Stroke, Vol 22, 910-914, Copyright © 1991 by American Heart Association
C Werner, WE Hoffman, E Kochs, SF Rabito and DJ Miletich
We investigated the effects of the angiotensin-converting enzyme inhibitor
captopril on neurologic outcome in a rat model of incomplete cerebral
ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70%
nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25
micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n =
10) received no angiotensin-converting enzyme inhibitor while animals in
group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to
the ischemic period. Ischemia was produced by unilateral carotid artery
ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body
temperature, arterial blood gases, and arterial pH were maintained
constant. Neurologic outcome was evaluated every 24 hours for 3 days using
a graded deficit score (0, normal; 18, stroke-related death). On the third
day after ischemia, captopril significantly improved neurologic outcome
(median deficit score = 4) compared with controls (median deficit score =
18) (p less than 0.05). These results suggest that reduced angiotensin II
levels or increased tissue kinin concentrations may decrease ischemic brain
injury.
ARTICLES
Captopril improves neurologic outcome from incomplete cerebral ischemia in rats
Department of Anesthesiology, University of Illinois, Chicago.
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