Stroke, Vol 21, 589-595, Copyright © 1990 by American Heart Association
Y Saku, J Choki, R Waki, J Masuda, K Tamaki, M Fujishima and J Ogata
The purpose of this experiment was to determine whether an acute rise in
brain perfusion pressure causes hemorrhagic transformation of an infarct
without a reopening of the occluded artery. We raised the blood pressure of
22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral
artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial
blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11
cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11
remaining cats with pale brain infarcts (p less than 0.05). Induction of
hypertension increased regional cerebral blood flow in the ischemic
cortical gray matter more in three cats with hemorrhagic infarcts than in
seven with pale infarcts. Our results demonstrate that hemorrhagic
transformation of an infarct can be induced by a rapid increase in
perfusion pressure to brain tissue already exposed to focal ischemia. We
also suggest that the restoration of blood flow through leptomeningeal
collaterals plays an important role in the pathogenesis of hemorrhagic
infarction in cases without reopening of occluded arteries.
ARTICLES
Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion
National Cardiovascular Center, Research Institute, Osaka, Japan.
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