Ischemic preconditioning mediated by activation of KATP channels in rat small intestine
Abstract
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.
Keywords:
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.