Herland J, Julian F J, Stephenson D G
School of Zoology, La Trobe University, Bundoora, Victoria, Australia.
Am J Physiol. 1996 May;270(5 Pt 2):H1662-71. doi: 10.1152/ajpheart.1996.270.5.H1662.
Rapid cooling contractures (RCCs) have been elicited in rat ventricular cardiac muscle skinned by saponin (50 micrograms/ml). The size and shape of the RCC in skinned cardiac muscle were similar to those observed in intact cardiac muscle. The ATP-dependent Ca2-uptake pump in the sarcoplasmic reticulum (SR) was active at low temperature and could efficiently load the SR with Ca2+ even at 3 degrees C. Halothane reduced both RCC and caffeine contracture in a dose-dependent way when halothane treatment was applied before either RCC or caffeine. This action is consistent with halothane-induced depletion of the SR Ca2+. Under similar conditions, isoflurane inhibited RCC but had little effect on the caffeine contracture. This may suggest that rapid cooling and caffeine have different modes of action on the SR Ca(2+)-release channel. Our results provide further strong supporting evidence for differential inhibitory actions on a key intracellular organelle in cardiac muscle by two vapor anesthetic agents.
用皂苷(50微克/毫升)剥除细胞膜的大鼠心室心肌已引发快速冷却挛缩(RCCs)。剥除细胞膜的心肌中RCC的大小和形状与完整心肌中观察到的相似。肌浆网(SR)中依赖ATP的Ca2+摄取泵在低温下活跃,即使在3℃时也能有效地将Ca2+加载到SR中。当在RCC或咖啡因处理之前应用氟烷时,氟烷以剂量依赖的方式降低RCC和咖啡因挛缩。这种作用与氟烷诱导的SR Ca2+耗竭一致。在类似条件下,异氟烷抑制RCC,但对咖啡因挛缩影响很小。这可能表明快速冷却和咖啡因对SR Ca(2+)释放通道有不同的作用模式。我们的结果为两种挥发性麻醉剂对心肌关键细胞内细胞器的不同抑制作用提供了进一步有力的支持证据。