학술논문
Noninvasive delayed limb ischemic preconditioning attenuates myocardial ischemia-repertusion injury in rats by a mitochondrial K(ATP) channel-dependent mechanism
Document Type
Text
Author
Source
Physiological research | 2011 Volume:60 | Number:2
Subject
Language
English
Abstract
Y.-N. Wu ... [et al.].
Obsahuje bibliografii a bibliografické odkazy
b1_We previously demonstrated in rats that noninvasive delayed limb ischemic preconditioning (LIPC) induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb per day for three days confers the sa me cardioprotective effect as local ischemic preconditioning of the heart, but the mechanism has not been studied in depth. The aim of this project was to test the hypothesis that delayed LIPC enhances myocardial antioxidative ability during ischemia-reperfusion by a mitochondrial KATP channel (mito KATP)-dependent mechanism. Rats were randomized to five gr oups: ischemia-reperfusion (IR)- control group, myocardial ischemic preconditioning (MIPC) group, LIPC group, IR-5HD group and LIPC-5HD group. The MIPC group underwent local ischemic precondi tioning induced by three cycles of 5-min occlusion and 5-min reperfusion of the left anterior descending coronary arteries. The LIPC and LIPC-5HD groups underwent LIPC induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb using a modified blood pressure aerocyst per day for three days. All rats were subjected to myocardial ischemia-reperfu sion injury. The IR-5HD and LIPC-5HD groups received the mito KATP channel blocker 5-hydroxydecanoate Na (5-HD) before and during the myocardial ischemia-reperfusion injury. Compar ed with the IR-control group, both the LIPC and MIPC groups showed an amelioration of ventricular arrhythmia, reduced my ocardial infarct size, increased activities of total superoxide dismutase, manganese-superoxide dismutase (Mn-SOD) and glutathione peroxidase, increased expression of Mn-SOD mRNA and decreased xanthine oxidase activity and malondialdehyde concentration. These beneficial effects of LIPC were prevented by 5-HD. In conclusion,delayed LIPC offers similar cardioprotecti on as local IPC.
b2_These results support the hypothesis that the activation of mito K ATP channels enhances myocardial antioxidat ive ability during ischemia- reperfusion, thereby contributing, at least in part, to the anti- arrhythmic and anti-infarct effects of delayed LIPC.
Obsahuje bibliografii a bibliografické odkazy
b1_We previously demonstrated in rats that noninvasive delayed limb ischemic preconditioning (LIPC) induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb per day for three days confers the sa me cardioprotective effect as local ischemic preconditioning of the heart, but the mechanism has not been studied in depth. The aim of this project was to test the hypothesis that delayed LIPC enhances myocardial antioxidative ability during ischemia-reperfusion by a mitochondrial KATP channel (mito KATP)-dependent mechanism. Rats were randomized to five gr oups: ischemia-reperfusion (IR)- control group, myocardial ischemic preconditioning (MIPC) group, LIPC group, IR-5HD group and LIPC-5HD group. The MIPC group underwent local ischemic precondi tioning induced by three cycles of 5-min occlusion and 5-min reperfusion of the left anterior descending coronary arteries. The LIPC and LIPC-5HD groups underwent LIPC induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb using a modified blood pressure aerocyst per day for three days. All rats were subjected to myocardial ischemia-reperfu sion injury. The IR-5HD and LIPC-5HD groups received the mito KATP channel blocker 5-hydroxydecanoate Na (5-HD) before and during the myocardial ischemia-reperfusion injury. Compar ed with the IR-control group, both the LIPC and MIPC groups showed an amelioration of ventricular arrhythmia, reduced my ocardial infarct size, increased activities of total superoxide dismutase, manganese-superoxide dismutase (Mn-SOD) and glutathione peroxidase, increased expression of Mn-SOD mRNA and decreased xanthine oxidase activity and malondialdehyde concentration. These beneficial effects of LIPC were prevented by 5-HD. In conclusion,delayed LIPC offers similar cardioprotecti on as local IPC.
b2_These results support the hypothesis that the activation of mito K ATP channels enhances myocardial antioxidat ive ability during ischemia- reperfusion, thereby contributing, at least in part, to the anti- arrhythmic and anti-infarct effects of delayed LIPC.