K_(ATP)通道激活介导大鼠小肠的缺血预处理(英文)

Ischemic preconditioning mediated by activation of K^(ATP) channels in rat small intestine

目的:研究缺血预处理对大鼠缺血再灌注损伤小肠的保护作用是否由K_(ATP)通道开放剂介导的,方法:用短暂反复夹闭肠系膜上动脉诱导预处理,观察其对长期缺血再灌注损伤小肠的保护作用,并用K_(ATP)通道开放剂色满卡林(Cro)和拮抗剂格列苯脲(Gli)进一步探讨其作用机制,结果:预处理对大鼠缺血再灌注损伤小肠具有保护作用,其作用可被Cro模拟,并被Gli取消,结论:预处理对大鼠缺血再灌注损伤小肠的保护作用是由K_(ATP)通道开放剂介导的。

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 μg·kg-1) and glibenclamide (Gli 8 mg·kg-1) were injected iv 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 <0.0l), 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.