(Stroke. 1997;28:2259-2265.)
© 1997 American Heart Association, Inc.
Articles |
From the Departments of Anesthesiology and Critical Care Medicine and Neurology and Pathology, The Johns Hopkins Medical Institutions, Baltimore, Md.
Background and Purpose We attempted to determine whether
N
-nitro-L-arginine methyl ester
(L-NAME) would improve neurological outcome and whether
L-arginine (L-ARG) would worsen neurological outcome
after transient global ischemia.
Methods Halothane-anesthetized cats (n=6 for each group) were treated with intravenous saline, L-NAME (5 mg/kg or 10 mg/kg), or L-arginine (300 mg/kg) 30 minutes before 10 minutes of ischemia (temporary ligation of the left subclavian and brachiocephalic arteries with hemorrhagic hypotension to 50 mm Hg). At 30 minutes of reperfusion, cats in the L-ARG group were administered an additional 300 mg/kg dose of intravenous L-arginine.
Results Time (mean±SE) to isoelectric electroencephalography was similar among groups (saline, 26±11 seconds; L-NAME5, 15±4 seconds; L-NAME10, 36±27 seconds; and L-ARG, 22±7 seconds). At 72 hours, reperfusion pathological injury was severe and neurological deficit score (mean, range) was similar among groups (saline, 38 [11 to 70]; L-NAME5, 52 [40 to 73]; L-NAME10, 47 [23 to 70]; and L-ARG, 40 [0 to 79]).
Conclusions Nitric oxide is not important in the mechanism of brain injury after global ischemia in cats.
Key Words: cerebral ischemia, global neuroprotection nitric oxide neuronal death cats
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