Sekamova S M, Kuzin M I, Korolev V V, Beketova T P, Sorokina M I
Arkh Patol. 1982;44(6):42-9.
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.
对处于严重压迫综合征（压迫6 - 9小时及减压后2 - 4 - 7小时）的大鼠和犬的心肌进行组织学、电子显微镜和生理学研究发现，心脏功能不全存在三组形态学变化：（1）主要是微循环障碍，心动过缓时可检测到心肌细胞有轻微变化。在这些情况下，心脏衰弱的发展可能基于钙超载以及心脏活动的反射性减弱；（2）微循环障碍与心动过速条件下可检测到的心肌细胞结构明显缺氧损伤相结合，可能是心肌衰弱的独立原因；（3）负责神经冲动传导的心肌细胞结构变化：肌膜及其衍生物。在这种情况下，心脏疾病的可能原因可能是压迫后毒血症伴随的电解质失衡。
