Stroke, Vol 19, 991-996, Copyright © 1988 by American Heart Association
M Kobari, F Gotoh, M Tomita, N Tanahashi, T Shinohara, Y Terayama and B Mihara
Acute cerebral circulatory changes following experimental cerebral
hemorrhage were investigated in eight cats. The cerebral hemorrhage was
produced in the right basal ganglia by introducing arterial blood via a
thin catheter, using the systemic arterial blood pressure of the cat as a
driving force. Local cerebral blood volume was measured continuously in the
bilateral parietotemporal cortexes employing photoelectric apparatuses.
Carbon black dilution curves were recorded from the regions, and the mean
transit time of blood was calculated. Local cerebral blood flow was
estimated from mean transit time and cerebral blood volume. Intracranial
pressure was monitored continuously in the right parietal epidural space.
Five minutes after cerebral hemorrhage, intracranial pressure increased by
24.0 +/- 6.1 mm Hg, while mean arterial blood pressure increased by only
2.9 +/- 2.0 mm Hg. Cerebral blood volume decreased by 1.60 +/- 0.24 vol% in
the hemorrhagic and 1.14 +/- 0.30 vol% in the nonhemorrhagic hemisphere.
Cerebral blood flow decreased by 30.0 +/- 4.5 ml/100 g brain/min in the
hemorrhagic (initially 64.5 +/- 13.6) and by 30.3 +/- 7.5 ml/100 g
brain/min in the nonhemorrhagic (initially 60.9 +/- 6.9) hemisphere.
Increased intracranial pressure appeared to be the main cause of the
observed cerebral blood volume/flow reduction shortly after experimental
hemorrhage in the basal ganglia. Several other factors and mechanisms
involved are discussed.
ARTICLES
Bilateral hemispheric reduction of cerebral blood volume and blood flow immediately after experimental cerebral hemorrhage in cats
Department of Neurology, School of Medicine, Keio University, Tokyo, Japan.
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