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.