Liu M S, Wu L L
Department of Pharmacological and Physiological Science, St. Louis University School of Medicine, MO 63104.
Biochem Biophys Res Commun. 1991 Feb 14;174(3):1248-54. doi: 10.1016/0006-291x(91)91555-q.
Effects of endotoxin administration on the Ca2(+)-induced Ca2+ release from canine cardiac sarcoplasmic reticulum (SR) were studied. Results show that the Ca2(+)-induced Ca2+ release from either passively or actively loaded SR vesicles was decreased by 28 to 46% (p less than 0.05) 4 h after endotoxin administration. Kinetic analysis reveals that the Vmax for Ca2+ was decreased significantly without changing the S0.5 and the Hill coefficient values. The binding of [3H]ryanodine to cardiac SR was reduced by 25.3% (p less than 0.01) following endotoxin administration. These data demonstrate that the Ca2(+)-induced Ca2+ release via the ryanodine-sensitive Ca2+ channel in canine cardiac SR was reduced during endotoxin shock. A reduction in the SR Ca2(+)-induced Ca2+ release may have a pathophysiological significance in contributing to the development of myocardial depression during endotoxin shock.
研究了内毒素给药对犬心肌肌浆网(SR)中Ca2+诱导的Ca2+释放的影响。结果显示,内毒素给药4小时后,被动或主动加载的SR囊泡中Ca2+诱导的Ca2+释放减少了28%至46%(p<0.05)。动力学分析表明,Ca2+的Vmax显著降低,而S0.5和希尔系数值不变。内毒素给药后,[3H]ryanodine与心肌SR的结合减少了25.3%(p<0.01)。这些数据表明,内毒素休克期间,犬心肌SR中通过ryanodine敏感的Ca2+通道的Ca2+诱导的Ca2+释放减少。SR中Ca2+诱导的Ca2+释放减少可能在导致内毒素休克期间心肌抑制的发展中具有病理生理学意义。