Transformations of mitochondria in damaged cardiomyocytes

Abstract

Time course of intermitochondrial contacts in rat cardiomyocytes is studied in myocardial hypertrophy followed by its regression, alcoholic cardiomyopathy, acute pancreatitis, and acute diffuse purulent peritonitis. Contacts between mitochondria do not depend on the type of disease. Subacute and chronic myocardial hyperfuntion is characterized by hyperplasia of contacts involving an increase in the number and extent of mitochondrial associations resulting from these contacts during exposure to a damaging factor and a decrease in the number of contacts and mitochondrial associations after liquidation of the cause of pathological process. In a severe disease (acute diffuse purulent peritonitis) the number of contacts between mitochondria drops and associations of damaged mitochondria disintegrate, causing exhaustion of cardiac muscle energy. The results confirm Sarkisov's recombination theory that rearrangements of elements in biological system involve alterations of the quantity and quality of its function. This helps the heart overcome the critical stage of disease and later ensure hyperplasia of mitochondria and other structures in cardiomyocytes. This phenomenon possesses the characteristics of a biological regularity and is one of the earliest compensatory adaptive reactions of injured heart.