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首页> 外文期刊>Life sciences >Role of constitutive nitric oxide synthase and peroxynitrite production in a rat model of splanchnic artery occlusion shock.
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Role of constitutive nitric oxide synthase and peroxynitrite production in a rat model of splanchnic artery occlusion shock.

机译：本构型一氧化氮合酶和过氧亚硝酸盐产生在内脏动脉阻塞性休克大鼠模型中的作用。

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Peroxynitrite, a potent cytotoxic oxidant formed by the reaction of nitric oxide with superoxide anion, is an important mediator of reperfusion injury. In a rodent model of mesenteric ischemia and reperfusion injury we evaluated the contribution of the constitutive and/or inducible nitric oxide synthase (cNOS or iNOS) in the formation of peroxynitrite. Splanchnic artery occlusion (SAO) shock was induced in rats by clamping both the superior mesenteric artery and the celiac trunk for 45 min, followed by release of the clamps (reperfusion). A significant peroxynitrite production was found in the plasma of the splanchnic occlusion shocked rats at 60 minutes after reperfusion. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine, a specific "footprint" of peroxynitrite, in the necrotic ileum and the aorta of shocked rats. No change in plasma levels of nitrateitrite, tissue iNOS expression (by western blotting detection) or iNOS activity was found in the intestine at 60 minutes after reperfusion. On the contrary, activity of the cNOS was reduced (approximately 50%) in the reperfused ischemic intestinal tissue. Treatment with NG-nitro-L-arginine methyl ester, a non selective inhibitor of nitric oxide synthase (given at 3 mg/kg i.v., 5 min prior to reperfusion), significantly reduced plasma level of peroxynitrite and the immunohistochemical staining for nitrotyrosine in the ileum and aorta. Our results suggest that during splanchnic artery occlusion shock peroxynitrite formation is likely to be correlated with nitric oxide production from constitutive nitric oxide synthase activation rather than from the inducible isoform enzyme.
机译：过氧亚硝酸盐是一氧化氮与超氧阴离子反应形成的有效的细胞毒性氧化剂，是再灌注损伤的重要介质。在肠系膜缺血和再灌注损伤的啮齿动物模型中，我们评估了组成型和/或诱导型一氧化氮合酶（cNOS或iNOS）在过氧亚硝酸盐形成中的作用。钳夹肠系膜上动脉和腹腔干45分钟，然后松开夹钳（再灌注），在大鼠中诱发内脏动脉阻塞（SAO）休克。再灌注后60分钟，内脏阻塞休克大鼠血浆中发现大量过氧化亚硝酸盐。免疫组织化学检查显示，在坏死的回肠和休克大鼠的主动脉中，对硝基酪氨酸（过氧亚硝酸盐的特定“足迹”）的免疫反应性显着增加。再灌注后60分钟，小肠中硝酸盐/亚硝酸盐，组织iNOS表达（通过蛋白质印迹检测）或iNOS活性的血浆水平未见变化。相反，在再灌注的缺血性肠组织中，cNOS的活性降低了（约50％）。用一氧化氮合酶的非选择性抑制剂NG-硝基-L-精氨酸甲酯处理（再灌注前5分钟，以3 mg / kg静脉内给药），显着降低了血浆过氧亚硝酸盐水平，并对免疫组化染色了回肠和主动脉。我们的结果表明，在内脏动脉阻塞期间，过氧化亚硝酸盐的形成可能与组成型一氧化氮合酶激活而不是诱导型亚型酶产生的一氧化氮有关。

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