12- Circulation through special regions
Coronary circulation
Anatomical considerations :
The two coronary arteries that supply the myocardium arise behind the
aortic valve at the root of the aorta. Eddy currents keep the valves away
from orifices of the coronary arteries. Venous blood returns to the heart
through the coronary sinus and anterior cardiac veins which drain into the
right atrium. Anastomoses between coronary arteries in humans are only
less than 40 µm in diameter, but there is evidence that these channels
enlarge and increase in number in patient with coronary artery disease.
Regulation of coronary Blood flow:
1-Neural factor:
Coronary arterioles contain α-adrenergic receptors which mediate
vasoconstriction and β2-adrenergic receptors which mediate
vasodilation. The predominant effect of sympathetic stimulation in
coronary arteries is vasodilation. Parasympathetic stimulation also causes
modest dilatation of normal coronary arteries. Healthy coronary
endothelium release nitric oxide (NO) which promotes vasodilation, but
if endothelium is damaged by atheroma, endothelium dependent
vasodilation may be impaired.
2-Chemical factor:
When metabolism of myocardium is increased, vasodilator substances
increase which cause coronary vasodilation such as O2 lack, increase
concentration of CO2, H+, K+, lactate, and adenosine. Adenosine is
powerful vasodilator in coronary vessels. 3-Aortic pressure: When the
systemic blood pressure fall, the noradrenergic discharge increases due to
effect of the sympathetic reflex and coronary blood flow increases. At
same time cutaneous, renal, splanchnic vessels are constricted. So the
coronary circulation shows autoregulation.
Coronary blood flow at rest in humans is about 250 ml / min. (5 % of
cardiac output). The coronary vessels are severely compressed during
systole. BF to left ventricle is during diastole only, while BF to right
ventrile and atria are reduced during systole. So subendocardial portion
of left ventricle is prone to ischemic damage which is most common site
of myocardial infarction (MI). The narrowing coronary artery by
atheromatous does not limit blood flow even during exercise until the
cross-sectional area of vessel is reduced by at least 70%.
Coronary artery diseases :
1- Stable angina. The most cause of angina is atherosclerosis. See
figure 49.
2-Unstable angina. Coronary arteries can be constricted by vasospasm to
produce anginal symptoms.
3-Myocardial infarction (MI).
If myocardial ischemic is sever and prolonged, irreversible changes
occur in the Myocardial muscle lead to MI. The cause of MI is
atherosclerotic plaque or hemorrhage into it which triggers the formation
of coronary clot at site of plaque.
Figure (49): Atherosclerotic plaque.
Coronary arteries bypass grafting (CABG):
The internal mammary arteries, radial arteries or segment of patient's
own saphenous vein can be used for bypass coronary artery stenosis. This
usually involves major surgery under cardiopulmonary bypass. See
figure50.
Figure (50): Coronary arteries bypass grafting.
Microcirculation
The major mechanisms for exchange are diffusion and filtration.
Substances pass through the junction between endothelial cells and
through fenestrations, when they are present. Some also pass through the
cells by vesicular transport or through the cytoplasm in the case of lipidsoluble substances. Diffusion is much more important in exchange of
nutrients and waste materials between blood and tissue. O 2 and glucose
are in higher concentration in bloodstream than in the interstitial fluid, so
they diffuse to the interstitial fluid, whereas CO 2 diffuses in the opposite
direction. The rate of filtration at any point depends upon a balance of
Starling forces.
Cerebral circulation
Anatomic consideration of vessels: The principal arterial inflow to
brain in humans is via four arteries. Two internal carotid and two
vertebral arteries. The vertebral arteries unit to form the basilar artery.
The basilar and the carotids artery form the circle of Willis below the
hypothalamus. The circle of Willis is the origin of the six
large vessels supplying the central cortex. Figure 51.
Figure (51): Cerebral circulation.
Venous drainage from the brain by deep veins and dural sinuses empties
principally into the internal jugular veins in humans.
The cerebral vessels have a number of anatomic features:
1- In choroid plexus there are gaps between the endothelial cells of
capillary walls, but the choroid epithelial cells that separate them from
CSF are connected to one another by tight junction.
2- Capillaries in the brain substance are non-fenestrated resemble
capillaries of muscles, tight substance between endothelial cells.
Substance transport through capillaries is by vesicular transport.
3- Brain capillaries are surrounded by end feet of astrocytes. These end
feet are closely applied to the basal lamina of the capillaries but they do
not cover the entire capillary wall and there are gaps about 20 nm
between end feet. See figure 52.
Figure (52): Transport across cerebral capillaries (Ganong's review of
medical physiology 2010).
Innervations: three systems of nerve innervate the cerebral blood vessels
postganglionic sympathetic neurons, their ending contain norepinephrine
many contain neuropeptide Y, they cause vasoconstriction. Cholinergic
neurons also innervate the cerebral vessels and their ending contain
acetylcholine many contain vasoactive intestinal peptide (VIP), they
cause vasodilation. While sensory nerves are found on most distal
arteries, their cell bodies in the trigeminal ganglia and contain P
substance. Toughing or pulling cerebral vessel cause pain.
Cerebral blood flow: There are many methods to measure cerebral
blood flow as Kety method which depends on Fick principle by use
inhaled nitric oxide (N2O) Blood flow in the cerebral cortex and
cerebellar cortex is high, but the part of the brain with highest blood flow
per gram is the inferior colliculus. The blood flow in gray matter is much
greater than in white matter. The average cerebral blood flow in young
adult is about 54 mi/ 100 g / min. If the weight of brain is 1400 gm, so
the cerebral blood flow is 765 ml/min.
Regulation of cerebral circulation:
In site of marked local fluctuation in brain blood flow, the blood flow
remains relatively constant. The factors that effect blood flow are:
1- Intracranial pressure: the cerebral vessels are compressed
whenever the cranial pressure rises.
2- Mean venous pressure: any change in venous pressure causes a
similar change in the intracranial pressure.
3- Concentration of vasodilator substances: There are marked local
fluctuation in blood flow by vasodilator metabolites such as K ions, H
ions and adenosine. The most important local vasodilator for the
cerebral circulation is CO2
4-Viscosity of blood.
5- Mean arterial pressure at brain level. Neural sympathetic control
help to maintain constant blood flow with elevated blood pressure, but it
play a minor role. The autorgulation maintains a normal cerebral blood
flow at arterial pressure of 65 – 140 mmHg.
Brain is sensitive to hypoxia, and occlusion of its blood supply produces
unconsciousness in short period as 10 second. Glucose enters the brain via
glucose transporter, found in high concentration in cerebral capillaries. There
is decrease glucose utilization during sleep. Glucose utilization at rest
parallels to blood flow or oxygen consumption. Because of low stored
glucose and glycogen, the brain can not stand when total blood occlusion for
more than 2 minute (which is longer time than it can withstand hypoxia).
The cortical regions are more sensitive to hypoglycemia than centers in the
brain stem. Ammonia is very toxic to nerve cells and ammonia intoxication
is major neuralgic symptoms in hepatic failure. Insulin is not required for
most central cells to utilize glucose.
Effect of gravity on the body
The following changes occur when an individual move from a supine
position to standing position:
1- A significant increase blood pools in the lower extremities.
2- Increase venous pressure in legs.
3- Decrease venous return, both stroke volume, COP decrease (FrankStarling relationship), and decrease in arterial pressure
4- If COP decrease cerebral blood pressure becomes low, fainting may
occur.
Compensatory mechanism: Vasomotor center then increases sympathetic
outflow to the heart and blood vessels and decreases parasympathetic
outflow to heart. As a result, heart rate and TPR increase and blood pressure
increases toward normal
Effect of altitude on the body:
As we ascend to higher altitude in aviation, The following changes occur:
1-The oxygen partial pressure decreases, hypoxia beginning at altitude of
about 12,000 feet ( drowsiness, lassitude, mental and muscle fatigue,
sometime headache).
2-Hypoxia stimulates arterial chemoreceptors to increase ventilation to a
maximum of about 1.65 times of normal. This is an immediate compensation
with in seconds.
3-It increases red blood cell production, hematocrit from 40 – 45 to about
60.
4- Increase concentration of hemoglobin from 15 gm /dl to about 20 gm
/dl.
5- It increases diffusing capacity for O2 through the pulmonary
membrane 3 fold as much as during exercise. Normal capacity 21 ml /
mmHg / minute.
6- Increase the cardiac output (COP) 30% immediately after a person
ascends to high altitude but then decrease back toward normal as the blood
hematocrit incre es.
7- Increase in number of systemic circulatory capillaries.
8- In animals native to altitude of 13,000 to 17,000 feet, cell mitochondria
and cellular oxidative enzyme systems are slightly more plentiful.