[Ultrastructural bases of heart failure in the early period of the prolonged crush syndrome].

Histological, electron microscopic, and physiological studies on the myocardium of rats and dogs in severe forms of compression syndrome (6-9 hours of compression and 2-4-7 hours after decompression) revealed three groups of morphological changes underlying cardiac insufficiency: (1) predominantly microcirculatory disorders with mild changes in cardiomyocytes detectable in bradycardia. Under these conditions the development of cardiac weakness may be based on both calcium overloading and reflectory weakening of the heart activity; (2) combination of microcirculatory disorders with marked hypoxic damage of the cardiomyocytes structure detectable under conditions of tachycardia may be an independent cause of the cardiac muscle weakness; (3) changes in the structures of cardiomyocytes responsible for nervous impulses conduction: sarcolemma and its derivatives. Under this condition, the probable cause of cardiac disorders may be electrolyte imbalance accompanying postcompression toxemia.