Effect of ATP-potassium channel opener nicorandil on long-term cardiac preservation

Background. ATP-sensitive potassium channels have been shown to be one of t he important protective mechanisms for the ischemic myocardium. The purpose of this study was to evaluate the protective effect of nicorandil, an ATP- sensitive potassium channel opener, on myocardium during 6 hours hypothermi c preservation. Methods. preserved rat hearts were randomly divided into 4 groups according to cardioplegia and preservation protocols as follows: (1) histidine-trypt ophan-ketoglutarate solution (HTK) for both cardioplegic and immersing solu tions (group A); (2) nicorandiladded HTK for cardioplegic solution and nico randil-free HTK for immersing solution (group B); (3) nicorandil-free HTK f or cardioplegic solution and nicorandil-added HTK for immersing solution (g roup C); and (4) nicorandil-added HTK for both cardioplegic and immersing s olutions (group D). Results. The recovery of postischemic cardiac function, including left vent ricular developed pressure and end-diastolic pressure, was significantly im proved in group B and group C as compared with the other groups (p<0.05). P ostischemic intracellular calcium concentration was significantly lower in group B and group C than in group A (p<0.05). Conclusions. We concluded that nicorandil-induced hyperpolarizing arrest co uld reduce ischemia-derived myocyte injury and inhibit the influx of calciu m into the myocytes in long-term cardiac preservation.