The effects of cardiac cooling under surface-induced hypothermia on the cardiac function in the in situ heart.

It has been reported that in the excised cross-circulated dog heart model, cardiac cooling increases Emax (contractility index) and the external work (EW) of the left ventricle without affecting the systolic pressure volume area (PVA)-independent myocardial oxygen consumption (VO2). However, it remains unclear whether this cooling inotropism and oxygen-saving effect can also be demonstrated in an in situ heart. In the present study, we investigated the effect of cardiac cooling under surface-induced hypothermia in the in situ heart to assess the practical application of this method. Adult mongrel dogs were examined under surface-induced hypothermia with or without vasodilator. Using conductance catheter, pressure-volume relationship were obtained and mechanoenergetical parameters were measured. Optimal temperature for cardiac cooling was also examined. Simple hypothermia increased Emax compared with normothermia without affecting PVA-independent VO2, but EW did not increase. However, with concurrent vasodilator administration, cardiac cooling increased not only Emax but also EW without affecting PVA-independent VO2 compared with normothermia. However, at temperature below 32 degrees C, Tau increased significantly and diastolic dysfunction was noted. Cardiac cooling with concurrent vasodilator administration in the in situ heart has inotropic and oxygen-saving effects and optimal temperature for cardiac cooling is thought to be 34 degrees C.