Allshire A, Piper H M, Cuthbertson K S, Cobbold P H
Department of Zoology, University of Liverpool, U.K.
Biochem J. 1987 Jun 1;244(2):381-5. doi: 10.1042/bj2440381.
Free Ca2+ in the cytosol ([Ca2+]i) of individual rat ventricle cells injected with aequorin was measured under anoxia. In glucose-free medium myocytes spontaneously shortened after about 60 min, although [Ca2+]i was still at or near resting levels. However, within minutes a net inward movement of Ca2+ across the sarcolemma developed and [Ca2+]i began to rise. Provided oxygen was readmitted before [Ca2+]i exceeded 2-3 microM, cells were able to restore [Ca2+]i to resting levels through caffeine-sensitive sequestration of Ca2+ in the sarcoplasmic reticulum. We suggest that Ca2+-independent shortening of anoxic cardiomyocytes reflects onset of rigor which triggers loss of [Ca2+]i homoeostasis.
在缺氧条件下，对注射了水母发光蛋白的大鼠单个心室细胞胞质溶胶中的游离钙离子浓度（[Ca2+]i）进行了测量。在无糖培养基中，心肌细胞在约60分钟后自发缩短，尽管[Ca2+]i仍处于或接近静息水平。然而，几分钟内，钙离子跨肌膜的净内向移动开始出现，[Ca2+]i开始升高。如果在[Ca2+]i超过2 - 3微摩尔之前重新通入氧气，细胞能够通过将钙离子在肌浆网中进行咖啡因敏感型隔离，将[Ca2+]i恢复到静息水平。我们认为，缺氧心肌细胞的钙离子非依赖性缩短反映了僵直的开始，这触发了[Ca2+]i稳态的丧失。
