The dynamic detection of NO during stroke and reperfusion in vivo

• Published in: Brain injury 2009-01, Vol.23 (5), p.450-458
• Main Authors: Liu, Kezhou, Li, Qian, Zhang, Le, Zheng, Xiaoxiang
• Format: Article
• Language: English
• Subjects: Animals; Disease Models, Animal; Enzyme Inhibitors - pharmacology; Hippocampus - metabolism; Imines - pharmacology; Indazoles - pharmacology; Infusions, Intravenous; Male; Nitric Oxide - analysis; Nitric Oxide - metabolism; Nitric Oxide Synthase - antagonists & inhibitors; Rats; Rats, Sprague-Dawley; Reperfusion Injury - metabolism; Stroke - metabolism
• ISSN: 0269-9052; 1362-301X
• DOI: 10.1080/02699050902838173

Nitric oxide (NO) 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 NO concentration in rat hippocampus during global cerebral ischemia and reperfusion in vivo and to reveal effects of different NO synthases (NOS). In the present study, the real-time record of NO levels in rat hippocampus was obtained by using a NO sensor during the global cerebral ischemia and the initial stage of reperfusion. The effects of two inhibitors of NOS on NO concentration were also observed. The two inhibitors were respectively administrated intravenously at the onset of reperfusion and 1 hour later. The change of the NO concentration in the initial stage of reperfusion was 0.768 +/- 0.029 microM. 7-nitroindazole (7-NI, inhibitor of nNOS) had a strong inhibitive effect on NO synthesis at both time points, while 1400W dihydrochloride (1400W, inhibitor of iNOS) had no significant effect on the NO synthesis. The in vivo detection revealed the real dynamic change of NO concentration, which is much more reliable than the in vitro method. The results showed that, during the initial stage of reperfusion, NO biosynthesis was mainly in an nNOS-dependent manner. Thus, the toxicity of NO in this process had a close relationship with the activity of nNOS but not iNOS.