Effects of 5-hydroxydecanoate and ischemic preconditioning on the ischemic-reperfused heart of fed and fasted rats

ABSTRACT

This investigation aimed to assess whether the mitochondrial ATP-sensitivepotassium channel blocker 5-hydroxydecanoate (5-HD) could abolish the protectionconferred by fasting and ischemic preconditioning (IPC) and to ascertainwhether these effects are associated with glycogen breakdown and glycolytic activity.Langendorff perfused hearts of fed and 24-h fasted rats were exposed to 25 minischemia plus 30 min reperfusion. IPC was achieved by a 3 min ischemia plus a 5 minreperfusion cycle. 5-HD (100 µM) perfusion begun 5 min before IPC or 13 minbefore sustained ischemia in the non preconditioned groups. Fasting improved thereperfusion recovery of contraction, decreased the contracture and the lactate production,increased glycogenolysis and did not affect the percentage of viable tissue.5-HD abolished the effects of fasting on the contractile recovery but did not affectthe contracture. 5-HD decreased the lactate production in the fed group, increasedthe preischemic glycogen content in both nutritional groups and did not affect theischemic glycogen fall. IPC improved the contractile function but prevented thecontracture only in the fed group, reduced lactate accumulation and glycogenolysisand evoked an increase of the viable tissue. 5-HD abolished the effects of IPC on thecontractile recovery and did not affect its effect on the contracture, lactate production,glycogenolysis and viable tissue. These data suggest that the mitocondrial ATPsensitivepotassium channel is involved in the effects of fasting and IPC on the contractilefunction but the other cardioprotective and metabolic effects appear evokedthrough other mechanisms. Also suggest that besides the inhibition of the mitochondrialpotassium channel, other mechanisms mediate the effects of 5-HD (AU)

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