Background. This study was designed to assess the protective effects of the mitochondrial adenosine triphosphate-sensitive potassium channel (K ATP) opener diazoxide as an additive to heart preservation solution.
Methods. Forty isolated isovolumic buffer-perfused rat hearts were divided into four groups. Groups I and III hearts were arrested with and cold-stored in Celsior solution for 4 hr and 10 hr, respectively. In Groups II and IV, hearts underwent a protocol similar to that used in Group I and III, respectively, except that Celsior was supplemented with 100 μmol/L of diazoxide.
Results. The protective effects of diazoxide were primarily manifest as a better preservation of diastolic function and a reduction of myocardial edema. The improvement of postischemic systolic function was observed only after prolonged exposure to diazoxide in Group IV, compared with Group III. The endothelium-dependent and endothelium-independent coronary flow postischemic responses were not affected by the supplementation of Celsior with diazoxide.
Conclusions. Pharmacologic activation of mitochondrial K ATP channels seems to be an effective means of improving preservation of cold-stored hearts, which is consistent with the presumed role of these channels as end effectors of the cardioprotective preconditioning pathway.