Borgers M, Piper H M
J Mol Cell Cardiol. 1986 Apr;18(4):439-48. doi: 10.1016/s0022-2828(86)80906-3.
Cultivated heart muscle cells from adult rats were exposed to anoxia in a substrate-free Tyrode solution at constant pH. It has been shown previously that in this system anoxic changes of metabolism and morphology develop gradually during the first 60 min. In this study, intracellular Ca2+ localization was pursued cytochemically. Under aerobic control conditions, Ca2+-deposits are only detected along the sarcolemma and T-tubules. Under anoxia the pattern changes gradually. During the first 60 min, the number of sarcolemmal deposits is transiently increased and single deposits appear inside mitochondria. After 90 and 120 min of anoxia, an increasing number of cells have lost their ability of sarcolemmal Ca2+ binding, but exhibit clustered deposits in single mitochondria. These cells are hypercontracted, often contain condensed myofibrillar masses and are covered with large sarcolemmal protrusions, indicating that they are irreversible injured. Loss of sarcolemmal Ca2+ binding ability seems to be a crucial event on the edge of the development of irreversible injury. Since the sarcolemmal Ca2+-deposits in normal cells are believed to be causally related to a binding of Ca2+ to anionic phospholipids, a decrease of Ca2+ affinity of these phospholipids and a change in the sarcolemmal phospholipid composition may be considered as causes for the disappearance of sarcolemma-bound Ca2+.
将成年大鼠培养的心肌细胞置于pH恒定的无底物台氏液中进行缺氧处理。先前已经表明，在该系统中，代谢和形态的缺氧变化在最初60分钟内逐渐发展。在本研究中，采用细胞化学方法追踪细胞内Ca2+的定位。在有氧对照条件下，仅在肌膜和T小管沿线检测到Ca2+沉积物。在缺氧条件下，模式逐渐改变。在最初的60分钟内，肌膜沉积物的数量短暂增加，并且在线粒体内出现单个沉积物。缺氧90分钟和120分钟后，越来越多的细胞失去了肌膜结合Ca2+的能力，但在单个线粒体中表现出聚集的沉积物。这些细胞过度收缩，通常含有凝聚的肌原纤维团块，并被大的肌膜突起覆盖，表明它们受到了不可逆损伤。肌膜Ca2+结合能力的丧失似乎是不可逆损伤发展边缘的一个关键事件。由于正常细胞中的肌膜Ca2+沉积物被认为与Ca2+与阴离子磷脂的结合有因果关系，这些磷脂的Ca2+亲和力降低以及肌膜磷脂组成的变化可能被认为是肌膜结合Ca2+消失的原因。
