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Effect of ischemic postconditioning on the oxidative stress and tissue injury in the intestinal warm ischemia/reperfusion model

机译:缺血性后处理对肠道温缺血/再灌注模型氧化应激和组织损伤的影响

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Intestinal ischemia/reperfusion (I/R) injury is resulting from some pathological and surgical procedures. Ischemic postconditioning (IPO) phenomenon was described as brief periods of reperfusion alternating with re-occlusion applied during the early minutes of reperfusion. We aimed to investigate the effect of IPO in the warm intestinal I/R model. Warm ischemia was performed by occlusion of superior mesenteric artery for 1, 3 and 6 hours on white domestic pigs (n=30). Reperfusion lasted 3 hours in all groups. Before reperfusion intestine were postconditioned by 3 cycles of 30-seconds ischemia and 30-seconds reperfusion. Small intestine tissue was collected after laparotomy (control) and at the end of the reperfusion periods. From oxidative stress markers tissue value of malondialdehyde (MDA) and reduced glutathione (GSH), and the activity of superoxide dismutase (SOD) were determined. Tissue damage was evaluated by quantitative method. IPO significantly decreased this injury in each group. IPO prior to reperfusion mitigated the oxidative stress and histological damages in our experimental warm I/R model.
机译:肠缺血/再灌注(I / R)损伤是由某些病理和外科手术产生的。缺血性后处理(IPO)现象被描述为在再灌注早期占用的再堵塞再挤出的再灌注交替。我们旨在探讨IPO在暖肠I / R模型中的影响。通过在白色家养猪上闭塞的高级肠系膜动脉(N = 30)闭塞,通过闭塞1,3和6小时进行温暖的缺血。再灌注持续了所有群体3小时。在再灌注肠道之前,在30秒的30秒缺血和30秒再灌注中被3次循环后处理。在再灌注时期和再灌注期结束后收集小肠组织。从氧化应激标记物中测定丙二醛(MDA)的组织值和降低的谷胱甘肽(GSH),并测定过氧化物歧化酶(SOD)的活性。通过定量方法评价组织损伤。 IPO在每组中显着降低了这种伤害。在再灌注之前,IPO在我们的实验温度I / R模型中减轻了氧化应激和组织学损伤。

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