S P Yang, Y B Hao, Y X Wu, W Dun, L H Shen, Y Zhang
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引用次数: 0
摘要
目的:研究缺血预处理对大鼠小肠缺血再灌注损伤的保护作用是否可通过KATP通道开启剂介导。方法:在长时间缺血前,采用8 min肠系膜上动脉(SMA)闭塞和10 min再灌注3个周期诱导预适应(Pc)。延长缺血前10 min静脉注射克罗卡林(Cro 75 mg.kg-1)和格列本脲(Gli 8 mg.kg-1)。结果:与缺血再灌注(IR)组相比,延长缺血前Pc组(Pc + IR)降低了LDH释放[(380 +/- 55)vs (559 +/- 49) U.L-1, P < 0.05],减轻了肠道水肿[湿重/干重(WW/DW), 5.6 +/- 0.6 vs 6.34 +/- 0.29, P < 0.05],改善了肠道组织损伤(分级,3.4 vs 5.7, P < 0.01),改善了再灌注性低血压。Cro [LDH]对Pc的影响与(298 +/- 40)vs (559 +/- 49) ul -1相似,P < 0.05;WW/DW, 5.6 +/- 0.4 vs 6.34 +/- 0.29, P < 0.05;分级评分,3.6 vs 5.7, P < 0.01], Gli [LDH]存在时消失,(624 +/- 44)vs (559 +/- 49) U.L-1;WW/DW, 6.6 +/- 0.6 vs 6.34 +/- 0.29;分级标准,5.7 vs 5.7;P > 0.05],与IR组比较。结论:大鼠小肠缺血预处理是通过激活KATP通道介导的。
Ischemic preconditioning mediated by activation of KATP channels in rat small intestine.
Aim: To study whether the protective effects of ischemic preconditioning against rat small intestine ischemia/reperfusion injury could be mediated by KATP channel opener.
Methods: Preconditioning (Pc) was induced by 3 cycles of 8-min superior mesenteric artery (SMA) occlusion and 10-min reperfusion before prolonged ischemia. Cromakalim (Cro 75 micrograms.kg-1) and glibenclamide (Gli 8 mg.kg-1) were injected i.v. 10 min before prolonged ischemia and Pc, respectively.
Results: Compared with ischemic reperfusion (IR) group, Pc before prolonged ischemia (Pc + IR) decreased LDH release [(380 +/- 55) vs (559 +/- 49) U.L-1, P < 0.05], attenuated intestinal edema [wet weight/dry weight (WW/DW), 5.6 +/- 0.6 vs 6.34 +/- 0.29, P < 0.05], ameliorated intestinal histological damage (grading scale, 3.4 vs 5.7, P < 0.01), and improved reperfusion-induced hypotension. These effects of Pc were mimicked by Cro [LDH, (298 +/- 40) vs (559 +/- 49) U.L-1, P < 0.05; WW/DW, 5.6 +/- 0.4 vs 6.34 +/- 0.29, P < 0.05; grading scale, 3.6 vs 5.7, P < 0.01] and abolished in the presence of Gli [LDH, (624 +/- 44) vs (559 +/- 49) U.L-1; WW/DW, 6.6 +/- 0.6 vs 6.34 +/- 0.29; grading scale, 5.7 vs 5.7; P > 0.05] compared with IR group, respectively.
Conclusion: Ischemic preconditioning on the rat small intestine is mediated by activation of KATP channels.