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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.
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Autoregulation
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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