The effect of ketamine on myocardial contractile force was examined in rabbit papillary muscles in order to determine the underlying mechanism of action of the anesthetic. Ketamine HCl (20 and 40 mg/L) inhibited rested-state contractions that are dependent on the transsarcolemmal influx of Ca2+ for activation and reduced the upstroke velocity of the slow action potential, which reflects Ca2+ influx through the slow Ca2+ channel. On the other hand, ketamine had a relatively small effect on potentiated-state contractions and no effect on rapid cooling induced contractures, both of which are activated by the release of Ca2+ stored in the sarcoplasmic reticulum. These results suggest that ketamine inhibition of transsarcolemmal Ca2+ influx plays a major role in the negative inotropic action of the anesthetic.

译文

在兔乳头肌中检查了氯胺酮对心肌收缩力的影响,以确定麻醉剂作用的潜在机制。氯胺酮HCl (20和40 mg/L) 抑制了依赖于Ca2的跨膜内流激活的静息状态收缩,并降低了慢动作电位的上行速度,这反映了通过慢速Ca2通道的Ca2内流。另一方面,氯胺酮对增强态收缩的影响相对较小,而对快速冷却引起的挛缩没有影响,这两者均被存储在肌浆网中的Ca2释放激活。这些结果表明,氯胺酮对跨肌膜Ca2内流的抑制在麻醉剂的负性肌力作用中起主要作用。

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