To the Pathogenesis of Heart Failure in Pancreonecrosis: Experimental Study

Abstract

Objective: to evaluate the severity of a cardiac lesion in pancreonecrosis and possible mechanisms of pancreatogenic heart failure. Materials and methods. Experiments were made on albino male Wistar rats. In 32 animals anesthetized with ether, pancreonecrosis was simulated by injecting autobile (0.15 ml/kg) into the pancreas with later ligation of the common bile duct. In 18 animals, immunosuppression was induced by triple hydrocortisone administrations and pancreonecrosis was then simulated. Thirty intact anesthetized rats served as a control. Cardiac contractility was studied using an isolated isovolumi-cally contracting heart preparation, by recording the force and velocity indices of contractility, glucose uptake, and enzymatic leakage into the coronary stream. The severity of endotoxemia, the rate of free radical processes, and the serum levels of cardiospecific and pancreatic enzymes were estimated. Results. Pancreonecrosis induces a cardiac lesion, followed by its contractile depression and increased glucose uptake per performed function unit. There is an enhanced susceptibility of isolated hearts to hypoxia, reoxygenation, and exogenous calcium. The hearts of immunosuppressed animals are damaged to a greater extent. Conclusion. Activation of free radical oxidative processes, inadequacy of the antioxidant defense system, impaired cardiac bioenergy, endotoxemia, and depressed phagocytosis have been established to be the leading pathogenetic factors of pancreatogenic myocardial depression. Key words: pancreonecrosis, pathogenesis of heart failure.