The purpose of this study was to assess the effects of the addition of calcium to University of Wisconsin solution in long-term myocardial perfusion. In a heterotopic heart transplantation model, performed in pigs, the donor heart was preserved for 24 hours by means of continuous perfusion in this solution, without (24hUW group) or with calcium, 2.4 mmol/L (24hUW+Ca). During this period, the oxygenation and pH of the solution were measured, as were the calcium and lactate concentrations and enzyme release. After two hours of reperfusion, samples were collected from both ventricles for the morphological study. In the control group, there were no signs that reperfusion had triggered the calcium paradox. The addition of this cation to the preservation solution improved the intercellular junction integrity but, at the same time, favored intracellular calcium overload. This is manifested by increased enzyme release during preservation (LDH: 242+/-95 vs 140+/-25; CK: 668+/-371 vs 299+/-83 (U/L). p<0.01 in both cases) and signs of ventricular contracture: hardness and stiffness were significantly more prominent than in the group without calcium supplementation. Moreover, in comparison with the control group, the structural morphology of 24hUW+Ca is characterized by the more prominent and extensive presence of contraction bands and disorganized actin structure. Thus, under the experimental conditions employed in this study, we consider the addition of calcium to Wisconsin solution to be unadvisable.