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

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. 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. 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. 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.