Arresto Cardioplegico con una soluzione arricchita di Urocortina. Modello in vivo e confronto nel ratto diabetico e non diabetico

The protection of the myocardium in cardiac surgery will always be one of the most important and of concern moment for the surgeon when deciding to operate on a patient. Always keeping in mind that this procedure should aim to improve the quality of life of the patient, especially in those who show, (already before the operation), a certain degree of contractile deficit. The conflicting results of experimental studies in the last decade again raise many doubts about their effectiveness in the clinical setting. A solution to the dispute may only result from a better understanding of the fundamental concepts on the metabolism of the heart muscle and damage by ischemia and reperfusion injury during cardioplegic arrest. Basic research is therefore not only useful, but necessary and indispensable to try to resolve these doubts by applying experimental models that are as close as possible to clinical reality, as occurred in our experimental model. Recent studies have shown a certain cellular metabolic activity even during cardiac arrest induced with cardioplegic solution, thus demonstrating the need to add to a standard cardioplegic solutions , appropriate substrates that acts to improve the protection itself. Other studies have also demonstrated the superiority of blood cardioplegia compared to crystalloid, especially for its more physiological features. As regards the temperature and the routes of administration to induce cardiac arrest remains at the discretion of the surgeon. We have shown that the cardioplegic arrest induces overexpression of endogenous UCN and the addition of UCN in the cardioplegic solution infused in diabetic rat versus control probably induces both at, mRNA level and at protein level a colocalization of PKCepsilon with mitochondrial translocation, inducing the survival of myocytes against cell death by apoptosis. Whereas the loss and / or functional impairment of myocytes after cardioplegic arrest is known to cause reduction of cardiac contractility and resulting in increased mortality and morbidity, functional data measured with conductance catheter appear to reduce the extent of cardiac dysfunction if opposed to the control group that had received a cardioplegia devoid of UCN. This strategy is a proposed cardioplegic solutions supplementation with exogenous UCN that seems to be promising to reduce the risk of cardiac dysfunction and cell apoptosis after surgery in patients exposed to damage from I / R associated with cardioplegic arrest.