The effects of mannitol, albumin, and cardioplegia enhancers on 24-h rat heart preservation

During 24 h in vitro heart preservation and reperfusion, tissue damage occurs that seriously reduces cardiac function. Prevention of free radical production during preservation and reperfusion of ischemic tissue using free radical scavengers is of primary importance in maintaining optimal heart function in long-term preservation protocols. We examined whether mannitol (68 mM) and albumin (1.4 mu M) in combination with other cardioplegia enhancers decreased free radical formation and edema and increased cardiac function during 24-h cold (5 degrees C) heart preservation and warm (37 degrees C) reperfusion in the Langendorff-isolated rat heart. The performance of mannitol-treated hearts was significantly decreased compared with that of hearts without mannitol treatment after 24 h of preservation with regard to recovery of diastolic pressure, contractility (+dP/dt), relaxation (-dP/dt), myocardial creatine kinase release, coronary flow, and lipid peroxidation. Albumin-treated hearts demonstrated higher cardiac function (contractility and coronary flow especially) than hearts not treated with albumin or hearts treated with mannitol, and this appears to be due to the positive effects of increased cellular metabolism and the enhancement of membrane stability.