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ISOFLURANE PC, VIA K_ATP CHANNELS, PROTECTS THE HYPOTHERMIC HEART

Department of Anesthesiology and Pain Medicine, University of Alberta, Edmonton, Alberta, Canada

INTRODUCTION

Preconditioning (PC) alters exogenous glucose metabolism, reducing glycolysis in aerobically perfused hearts and hearts subject to reperfusion following prolonged ischemia. Isoflurane exposure prior to regional ischemia reduces infarct size. We assessed the metabolic and mechanical functional effects of isoflurane preconditioning in hearts subjected to prolonged no-flow hypothermic arrest.

METHODS

Following animal ethics committee approval, rat hearts were subject to a 10-min Langendorff perfusion (L), a storage phase in which hearts were arrested with cold St. Thomas' II cardioplegia solution and stored at 3°C ± 1°C for 8 hours (S); a Langendorff reperfusion phase (LR) and finally a working mode reperfusion phase (WR). To assess mechanical function three groups of hearts were studied, each undergoing L, S, LR and WR: a group received no intervention; a group underwent isoflurane PC and a group underwent isoflurane PC and treatment with 5-hydroyxdecanoate (5-HD), a selective mitochondrial K_ATP antagonist during the S phase only. Other groups of hearts were frozen at the end of S to assess metabolic parameters.

RESULTS

Isoflurane PC effectively protected the heart with LV work recovering to 68% of that observed in the untreated group. The presence of 5HD during the S phase abolished the protective effect on mechanical functional recovery of isoflurane PC. In groups of hearts studied only during L and S, glycogen content was preserved by isoflurane PC but this effect was not seen when 5-HD was present during S. HMR 1098, a sarcolemmal K_ATP channel-selective blocker, did not antagonize the metabolic effect of isoflurane.

DISCUSSION

Brief exposure to isoflurane (in this study 10 min) is effective in enhancing mechanical functional recovery in hearts subject to prolonged hypothermic cardioplegic arrest and storage. Isoflurane appears to trigger a protective effect that is mediated by the opening of mitochondrial, but not sarcolemmal K_ATP channels. Alteration in energy substrate metabolism during the storage interval may be one mechanism of isoflurane-induced PC.

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