[Verapamil pretreatment extended the viability of non-beating donor hearts in situ]

An animal study was designed to examine whether the viability of asphyxiated cadaver hearts in situ could be extended by the verapamil pretreatment. Verapamil was administered separately at a dose of 0.1 (n = 9), 1.0 (n = 9), or 10 mg/kg (n = 16) to male adult Sprague-Dawley rats (440-500 g) 15 minutes prior to asphyxiation to death. Verapamil was not administered in control rats (n = 9). All dead rats were left at room temperature for 30 minutes followed by excision of their hearts and washout of coronary vascular beds with a cold University of Wisconsin solution. After simple cold storage for 30 minutes, hearts were reperfused on an isolated working rat heart apparatus in a nonworking mode with modified Krebs-Henseleit buffer for 60 minutes. After 30 minutes of the subsequent working mode, hemodynamics were measured and the hearts were perfused with 3% glutaraldehyde for the ultrastructural examination using electron microscopy. The hearts of the 10 mg/kg group were irreversibly contracted (0/16 vs. 8/9 in control hearts, p < 0.0001) during reperfusion, and most of them could make a pressure enough to keep a working mode (14/16 vs. 1/9 in control hearts, p = 0.0003). Satisfactory results were not found with 0.1 and 1.0 mg/kg verapamil groups. In ultrastructural examination, coronary vessels after preservation were dilated in the 10 mg/kg group, whereas were not dilated enough to washout of the red blood cells by the solution in controls. Irreversible changes of myocytes after reperfusion such as contraction bands and amorphous densities were presented in controls, but not in the 10 mg/kg group. Verapamil pretreatment before cardiac arrest may contribute to preserve cadaver hearts with dilating the coronary vessels and probably preventing the calcium influx into cardiomyocytes during ischemia and reperfusion. Verapamil provides dose-dependent extension of viability of non-beating donor hearts in situ.