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Dr. Yasser Mokhtar, M.D.


Physiology of the cerebral circulation

A. Blood Brain Barrier

This barrier insulates the brain and its extracellular fluid, including the cerebrospinal fluid (CSF), from many of the body?s blood borne chemical perturbations, such as circulating drugs, immunogenic antigens and electrolyte changes. The anatomic barrier lies in the intracranial endothelium, where tight intracellular junctions weld the entire inner vascular surface into a continuous membranous sheet. As a result, only nonpolar materials that have a small molecular size, are lipid soluble or are transported across the membrane by specific carrier systems or pumps transgress the endothelium with any rapidity (Bronner et al., 1995).

Transient breaches of the barrier occur under a variety of circumstances but have little ill effect on brain function. Sustained, partial barrier alterations occur in areas of cerebral neoplasms, inflammation or edema associated with such conditions. Severe damage to barrier transport mechanisms can intensify brain infarction during ischemia (Bronner et al., 1995).   

B. Regulation of cerebral blood flow

Cerebral blood flow (CBF) in man is about 50 ml / 100 g of brain / minute. It has been shown that CBF, cerebral blood volume (CBV) and cerebral energy metabolism measured as cerebral metabolic rate of oxygen (CMRO2) or of glucose (CMRglu) are all coupled and higher in gray than white matter. This means that the oxygen extraction fraction (OEF) remains about the same (approximately forty per cent) throughout the brain, therefore, in normal resting human brain, CBF (i.e. flow) is a reliable reflection of CMRO2 (i.e. function) (Leenders et al., 1990).

CBF depends on cerebral perfusion pressure (CPP) and cerebrovascular resistance. The perfusion pressure is the difference between systemic arterial pressure and venous pressure at exit of the subarachnoid space, the latter being approximated by the intracranial pressure.


It is a characteristic of the brain to adjust its own blood supply. In normal individuals, CBF remains constant when the mean arterial pressure is between 60 and 160 mmHg which, in normal circumstances, when the intracranial venous pressure is negligible, is the same as the CPP (Powers 1991). Whether myogenic, metabolic or neurogenic processes are responsible for this process is unknown (Aaslid et al., 1989). Autoregulation is impaired or abolished in damaged areas of the brain (e.g. by ischemia, trauma, etc.) so that CBF becomes pressure passive and follows perfusion pressure (Strandgaard and Paulson 1984 and Deardin 1985).  

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