Blood Flow
A- Regulation of local blood flow to tissues:
Blood flow in different organs is physiologically maintained by
adjusting the diameter of their arterioles. The mechanisms of regulation
of regional: local blood flow can be classified into; Short-term and long
tent regulation mechanisms.
Short-tern regulation mechanisms:
These mechanisms adjust the minute-to-minute flow to the organs
according to their metabolic needs. Four mechanisms are involved:
a- Metabolic auto regulation. c- Hormonal regulation.
b- Nervous regulation.
d- Myogenic auto regulation.
Metabolic auto regulation:
Increased metabolic activity dilates the blood vessels. This effect is
mediated by:
A- Hypoxia, The increased O
2
utilization by the tissues produces local
hypoxia. The degree of vascular dilation is directly proportionate to the
degree of hypoxia in arteriolar blood. in contrast, an increase in O
2
, level
(hyperoxia) produce local vasoconstriction and decrease in blood flow.
B- Vasodilator metabolites, hid metabolism with hypoxia produces a
number of vasodilator metabolites, which include:
1- Adenosine; which is the most important vasodilator substance released
from active tissues. An ischernic or hypoxic heart releases adenosine
which dilates the coronaries and corrects the ischemia or hypoxia.
Adenosine is also released by skeletal muscles and other tissues.
2. ADP and AMP which are produced by hydrolysis of AT?.
3. CO
2
and H
+
ions which act directly on the vascular smooth muscles
and relax them. CO
2
is a very powerful dilator of the cerebral blood
vessels
4. Lactic acid which is produced by anaerobic glycolysis. it has no direct
vasodilator effect, hut acts through elevation of H ion concentration.
5. IC released from active cells. It relaxes the vascular smooth muscles.
C- The endothelium produces several molecules that promote smooth
muscle relaxation (vasodilators), including nitric oxide (NO), bradykinin,
and prostacyclin.
D- The Endothelium-Derived Relaxing Factor (EDRE): This is a
powerful vasodilator substance secreted by the vascular endothelium.
This substance chemically was found to he nitric oxide. it is released
from the arterial endothelium when stimulated by bradykinin, VIP or
ACH (acetylcholine). i.e. these vasodilator substances act through
releasing EDRF and it is the EDRF which mediates the vasodilator effect
or these substances. in the absence of EDRE, bradykinins and VIP are
ineffective and ACH produces vasoconstriction not dilation, EDRE is
also produced when the blood flow to a tissue is increased as a result of
arteriolar dilatation, thus further increasing the blood flow to that tissue.
Nervous regulation:
All blood vessels except the capillaries are innervated. Regional
vasodilator fibers supply the vessels of some organs. Vasodilation in
specific organs occurs by the following mechanisms:
• Activation of parasympathetic vasodilator nerves produces vasodilation
in their specific organs, e.g. the salivary glands.
• Stimulation of the sympathetic vasodilator system dilates the skeletal
muscle vessels and increases the blood flow in the skeletal muscles.
• Stimulation of sympathetic cholinergic nerve supply to sweat lands
dilates the gland vessels and increases the local blood flow.
• Inhibition of the basal sympathetic vasoconstrictor tone to the vessels.
Some organs receive no vasodilator fibers (e.g. the skin), constriction or
dilation of their vessels occurs by changing the sympathetic vasomotor
tone.
Hormonal Regulation
This is regulation by vasoactive substances released from the tissues into
the blood and tissue fluids, examples:
Serotonin: This is a vasoconstrictor substance released from platelets
during the platelet release reaction. It helps to stop bleeding from
wounds. Serotonin is also found in chromatin cells in the intestine.
Histamine: This is a strong vasodilator substance which is released from
mast cells and halophiles in damaged or inflamed tissues. It is also
released during allergic reactions. In small doses, histamine dilates the
arterioles, but in large doses, it dilates all the vessels.
Prostaglandins (PC): These are hormone-like substances, some of them
(PG F) are constrictors, but most of them (PG A and PG E) are dilators.
Bradykinins: these are strong vasodilator substances formed in tissues
during inflammations or increased activity. The tissues release an
activator substance to activate prekallikrein in tissue fluids into active
kailikrein. Kailikrein acts on a2-giobuiin in tissue fluids to produce
kallidin. Kallidin is then converted by tissue enzymes into bradvkinin,
Bradykinin is now believed to be the mediator of vasodilation in sweat
and digestive glands when they are activated. Kallikreiri and
ߙ2-globulin
are also found in plasma.
Myogenic auto regulation:
This is done by constriction when pressure increases and dilation
when pressure decreases. This phenomenon is found in she vascular beds
of certain organs like the kidney, brain, skeletal muscles. mesentery and
the liver.
The mechanism of myogenic auto regulation is that when the blood
pressure increases → distention of arteriole and stretch of its wall →
intrinsic myogenic contraction response → vasoconstriction→ decrease
in blopd flow back towards normal.
The opposite reaction, occurs when the blood pressure fails. This
enable an organ like the kidney to maintain- an almost constant blood
flow in arterial blood pressure range of 80-160mmHg. In the brain,
changes in systemic arterial pressure are compensated by the appropriate
responses of vascular smooth muscle.
A decrease in arterial pressure causes cerebral vessels to dilate, so
that adequate rates of blood low cart he maintained despite the decreased
pressure. While, high blood pressure causes cerebral vessels to constrict,
so that finer vessels downstream are protected from the elevated pressure.
These responses are myogenic; they are direct responses by the vascular
smooth muscle to changes in pressure.
Long-term regulation mechanisms:
These mechanisms adjust the basal blood flow over long periods of
time. Thai mite few hours up to few weeks to he filly effective, They
correct any change in basal flow at blood pressure range of 50-250
mmHg. Three mechanisms are involved:
a- Opening of closed collaterals.
b- Formation of new vessels.
c-Narrowing or closure of some vessels.
Opening of closed collaterals:
When an artery or a vein is blocked, hew vascular channels, which
bypass the blocked segment, opens within one to two minutes, Such
alternative vascular channels are normally found, but they are closed,
Hypoxia and the metabolic vasodilators of the ischemic segment lead to
their opening.
Formation of new vessels (angiogenesis):
Hypoxic tissues (either due to lack of O
2
supply or high metabolic
rate) produce angiogenic substances called angiogenins. These substances
stimulate the sprouting of new vessels from the wall of venules and
capillaries. Some of these vessels may grow up to font arterioles or even
sin all arteries. The ability of young tissues to form new blood vessels in
response to hypoxia is very high.
Narrowing or closure of vessels:
Increased blood flow (e.g. by increase in arterial blood pressure) or
breathing air with high O
2
content or depression of tissue metabolism
elevates the local O
2
level (hyperoxia). Blood vessels constrict. If
hyperoxia. lasts for a long time, structural changes take place in the
vascular wail leading to permanent narrowing of the vascular lumen (e.g.
arteriosclerotic changes which occur with chronic hypertension) some
vessels might even get completely closed and obliterated.
B-Regulation of Blood Flow:
This is the Regulation of Blood Flow either by the autonomic
nervous system or by the endocrine system. Angiotensin II, for example,
directly stmu1ates vascular smooth muscle to produce generalized
vasocoristriction. Antidiuretic hormone (ADH) also has a vasocccstrictor
effect at high concentrations; this is why it is also called vasopressin. This
vasopressor effect of ADH is not believed to be significant under
physiological conditions in humans.
Regulation of blood flow by Sympathetic Nerves
Stimulation of the sympathoadrenal system produces an increase in
the cardiac output and an increase in total peripheral resistance through
ߙ-adrenergic simulation of vascular smooth muscle by norepinephrine
and to a lesser degree, by epinephrine. This produces vasoconstriction of
the arterioles in the viscera and skin.
In resting condition. when a person is calm, the sybathoadrenal
system is active to a certain degree and helps set the tone of vascular
smooth muscles. In this case adrenergic sympathetic fibers (those that
release norepinephrine) activate
ߙ-adrenergic receptors to cause a basal
level of vasoconstriction throughout the body.
During the fight-or-flight reaction, an increase in the activity of
adrenergic produces vasoconstriction in the digestive tract. Kidneys and
skin and vasodilation in the skeletal muscles which receive cholinergic
sympathetic fibers, that release acetylcholine as a neurotransmitter.
Vasodilation in skeletal muscles is also produced by epinephrine secreted
by the adrenal medulla, which stimulates beta-adrenergic receptors. in
other words, during the fight-or-flight reaction, blood flow is decreased to
the viscera and skin because of the a-adrenergic effects of
vasoconstriction in these organs, whereas blood flow to skeletal muscles
is increased.
Regulation of blood flow by Parasympathetic Nerves
Parasympathetic endings in arterioles are always cholinergic and
always promote vasodilation. Parasympathetic innervation of blood
vessels, however, is limited to the digestive tract, external genitalia, and
salivary glands. Because of this limited distribution, the parasympathetic
system is less important than the sympathetic system in the control of
total peripheral resistance.
Types of blood flow:
Laminar flow: The flow of blood in almost all vessels in the body is a
smooth, streamline, laminar flow. i.e. the blood flows in several layers or
laminar around a central layer. The central lamina moves at maximum
velocity whereas the outer laminar move at lower velocities. The
outermost lamina is practically static and adherent to the vascular
endothelium. Tie mean ve1oci’ of blood flow is the average of the
velocities of all layers in the vessel. The RBCs generally travel in the
central laminar, while the plasma generally travels in the outer laminar.
The laminar flow is silent (i.e. producing no sounds). So, normally no
sound is heard if a stethoscope is applied over a blood vessel. The friction
forces on the vascular endothelium are minimal.
Turbulent Flow: This is disturbed blood flow in the form of eddies in
various directions, in which fluide particules move in forward as well as
side-to-side directions. Turbulence produces sounds (bruits or murmurs)
that can be heard by the stethoscope. The friction forces of the turbulent
flow on vascular endothelium are high. It may 1ead to excess to excessive
shedding of lining endothelium (thus predisposing to intravascular
cloning and development atherosclerosis).
Methods for measuring the blood flow rate:
Measuring blood flow through an organ
1- Plethysn1oraphy: recording change in volume of an organ after
occluding its venous drainage. Rate of increase in volume of the organ
equals rate of blood flow.
2- Holds principle.
3- Plasma clearance: e.g., determination of renal blood flow.
Measuring blood flow through a blood vessel
1-Electromagnetic flow meters.
2-The ultrasonic Doppler flow meters.
