (volume)
vasomotor
vasodilatation x
vasoconstriction
β-2 adrenergic receptor↑Gs activity → ↑AC activity → ↑cAMP → ↑PKA activity → phosphorylation of MLCK → ↓MLCK activity →
dephosphorylation of MLC
↑α1 adrenergic receptorActivation of Gq --> ↑PLC activity --> ↑IP3 and DAG --> activation of IP3 receptor in SR --> ↑intracellular Ca2+
Regulation of blood circulation
Mechanisms of regulation:
 Local
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Humoral (chemical) – O2, CO2, H+
Nervous
Enzymatic and hormonal
General/systematic
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Fast = short-term (regulate blood pressure)
Slow = long-term (regulate blood volume) – several
days
Local chemical regulatory
mechanisms
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
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The most obvious in the heart and the brain
Goal: autonomic regulation of resistance by
organ based on its metabolic needs
Principle: accumulation of products of
metabolism (CO2, H+, lactic acid ) or
consumption of substances necessary for
proper function (O2) directly affects smooth
muscles of vessels and induce vasodilatation
Figure 1: Brain maps
illustrating increasing
activity and functional
connectivity of perisylvian
and extrasylvian areas in
both hemispheres as
subjects read
words, sentences
and narratives.
These emergent, contextdependent effects are
demonstrated using both
fMRI and EEG coherence
methods.
Figure 44: Across-subjects (N=10) z-statistic maps
overlaid on an anatomical template.
Congruent
audiovisual speech activated the auditory and
the visual cortical areas, as well as the inferior frontal,
the premotor and the visual-parietal areas bilaterally
(upper panel).
speech
Incongruent audiovisual
caused a similar but more extensive pattern
of brain activity (middle panel). The difference reached
significance in three left hemisphere areas: Brocat’s area
(BA44/45), superior parietal lobule (BA7) and prefrontal
cortex (BA10) (lower panel). In the contrast ’Congruent >
Incongruent’ no statistically significant voxels were
detected. Activation images were thresholded using
clusters determined by voxel-wise Z>3.0 and a cluster
significance threshold of p<0.05, corrected for multiple
comparisons.
Local nervous

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The most obvious in the skin and mucous
Goal: central regulation of blood distribution
Principle: Autonomic nervous system

Sympaticus
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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
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Platelets

Endothelium


balance
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Thromboxan A – vasoconstriction
Prostacyclin – vasodilatation
Endothel-derived relaxing factor = NO
(arginin =>nitric oxid synthetase=>NO=>G-cyclase =>cGMP =>
vasodilatation)

Endothelin1
most potent vaso/venoconstrictor, receptors in smooth muscles,
besides circulation in kidney GFR. Activated by Angiotensin-II,
catecholamines etc
Local enzymatic and hormonal

Plasma protein - Kinin ↑ = vasodilatation


bradykinin and kallikrein
A role in inflammation, coagulation, pain and gland
secretion (sweat, salivatory, pancreas -> increases blood flow
locally)
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Hormones of adrenal medula: adrenalin
(vasodilatation), noradrenalin (vasoconstriction)
General fast & slow regulatory
mechanisms
General fast (short-term)
regulatory mechanisms

Nervous autonomic reflexes
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Baroreflex
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glomus caroticum, glomus aorticum
Afferentation: IX and X spinal nerve
Centre: medulla oblongata, nucleus
tractus solitarii
Efferentation: X spinal nerve (ps),
sympathetic fibers
Effectors: heart (atriums), vessels
Effect: After acute increase of blood
pressure – activation of receptors –
decrease of blood pressure
(vasodilatation, decrease of effect
of sympathetic nerves)
SYMP
PARASYMP
right: Pathways within the lower brain stem and spinal cord that subserve the
baroreceptor and chemoreceptor reflex control of the sympathetic outflow to the
heart and blood vessels. The open triangles indicate excitatory synaptic inputs and
the filled triangles inhibitory synaptic inputs. CVLM, caudal ventrolateral medulla;
IML intermediolateral cell column in the spinal cord; KF, Kölliker-Fuse nucleus in
pons; NTS, nucleus tractus solidarus.
Carotid sinus massage
Purpose
Sinus, in this case, means an area in a blood vessel
that is bigger than the rest of the vessel. This is a
normal dilation of the vessel. Located in the neck just
below the angle of the jaw, the carotid sinus sits
above the point where the carotid artery divides into
its two main branches. Rubbing the carotid sinus
stimulates an area in the artery wall that contains
nerve endings. These nerves respond to changes in
blood pressure and are capable of slowing the heart
rate. The response to this simple procedure often
slows a rapid heart rate (for example, atrial flutter or
atrial tachycardia) and can provide important
diagnostic information to the physician.
Description
The patient will be asked to lie down, with the neck
fully extended and the head turned away from the side
being massaged. While watching an electrocardiogram
monitor, the doctor will gently touch the carotid sinus.
If there is no change in the heart rate on the monitor,
the pressure is applied more firmly with a gentle
rotating motion. After massaging one side of the neck,
the massage will be repeated on the other side. Both
sides of the neck are never massaged at the same
time.
General fast (short-term)
regulatory mechanisms

Humoral mechanisms


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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
slow (long-term)
Regulatory mechanisms of water and electrolytes
exchanges

autoregulation of total blood volume by kidneys

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Increase of ADH (vasopressin)


When ↓ blood volume → ↓ 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 (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
Intracardial regulatory
mechanisms (1)
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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
Myocardium – correlation length x
tension
beta receptor
activation
blockage


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