Real-Time Measurement of Murine HippocampusHippocampus NO Levels in Response to Cerebral Ischemia/ReperfusionReperfusion

Abstract

Nitric oxide has been implicated as a mediator of synaptic transmission and a pathological factor in stroke/reperfusion. The purpose of this study was to detect the change of nitric oxide concentration in rat hippocampus during global cerebral ischemia and reperfusion in vivo and to reveal effects of different nitric oxide synthases. In the present study, the real-time record of nitric oxide levels in rat hippocampus was obtained by using a nitric oxide sensor during global cerebral ischemia and the initial stage of reperfusion. We also observed the effects of two inhibitors of nitric oxide synthases on nitric oxide concentration. The two inhibitors were administrated intravenously at the onset of reperfusion and 1 h later. The change of the nitric oxide concentration in the initial stage of reperfusion was 0.768 ± 0.029 μM. 7-Nitroindazole (7-NI7-NI, inhibitor of nNOS) had a strong inhibitive effect on nitric oxide synthesis at both time points, while 1400 W1400 W dihydrochloride (1400 W, inhibitor of iNOSiNOS ) had no significant effect on nitric oxide synthesis. The results showed that during the initial stage of reperfusion, nitric oxide biosynthesis was mainly an nNOS-dependent process.