Meerson F Z, Malyshev V V, Kagan V E, Treshchuk L I, Rozhitskaia I I
Arkh Patol. 1980;42(2):9-12.
Emotional-pain stress reproduced in the form of so called anxiety-neurosis provokes long-term activation of lipid peroxidation associated with an increased content of its products in the myocardium and the development of focal lesions of the contracture type in myocytes. These heart lesions are likely to be related to the impairment of active calcium release from myofibrils due to lipid hydroperoxides-induced injury to cell membranes responsible for the cation transport. While progressing the morphologic changes in the heart reach maximum, i. e. lead to complete contracture and necrosis of myocardial cells.
以所谓焦虑神经症形式再现的情感疼痛应激会引发脂质过氧化的长期激活，这与心肌中其产物含量增加以及心肌细胞中挛缩型局灶性病变的发展相关。这些心脏病变可能与由于脂质氢过氧化物对负责阳离子转运的细胞膜造成损伤，导致肌原纤维主动钙释放受损有关。随着病情进展，心脏的形态学变化达到最大值，即导致心肌细胞完全挛缩和坏死。
