Barry W H, Peeters G A, Rasmussen C A, Cunningham M J
Department of Medicine, University of Utah, School of Medicine, Salt Lake City.
Circ Res. 1987 Nov;61(5):726-34. doi: 10.1161/01.res.61.5.726.
Mechanisms of energy deprivation contracture were investigated in cultured chick embryo ventricular cells. In the presence of zero-extracellular-Na+, (choline chloride substitution)-nominal-zero-Ca2+ [( Ca2+] approximately 5 microM), exposure of ventricular cells to 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG)-zero-glucose solution resulted in the development of a contracture (video motion detector) in 5.9 +/- 0.5 minutes. Early after contracture development, the resupply of extracellular Na+, in the continued presence of CN + 2-DG, resulted in a rapid partial relaxation (t1/2 = 1.9 +/- 0.3 seconds), associated with an increase in 45Ca efflux, presumably due to transsarcolemmal Ca2+ extrusion due to Na+-Ca2+ exchange. Resupply of glucose and removal of CN + 2-DG, in the continued absence of Na+, resulted in an initially slower (t1/2 = 11.6 +/- 2.5 seconds), but more complete relaxation of contracture, which was not associated with increased Ca2+ efflux. Pretreatment with 20 mM caffeine delayed the onset of contracture (9.2 +/- 1.1 minutes) and resulted in a contracture that could not be relaxed by resupply of external Na+ only. Studies using the fluorescent Ca2+ probe indo 1 demonstrated that in zero-Na+-zero-Ca2+ solutions, contracture due to CN + 2-DG was associated with an initial rise in [Ca2+]i but that this did not account for all of contracture force development. In cells exposed to CN + 2-DG in the presence of normal extracellular Na+ and Ca2+ concentrations, a small rise in [Ca2+]i was associated with initial contracture development, consistently preceding the development of a larger accelerated contracture presumably due to ATP depletion.(ABSTRACT TRUNCATED AT 250 WORDS)
在培养的鸡胚心室细胞中研究了能量剥夺性挛缩的机制。在细胞外钠浓度为零（用氯化胆碱替代）、名义钙浓度为零（[Ca²⁺]约5微摩尔）的情况下，将心室细胞暴露于1毫摩尔氰化物（CN）和20毫摩尔2-脱氧葡萄糖（2-DG）-零葡萄糖溶液中，5.9±0.5分钟后出现挛缩（视频运动检测器检测）。挛缩出现后早期，在持续存在CN + 2-DG的情况下重新供应细胞外钠，导致快速部分松弛（半衰期=1.9±0.3秒），伴有⁴⁵Ca外流增加，推测这是由于钠-钙交换导致跨肌膜Ca²⁺外排。在持续无钠的情况下重新供应葡萄糖并去除CN + 2-DG，导致挛缩最初松弛较慢（半衰期=11.6±2.5秒），但更完全，且与Ca²⁺外流增加无关。用20毫摩尔咖啡因预处理可延迟挛缩的发生（9.2±1.1分钟），并导致仅通过重新供应外部钠无法松弛的挛缩。使用荧光Ca²⁺探针indo 1的研究表明，在零钠-零钙溶液中，CN + 2-DG引起的挛缩与[Ca²⁺]i最初升高有关，但这并不能解释所有挛缩力的发展。在正常细胞外钠和钙浓度存在的情况下暴露于CN + 2-DG的细胞中，[Ca²⁺]i的小幅升高与最初的挛缩发展有关，始终先于可能由于ATP耗竭而出现的更大的加速挛缩的发展。（摘要截短于250字）
