BRAIN NITRITE PRODUCTION DURING GLOBAL-ISCHEMIA AND REPERFUSION - AN IN-VIVO MICRODIALYSIS STUDY

Nitric oxide (NO) is considered to be associated with the pathogenesis of cerebral ischemic injury. In the present study, NO production was continuously monitored employing in vivo microdialysis. A microdialysi s probe was inserted into the striatum. Levels of the major NO metabol ite, NO2-, in the dialysate were determined using the Griess reaction. Rats were subjected to global cerebral ischemia produced by occlusion of both common carotid arteries together with induced hypotension. Ce rebral ischemia induced a decrease in NO production, which was interru pted by a transient increase in NO synthesis. This increment was aboli shed in the presence of a NO synthase inhibitor, N-G-nitro-L-arginine methyl ester (L-NAME), suggesting that NO synthase activity is transie ntly activated during ischemia. Following reperfusion, NO synthesis wa s enhanced. To our knowledge, this is the first report concerning the continuous temporal profile of NO production during global cerebral is chemia and reperfusion.