Modulation by nitric oxide of cerebral neutrophil accumulation after transient focal ischemia in rats

被引:34
作者
Batteur-Parmentier, S [1 ]
Margaill, I [1 ]
Plotkine, M [1 ]
机构
[1] Univ Paris 05, Pharmacol Lab, F-75270 Paris 06, France
关键词
cerebral ischemia; neutrophil; N-G-nitro-L-arginine methylester; nitric oxide; reperfusion;
D O I
10.1097/00004647-200005000-00007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
beneficial role of nitric oxide (NO) after cerebral ischemia has been previously attributed to its vascular effects. Recent data indicate a regulatory role for NO in initial leukocyte-endothelial interactions in the cerebral microcirculation under basal and ischemic conditions. In this study, the authors tested the hypothesis that endogenous NO production during and/or after transient focal cerebral ischemia can also be neuroprotective by limiting the process of neutrophil infiltration and its deleterious consequences. Male Sprague-Dawley rats were subjected to 2 hours occlusion of the left middle cerebral artery and the left common carotid artery. The effect of N-G-nitro-L-arginine methyl ester (r-NAME) (10 mg/kg, intra-peritaneally), an NO synthase inhibitor, was examined at 48 hours after ischemia on both infarct size and myeloperoxidase activity, an index of neutrophil infiltration. L-NAME given 5 minutes after the onset of ischemia increased the cortical infarct volume by 34% and increased cortical myeloperoxidase activity by 60%, whereas administration of L-NAME at 1, 7, and 22 hours of reperfusion had no effect. Such exacerbations of infarction and myeloperoxidase activity produced when L-NAME was given 5 minutes after the onset of ischemia were not observed in rats rendered neutropenic by vinblastine These results suggest that after transient focal ischemia, early NO production exerts a neuroprotective effect by modulating neutrophil infiltration.
引用
收藏
页码:812 / 819
页数:8
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