RESUMO
We investigated the mitochondrial ATP-sensitive potassium channel [mito-K (ATP)] in exercise preconditioning of myocardial ischemia-reperfusion injury in rats. Eighty SD rats were randomly divided into high-, moderate-, low-intensity, and control groups. The exercise groups were divided into control and inhibited groups. The control group was divided into model and sham groups. Eight rats were randomly selected from each group for analysis. At 40 and 50 min after ischemia-reperfusion, respectively, J point and T-wave values and QT intervals were significantly higher in the control model group than in the control sham group; ECG parameters were significantly lower in the exercise group than in the control group; ECG parameters were lower in the 5-HD-inhibited group than in the corresponding exercise model group. The trends of serum enzymes (serum muscle kinase isoenzyme, lactate dehydrogenase, aspartate transaminase) were consistent with ECG parameter changes at 40 and 50 min after ischemia and reperfusion, respectively. Compared with the sham group, the control model group showed significantly decreased left ventricular systolic pressure (LVSP) and maximum rate of left ventricular pressure development (dP/dtmax) and significantly increased left ventricular end-diastolic pressure (LVEDP). LVSP and dP/dtmax were significantly higher and LVEDP was significantly lower in the control group than in the exercise model group. LVSP and dP/dtmax were significantly lower and LVEDP was significantly higher in the inhibited group than in the corresponding exercise group. Long-term exercise can produce a preconditioning effect that exerts an ischemia-reperfusion cardioprotective effect. Mito-K (ATP) mediates the cardioprotective effects of exercise preconditioning.
