Stroke, Vol 7, 410-416, Copyright © 1976 by American Heart Association
G Mchedlishvili, A Kapuscinski and L Nikolaishvili
Controlled cerebral ischemia was produced in rabbits by bilateral occlusion
of the common carotid arteries and restriction of collateral blood flow by
a decrease of the systemic arterial pressure to a desirable level (by
hemorrhage into a pressurized reservior system). The following circulatory
parameters were simultaneously monitored: systemic arterial pressure (SAP),
pressure in the circle of Willis (Pcw), systemic venous pressure (SVP), and
pressure in the sagittal venous sinus of brain (Pvs). The cerebral blood
flow (CBF) was measured by means of the H2-clearance method, and the brain
volume (BrV) changes were evaluated with a mechanical system of the
sterotaxic device. It has been concluded that the pre-edematous changes in
the brain tissue arise during deep ischemis but an important factor in the
brain edema development is the recovery of the CBF with and increase of the
intravascular pressure closely related to the brain blood volume
augmentation. The latter may be pronouced because of diminution of the
blood outflow from the brain when the SVP is increased. The compensation
for the BrV increase (caused either by brain blood volume augmentation or
by brain edema) is obtained by Pcw decrease probably due to resistance rise
in the internal carotid and vertebral arteries. The brain edema may be
additionally compensated by an active decrease of the systemic arterial
pressure.
ARTICLES
Mechanisms of postischemic brain edema: contribution of circulatory factors
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