Nicorandil ameliorates posttransplant dysfunction in cardiac allografts harvested from non-heart-beating donors.

OBJECTIVE: Warm ischemia is a major cause of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). We evaluated the cardioprotective effects of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on the early posttransplant left ventricular (LV) function of hearts harvested from asphyxiated canine NHBDs. METHODS: Hypoxic cardiac arrest was induced in 12 donor dogs. In 6, nicorandil was administered intravenously at 100 micrograms/kg + 25 micrograms/kg/min after respiratory arrest and hearts were preserved with nicorandil-supplemented cardioplegic solution (nicorandil group). The remaining 6 did not receive nicorandil at any time during the experiment (control group). Hearts were orthotopically transplanted after a mean myocardial ischemic time of 4 hours. RESULTS: All 12 recipients were weaned from cardiopulmonary bypass without inotropic support. In the control group, posttransplant cardiac indices and left ventricular end-systolic pressure (LVESP) decreased significantly, while LV max-dP/dt and Tau increased over pretransplant values. No differences were seen in parameters between pretransplant and posttransplant values in the nicorandil group. Posttransplant cardiac indices, LVESP, and LV max + dP/dt were higher in the nicorandil group than in controls, while posttransplant LV max-dP/dt in the nicorandil group was lower. CONCLUSIONS: Our results indicate that pretreatment with nicorandil during hypoxic perfusion before cardiac arrest and subsequent preservation with nicorandil-supplemented cardioplegia ameliorates early posttransplant LV dysfunction of hearts harvested from asphyxiated NHBDs.