Different roles of neuronal and endothelial nitric oxide synthases on ischemic nitric oxide production in gerbil striatum

Abstract

The production of nitric oxide (NO) in gerbil striatum during ischemia and reperfusion was monitored by measuring total NO metabolites in dialysates, and the effects of 7-nitroindazole (7-NI), a selective inhibitor of neuronal NO synthase, and N G-nitro- l-arginine methyl ester ( l-NAME), a non-selective inhibitor of NO synthase, were examined. The effects of these agents on ischemic neuronal damage were histologically evaluated 7 days after transient ischemia for 5 or 10 min. 7-NI and l-NAME decreased the NO production to similar extents in non-ischemic gerbils. 7-NI inhibited the increased NO production after 5 min of ischemia, and partly attenuated the increase in NO production after 10 min of ischemia, but had no effect on the increase after 15 min of ischemia. l-NAME completely abolished the increased NO production after different durations of ischemia. The extent of ischemic neuronal damage by 5-min ischemia was aggravated by either 7-NI or l-NAME, while damage by 10-min ischemia was marked in all groups. These results indicate that neuronal and endothelial NO synthases make different contributions to the post-ischemic NO production and the histological outcomes in gerbil striatum.