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Stroke. 1976 Jul-Aug;7(4):410-6.

Mechanisms of postischemic brain edema: contribution of circulatory factors.


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.

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