Nicorandil preserves myocardial function following brain death in rats by mitochondrial adenosine triphosphate-sensitive potassium channel-dependent mechanism.

OBJECTIVE: Interventions to preserve myocardial function after brain death may increase the donor pool for heart transplantation. The present study using a brain death model of rats was designed to examine the protective potential of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on myocardial function after brain death.

METHODS: Rats were anesthetized with sevoflurane. A Fogarty catheter was placed intracranially for induction of brain death. The conductance catheter was inserted into the left ventricle for measurement of myocardial function. Rats were assigned randomly to two groups, one receiving nicorandil before brain death and the other receiving saline (control group). Mean blood pressure, heart rate, maximal rate of rise of left-ventricular pressure and ejection fraction were measured every 30 min for 6h after brain death. The same protocol was performed in the presence of nicorandil combined with 5-hydroxydecanoic acid, a mitochondrial adenosine triphosphate-sensitive potassium channel inhibitor.

RESULTS: Nicorandil temporally, but significantly, improved ejection fraction compared with the control group. Furthermore, 5-hydroxydecanoic acid inhibited the effects of nicorandil.

CONCLUSIONS: Nicorandil was effective to preserve ejection fraction after brain death, and myocardial mitochondrial adenosine triphosphate-sensitive potassium channels may be involved in this action.