Cerebral Circulation in Human Beings: Anatomy and Factors | Biology

In this article we will discuss about:- 1. Anatomical Considerations of Cerebral Circulation 2. Normal Values of Cerebral Circulation 3. Regulation 4. Factors.

Anatomical Considerations of Cerebral Circulation:

Blood enters the cranium through four vessels, two internal carotid and two vertebral arteries. The last two combine to form the basilar artery which divides into two posterior cerebral arteries. Each internal carotid artery divides into two branches – the middle and anterior cerebral arteries. Intercommunicating branches unite the six arteries on two sides forming the circle of Willis (Fig. 7.102). These vessels supply the different parts of brain.

Brain has a rich blood supply. The grey matter is more vascular than the white matter. The total capillary length per cu. mm of the grey and white matter is about 1 metre and 200 mm respectively. The cerebral vessels are not strictly end arteries. They freely anastomose. The free anastomosis in the circle of Willis makes an adequate distribution of blood to the different parts of the brain tissue and this is the only contributory help during emergency. A red cell from one lobe can easily pass to another lobe.

Venous blood drains into large cerebral sinuses, e.g., the superior sagittal, inferior sagittal, cavernous, straight, etc., all of which ultimately unite to form the two transverse sinuses —which become continuous with the two internal jugular veins.

Method of Study – Nitrous Oxide Method—Fick Principle:

The subject inhales a mixture of air and 15% of N₂O. Blood samples are collected from a peripheral artery and from the jugular vein at frequent intervals during the period when the subject inhales the mixture. N₂O content of the arterial and venous blood is determined. Cerebral blood flow per minute is determined from the arteriovenous difference of N₂O and the partition coefficient for N₂O between blood and brain. Results are recorded in millilitre per 100 gm of brain tissue per minute.

Vasomotor Supply:

The sympathetic carries vasoconstrictor fibres. Their stimulation causes an average reduction in diameter between 7-8%. The dilator fibres pass in the vagus and the Vll^th nerve. The vagus carries the afferent fibres and the great superficial petrosal branch of the facial nerve carries the efferent fibres.

Hence, stimulation of the Vll^th nerve or that of the central cut end of the vagus increases the diameter to about 22%. Since, the flow of liquid through a capillary tube is directly proportional to the fourth power of its radius; a dilatation of 22% will increase the flow by about 150%. There is evidence that vascularity of a particular part of brain increases during the activity of that part and may be associated with vasoconstriction of the other parts of brain.

Normal Values of Cerebral Circulation:

i. The average blood flow of normal subjects in resting condition is 54 ml per 100 gm of brain tissue per minute. Taking the weight of brain as 1,400 gm, total cerebral blood flow is 750 ml.

ii. Blood pressure in the large cerebral arteries is 100 mm of Hg systolic and 65 mm of Hg diastolic. In the capillaries, it is about 13 mm of Hg. It rises during inspiration and falls during expiration. But forced expiratory efforts, specially with closed glottis, raise the pressure by 30-50 mm of Hg.

iii. The total oxygen consumption of the brain is 50 ml per minute. Hence, the rate of oxygen consumption is fairly high. Arteriovenous O₂ difference is 6.2 ml% (arterial -19 ml%, Jugular -12.8ml%).

iv. Respiratory quotient (R.Q.) is unity, showing that carbohydrates are mainly used {probably only as galactose).

v. Cranial circulation time (carotid to jugular) is 3 seconds (Radioactive method). The capillaries of the cerebral vessels, choroid plexus, etc., are less permeable. As a result of this less permeable crysalloid elements of the blood cannot pass into the cerebral tissue spaces. This is called blood-brain barrier (Fig. 7.103).

Regulation of Cerebral Circulation:

Cranium being a rigid box, the amount of blood in it, at any moment, cannot rise to any considerable degree. Only slight rise may take place by compressing the veins and displacing a little cerebrospinal fluid (CSF). Hence, blood supply to the brain can only be increased by raising the velocity of blood flow through it.

Broad­ly speaking, cerebral blood vessels have got no well-organised vasomotor control and the circulation can be maintained by:

(a) Adjusting the general blood pressure through the Sino-aortic mechanism, and

(b) Regulating the lumen of the cerebral vessels.

Existence of Auto-Regulation of Cerebral Blood Flow:

Auto-regulation in cerebral blood flow was first described by Fog in 1934. However, Sagawa and Guyton (1961) on the basis of their pressure/flow studies of cerebral circulation in dogs described the absence of such auto-regulation. But Harper (1963) has observed auto-regulation in normocapnoic dogs.

He described that in dogs having arterial CO₂ tension of about 40 mm of Hg, the pressure/flow relationship is absent after pressure head of 80 mm of Hg. But in hypercapnoic animal this auto-regulation is absent and cortical blood flow is increased with increase of pressure, i.e., the pressure/flow relationship is linear.

Thus it seems that in normal individual the auto-regulation of cerebral blood flow as if sub-serves a homeostatic function. As the increased CO₂ tension of the blood abolishes the auto-regulatory mechanism, it is quite likely that two factors may play. One is the myogenic response of smooth muscle which is effective with the increase of pressure and the other, the metabolic factors involving the tissue tensions of the respiratory gases, to which the cerebral arterioles are highly sensitive.

There is phenomenon which has interested physiologists for a long time is the cause of sleep. This has been discussed by many as the ischaemia of the brain. But Mangold and Sokoloff (1955) have been able to show no changes in the cerebral O₂ consumption along with circulation during sleep. Sometimes they have observed the increase of cerebral blood flow instead.

The cerebral circulation is higher in the youngest group particularly in the first decade but falls rapidly with the advent of puberty. This fall is possibly due to sex hormones (liberated during this age) which have got some constrictor effects on the cerebral blood vessels.

Factors Controlling Cerebral Circulation:

There are so many factors that may control the cerebral circulation. The main factors that generally operate are the driving force, i.e., the difference between the mean arterial blood pressure (MABP) and the internal jugular pressure (IJP), and the cerebrovascular resistance (CVR). So the cerebral blood flow (CBF) is directly proportional to driving force (the difference between the mean arterial blood pressure and the internal jugular pressure) and inversely proportional to the cerebrovascular resistance.

Driving Force or Arterial Pressure Head:

This factor depends upon the cardiac output and peripheral resistance. The arterial blood pressure is the sole determinant of driving force and internal jugular pressure has little role under normal condition. But in case, of positive g, this internal jugular pressure plays an immense role.

In human beings with centrifugal accelerative Stress, the cerebral circulation is still maintained for several seconds though the arterial blood pressure at head level is practically nil. This maintenance of pressure under such state is due to simultaneous fall of pressure in the internal jugular vein.

In normal individual having well-organised homeostatic control, any alteration of the systemic pressure will have practically no effect on the cerebral blood flow but if the homeostatic control fails, then hazard may occur. Sometimes cerebral haemorrhage or senselessness occurs possibly due to absence of this homeostatic control. Kety (1958) has described that there is a correlation between the cerebral blood flow and arterial blood pressure only at a very low pressure head, where the pressure level may be considered to be the limiting factor.

So long the pressure head remains above a certain minimal value, i.e., about 70 mm of Hg, the pressure no longer exerts a control on the circulation and the correlation disappears. Intrinsic factors play only when pressure drops further and the flow is maintained by lowering the cerebrovascular resistance.

Cerebrovascular Resistance:

The cerebrovascular resistance depends upon the following factors:

i. Intracranial Pressure:

Rise of intracranial pressure (brain tumour, meningitis, etc.) reduces the blood flow, by mechanically compressing the cerebral capillaries and veins. Cerebrovascular resistance has got mostly a linear relationship with intracranial pressure. The cerebral blood flow has got negative correlation with increased intracranial pressure; however this correlation only comes into play until pressure exceeds 500 mm of H₂O.

ii. Viscosity of Blood:

In Anaemia the viscosity of blood is decreased due to fall of haematocrit value and hence the increase of flow. But in case of polycythaemia vera the flow is decreased as the viscosity is higher due to raised haematocrit value.

iii. Diameter of the Cerebral Blood Vessels:

Cerebral vascular resistance has got inverse relationship with the diameter of the blood vessels. The diameter of the cerebral blood vessels are altered under the following factors, viz., neurogenic factors, CO₂ and O₂ level in blood, neurohormones, etc.

There is intrinsic nerve supply that possibly controls the state of constriction and dilatation of the cerebral blood vessels. These nerves originate from the plexus of nerves which surround the carotid and vertebral plexus as they enter the brain.

Fibres originating from the cervical sympathetic chains are constrictor, whereas the greater superficial petrosal nerve originated in the medulla is vasodilator. But the relative roles of these two nerves are not clear. Because bilateral blocking of the stellate ganglia has got little effect on CBF and CVR. Similarly the role of vasodilator fibres on the cerebral blood flow is not known.

iv. Carbon Dioxide Tension:

Increased CO₂ tension raises the flow. It causes cerebral vasodilatation by local action but general vasoconstriction through vasomotor centre (V.M.C.) and Sino-aortic reflexes. Cerebral blood flow increases by 75% after inhalation of 5-6% of CO₂.

v. O₂ Lack:

It increases cerebral circulation by local vasodilatation as well as by general vasoconstriction (V.M.C., Sino-aortic reflex, etc.) and thus raises blood pressure.

vi. Excess O₂:

It causes reduction of cerebral blood flow provided the concomitant hypocapnia is prevented.

vii. Adrenaline and Noradrenaline:

The adrenaline increases the cerebral blood flow through vasodilatation but the noradrenaline decreases the cerebral blood flow through profound vasoconstriction.

viii. There are other drugs which may modify the cerebral circulation. Ethyl alcohol in therapeutic doses has got no significant effect but, in severe alcoholic intoxication it may increase the cerebral blood flow. This effect is possibly due to effect of accumulated CO₂ in the blood.

ix. Papaverine is a good cerebral vasodilator.

x. Xanthine group of drugs have got some vasoconstrictor effects. Aminophylline in therapeutic dosage produces vasoconstriction. Caffeine has got similar effects. Nicotinic acid injected intravenously, though produces facial vasodilatation but does not produce any cerebral vasodilatation.

Though histamine produces cerebral vasodilatation yet it is not as effective as it simultaneously produces systemic vasodilatation causing fall of-systemic blood pressure.

Clinical Conditions:

In essential hypertension, the cerebral circulation remains unaltered though the vascular resistance is greatly increased. But in case of cerebral arteriosclerosis, the cerebral blood flow is diminished due to increased cerebrovascular resistance and loss of elasticity of the blood vessel wall.