Stroke, Vol 24, 1709-1716, Copyright © 1993 by American Heart Association
A Kader, VI Frazzini, RA Solomon and RR Trifiletti
BACKGROUND AND PURPOSE: Nitric oxide has been implicated as a mediator of
glutamate excitotoxicity in primary neuronal cultures. METHODS: A number of
indicators of brain nitric oxide production (nitric and cyclic guanosine
monophosphate [cGMP] concentrations and nitric oxide synthase activity)
were examined after bilateral carotid ligation and right middle cerebral
artery occlusion in adult rats. RESULTS: Brain nitrite was significantly
increased in the right versus left cortex 5, 10, and 20 minutes after
middle cerebral artery occlusion (P < .05), with a return to baseline at
60 minutes. There were no significant changes in cerebellar concentrations.
Cortical levels of cGMP were increased at 10, 20, and 60 minutes after
occlusion, with significant right-to-left differences (P < .05).
Cerebellar concentrations of cGMP were also increased but without
significant side-to-side differences. Nitric oxide synthase activity
increased approximately 10-fold from baseline 10 minutes after occlusion in
the right cortex but decreased markedly by 60 minutes from its peak at 10
minutes. The right-to-left difference in nitric oxide synthase activity was
significant at 20 minutes (P < .05). Pretreatment of rats with
NG-nitro-L-arginine, a nitric oxide synthase inhibitor, abolished the rise
in nitrite and cGMP. CONCLUSIONS: These results suggest that a sharp
transient increase in the activity of nitric oxide synthase occurs during
the first hour of cerebral ischemia, which leads to a burst in nitric oxide
production and activation of guanylate cyclase.
ARTICLES
Nitric oxide production during focal cerebral ischemia in rats
Department of Neurosurgery, Columbia University, College of Physicians and Surgeons, New York, NY 10032.
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