Ischemic preconditioning mediated by activation of K-ATP channels in rat small intestine

AIM: To study whether the protective effects of ischemic preconditioning ag ainst rat small intestine ischemia/reperfusion injury could be mediated by K-ATP 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 mu g.kg(-1)) and glibenclami de (Gli 8 mg.kg(-1)) were injected iv 10 min before prolonged ischemia and Pc, respectively. RESULTS: Compared with ischemic reperfusion (IR) group, P c before prolonged ischemia (Pc + IR) decreased LDH release [(380 +/- 55) v s (559 +/- 49) U.L-1, P < 0.05], attenuated intestinal edema [wet weight/dr y weight (WW/DW), 5.6 +/- 0.6 vs 6.34 +/- 0.29, P < 0.05], ameliorated inte stinal histological damage (grading scale, 3.4 vs 5.7, P < 0.01), and impro ved reperfusion-induced hypotension. These effects of Pc were mimicked by C ro [LDH, (298 +/- 40) vs (559 +/- 49) U.L-1, P < 0.05; WW/DW, 5.6 +/- 0.4 v s 6.34 +/- 0.29, P < 0.05; grading scale, 3.6 vs 5.7, P < 0.01] and abolish ed 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 r at small intestine is mediated by activation of K-ATP channels.