Stroke, Vol 15, 486-491, Copyright © 1984 by American Heart Association
JA Capraro, DP Reedy, JP Latchaw, RM Slugg, NT Stowe, RP Lesser and JR Little
Propranolol's potential as a protective agent against tissue injury has
been noted in experimental myocardial, renal and early acute focal cerebral
ischemia. The purpose of the present investigation was to study further the
effects of racemic (d,l) propranolol on blood-brain barrier permeability,
morphological changes, cortical electrical activity, and regional cerebral
blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult
cats, anesthetized with nitrous oxide, underwent 6 hours of right middle
cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats
were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7
hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately
before occlusion, both directly into the right carotid artery. Right
Sylvian rCBF did not significantly differ in the treated and untreated
groups. Carbon filling defects and vital dye (i.e., Evans blue and
fluorescein) extravasation were less severe in the propranolol treated
animals. Light microscopic findings demonstrated no difference in infarct
size between the two groups. The findings suggest that at doses given,
racemic propranolol does not exert a protective effect upon cerebral tissue
subjected to 6 hours of incomplete ischemia.
ARTICLES
Treatment of acute focal cerebral ischemia with propranolol
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