A cardiac intervention performed under extracorporeal circulation (ECC) is accompanied by diverse changes at all levels of neural reflex regulation, humoral activity and metabolic status. Intraoperative protection of organs and tissues, myocardium in particular, remains one of the challenges in cardio anesthesiology. The incidence of myocardial dysfunction in the early postoperative period varies from 3 to 30% of cases and is determined by a complex interaction of various mechanisms including a special pattern of metabolic processes in the myocardium, free-radical damage, ion paradox and endothelial dysfunction. One of the promising avenues in meeting this challenge is implementation of a preconditioning phenomenon. Ischemic and pharmacological preconditioning is considered to be a powerful method to increase the resistance of the organism to deleterious effects. However, due to possible worsening of symptoms and reduced reserves of the myocardium to protect the heart from intraoperative ischemia and reperfusion in cardiac patients, a pharmacologically induced preconditioning is thought of as the most suitable and safe technique. In this case, nitric oxide (NO) launching an infarction-limiting action through activation of cGMP (cyclic guanosine monophosphate)-dependent protein kinase G and formation of free radicals serves as a trigger to adapt the heart to ischemic-reperfusion injury. NO synthesis stimulation also plays a key role in mediating a late stage cytoprotective effects of the endogenous organ protection phenomenon. The study was designed to analyze the efficiency of NO delivery to the extracorporeal circulation line to protect the myocardium from ischemic-reperfusion damage when simulating acute myocardial infarction under cardiopulmonary bypass.

01 / Myocardium protection against ischemic-reperfusion injury by nitric oxide supply to the extracorporeal circulation line during cardiopulmonary bypass (experimental study)