Although the majority of recent scientific advances developed in the field of myocardial preservation have improved surgery procedures, it seems that during cardiothoracic surgery ischemia-reperfusion continues triggering clinical postoperative problems. This report focused on the changes human capillary endothelial cells and nerve endings suffer after cardiopulmonary bypass. The study involved four patients who received Bretschneider solution for cardioplegia during mitral stenosis surgery. Biopsies of right atrium were taken prior to and after CPB to be analyzed under electron microscopy. Samples taken after CPB showed detachment of myocardial capillary basal membrane, endothelial edema, and widespread nerve-ending destruction. Nevertheless, the shelter provided by the most advanced cardioplegic solutions, myocardial endothelial edema, and nerve-ending destruction cannot be completely prevented. Thus, it is possible to suggest that low interstitial concentration of Na(+), which activates Na(+)/Ca(++) exchanger, and inflow of Ca(++), present during ischemia-reperfusion, may lead to endothelial and neuronal cell damage, triggering cardiac contraction dysfunction. This mechanism would explain at least in part some of the problems patients face during the postoperative state.