Popov V G, Smetnev A S, Lazutin V K, Beskrovnova N N, Zhelnov V V
Kardiologiia. 1977 Sep;17(9):26-34.
The clinical manifestations of glycoside toxicosis were compared with the character of myocardial ultrastructural changes and the electrolyte shifts outside the infarction zone. Accumulation of glycogen in the cytoplasm of the muscle cells with simultaneous gross destruction of the myocardial ultrastructure in the pre-infarction zones are morphological manifestations of glycoside toxicosis on the ultrastructural level. The administration of strophanthin to patients with extremely severe cardiac insufficiency due to myocardial infarction may lead to disturbance in the mitochondrial energy-producing activity and the development of nodes of myofibril over-contractility with subsequent death of the cell, even to the development of smallfocal necrosis in the myocardium. The use of lidocaine and panangin in sufficiently high doses is an effective measure in the prevention and elimination of extrasystolic arrhythmias caused by glycoside toxicosis.
将洋地黄中毒的临床表现与心肌超微结构变化特征以及梗死区外的电解质变化进行了比较。在梗死前区，肌细胞胞质中糖原积聚，同时心肌超微结构严重破坏，这是洋地黄中毒在超微结构水平上的形态学表现。对因心肌梗死导致极度严重心脏功能不全的患者使用毒毛花苷，可能会导致线粒体能量产生活动紊乱，肌原纤维过度收缩节形成，随后细胞死亡，甚至会导致心肌出现小灶性坏死。大剂量使用利多卡因和潘南金是预防和消除洋地黄中毒引起的室性早搏性心律失常的有效措施。
