Stroke, Vol 15, 621-627, Copyright © 1984 by American Heart Association
JM Zabramski, RF Spetzler, WR Selman, UR Roessmann, LA Hershey, RC Crumrine and R Macko
Conflicting reports have appeared in the literature regarding the effect of
the opiate antagonist naloxone on ischemic neurologic deficits. We report
the results of a study using naloxone in our model of focal cerebral
ischemia in the awake primate. A total of 14 adult baboons were subjected
to six-hour occlusion of the left middle cerebral artery (MCA). Seven
animals served as controls and seven received treatment with naloxone (5
mg/kg) beginning 30 min after MCA occlusion and continuing until two hours
after reperfusion. All animals developed profound hemiparesis and
homonymous hemianopsia within seconds of inflating the MCA occluder.
Acutely, therapy with naloxone partially reversed ischemic neurologic
deficits in five of the seven treatment animals. Within minutes of
receiving the loading dose of naloxone, responding animals were more alert
and demonstrated improvements in motor function. Naloxone did not affect
mortality: Three animals in the treatment group and two in the naloxone
group died secondary to malignant intracranial pressure within 48 hours of
the ischemic episode. In animals surviving the ischemic insult however,
treatment with naloxone significantly improved neurologic outcome at 10
days (p less than 0.05). Neuropathologic examinations in these animals
revealed amelioration of ischemic tissue damage, with three of the five
suffering only small focal areas of infarction. (All control animals
suffered large infarcts of the MCA territory.) Our results verify that
naloxone can reverse ischemic deficits, and more importantly may improve
the outcome from focal ischemic insults.
ARTICLES
Naloxone therapy during focal cerebral ischemia evaluation in a primate model
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