Piper H M, Schwartz P, Spahr R, Hütter J F, Spieckermann P G
Basic Res Cardiol. 1985;80 Suppl 1:37-41. doi: 10.1007/978-3-662-11041-6_6.
Cultured adult cardiocytes were exposed to anoxia. The initial decrease of high-energy phosphates was accompanied by a moderate release of cytosolic enzymes and morphological changes: the appearance of sarcolemmal 'microblebs' (approximately 1 micron in diameter) and an increase of subsarcolemmal vesicles. At ATP levels above 2 mumol/gww, metabolic and morphological alterations were reversible. Probably the sarcolemmal changes are causally related to the loss of macromolecules from reversibly injured cells. At ATP levels below 2 mumol/gww, an increasing number of cells become irreversibly hypercontracted. In these cells cytoplasmic masses are protruded into large 'macroblebs' (10-30 micron in diameter), however sarcolemmal continuity is preserved. Thus, enzyme release, irreversible contracture and cytolysis do not occur simultaneously in anoxic isolated cardiocytes.
将培养的成年心肌细胞置于缺氧环境中。高能磷酸盐的初始减少伴随着胞质酶的适度释放和形态学变化：出现肌膜“微泡”（直径约1微米）以及肌膜下小泡增多。当ATP水平高于2微摩尔/克湿重时，代谢和形态学改变是可逆的。肌膜变化可能与可逆性损伤细胞中大分子物质的丢失存在因果关系。当ATP水平低于2微摩尔/克湿重时，越来越多的细胞会发生不可逆的过度收缩。在这些细胞中，细胞质团块突出形成大的“大泡”（直径10 - 30微米），然而肌膜的连续性得以保留。因此，在缺氧的分离心肌细胞中，酶释放、不可逆挛缩和细胞溶解不会同时发生。
