Direct measurement of nitric oxide release in gastric mucosa during ischemia-reperfusion in rats

Abstract

Nitric oxide (NO) generation in the rat gastric mucosa during ischemia-reperfusion was measured using an NO-sensitive electrode. Under pentobarbital sodium anesthesia, an electrode was inserted into the submucosa from the serous membrane side in the fundus. After steady-state baseline recording, the celiac artery was clamped for 30 min, and then ischemia-reperfusion was achieved by removing the clamp. The clamping of the celiac artery caused a decrease in blood flow and an increase in NO level in the gastric tissue. Just after the removal of the clamp, the NO level rapidly fell and returned to the baseline level. Administration of N G-nitro-l-arginine methyl ester (an NO synthase inhibitor, 30 mg/kg ip) before ischemia significantly attenuated both the increase in NO level during ischemia and the formation of acute gastric mucosal lesions observed after 60 min reperfusion. Administration of superoxide dismutase (a superoxide radical scavenger, 10,000 U/kg iv) at the end of ischemia inhibited both the rapid decrease in NO level during the reperfusion and the gastric mucosal erosions. Because NO and superoxide radical produce a highly reactive peroxynitrite, it can be argued that NO has an important pathological role in acute gastric mucosal injury induced by ischemia-reperfusion. Our conclusion was strongly supported by immunohistochemical staining of nitrotyrosine residues, an indication of peroxynitrite formation.

Protective Effect of Rutin on the Ischemia/Reperfusion Induced Damage in Rat Kidney

“…Afterwards, the electrons react with oxygen to generate even more superoxide radicals in a continuous cycle [33,34]. Numerous studies have shown that the overexpression and supplementation with MnSOD is protective during I/R [35,36]. We also observed histopathologic alteration in ischemic rat kidney as well as alteration of oxidative stress markers.…”

Role for complement in mediating intestinal nitric oxide synthase-2 and superoxide dismutase expression

“…The supply and/or overexpression of exogenous SOD in rat models of intestinal ischemia significantly reduce injury (11,39,53). This finding suggests that maintenance of endogenous SOD may provide protection in GI/R.…”

“…Several reports indicate that the overexpression of superoxide dismutase (SOD) can attenuate GI/R injury (11,22). The exogenous administration of SOD in a rat model of gastric ischemia-reperfusion increases luminal NO levels, suggesting that SOD-mediated protection is afforded by decreasing the local concentra-tion of superoxide that is available to react with NO (53). Because endogenous SOD levels are not adequate to quench the sudden surge in superoxide levels after reperfusion, attention has been directed toward the delivery of exogenous SOD (21,39).…”

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

“…Also, the contribution of nitric oxide (NO) in I/R-induced gastric lesions has been documented (Wada et al, 1998). It has been shown that NO reacts with ROS and produces highly toxic substances such as peroxynitrite and singlet oxygen (Beckman et al, 1990, Noronha-Dutra et al, 1993.…”