摘要
目的探讨七氟醚增强非去极化肌松药肌松作用的机制.方法从大鼠肌肉提取多聚腺嘌呤mRNA,注入去膜的非洲爪蟾卵母细胞以表达有功能的离子通道, 利用电压钳技术记录电压依赖性的离子通道电流.建立七氟醚、罗库溴铵和维库溴铵分别抑制乙酰胆碱所引起电流的量效曲线,再研究给予相当于50%抑制率浓度的七氟醚后,罗库溴铵和维库溴铵抑制作用的变化.结果七氟醚、罗库溴铵和维库溴铵均能产生快速、稳定、可逆、浓度依赖性的抑制.达到50%抑制率的浓度分别是823 μmol·L-1(95% CI:681～997 μmol·L-1)、 33.4 nmol·L-1(95% CI:27.1～41.7 nmol·L-1) 和9.2 nmol·L-1(95% CI:7.9～12.3 nmol·L-1).联合使用七氟醚、非去极化肌松药时,七氟醚增强非去极化肌松药的抑制效应.结论七氟醚增强非去极化肌松药肌松作用的机制可能是在受体水平增加拮抗剂的亲和力.
Aim To investigate the mechanism of sevoflurane enhancement of muscle relaxation. Methods Poly（A） ＋ mRNA isolated from the rat＇s muscle were microinjected into Xenopus oocytes to express functional ion channels. Voltage clamp technique was used to record the current of the voltage-dependent ion channels. Concentration-effect curves for the inhibition of acetylcholine-induced currents were established for sevoflurane, rocuranium and vecuronium. Subsequently, inhibitory effects of NDMRS were studied in the presence of the sevoflurane at a concentration equivalent to half the concentration producing a 50% inhibition alone. Results Sevoflurane, rocuranium and vecuronium produced rapid and readily reversible con- centration-dependent inhibition. The 50% inhibitory concentration values were 823μmol·L^-1 （95% CI： 681 -997μmol·L^-1） ,33.4 nmol（95% CI：27.1 - 41.7 nmol·L^-1） and 9.2 nmol·L^-1（95% CI：7.9 - 12.3 nmol·L^-1） for sevoflurane, rocuranium and vecuronium, respectively. Coapplication of sevoflurane significantly enhanced the inhibitory effects of rocuranium and vecuronium. Conclusion Sevoflurane increases the potency of NDMRs, possibly by enhancing antagonist affinity at the receptor site.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第9期1081-1084,共4页
Chinese Pharmacological Bulletin
关键词
七氟醚
非去极化肌松药
细胞膜
受体
胆碱能
sevoflurane
nondepolarizing muscle relaxants
cell membrane
receptors, cholinergic
