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利多卡因对鸡颈二腹肌骨骼肌的作用。

Effect of lignocaine on chick biventer cervicis skeletal muscle.

作者信息

Wali F A

出版信息

Pharmacol Res Commun. 1986 Jan;18(1):31-48. doi: 10.1016/0031-6989(86)90157-8.

Abstract

The effect of lignocaine (0.01-100 micrograms.ml-1) on amplitude of indirectly and directly-elicited twitch contractions and on contractures produced by acetylcholine (ACh) (0.1-10 mM) and tetraethylammonium (TEA) (1.2-12 mM) was studied in isolated biventer cervicis skeletal muscle of the chick. Lignocaine (0.01-0.9 microgram.ml-1) increased the amplitude of the indirectly-elicited twitch contractions. At high concentrations (10-100 micrograms.ml-1), lignocaine decreased or blocked the twitch tension and produced a contracture in the chick skeletal muscle. Lignocaine also reduced or blocked the directly-elicited twitch contractions in a dose-dependent manner. Lignocaine (10 micrograms.ml-1) reduced the ACh-induced contracture whereas it increased that produced by TEA. Physostigmine (2 micrograms.ml-1) increased the stimulating effect of lignocaine, at low concentrations. However, repeated exposures to lignocaine followed by physostigmine resulted in both increase and decrease in the indirectly-elicited twitch contractions. It was concluded that lignocaine had a dual action at the neuromuscular junction. In low concentrations, lignocaine increases the twitch tension, possibly by an anticholinesterase action, and in high concentrations it reduces or blocks the twitch tension, produces a contracture in the muscle, and reduces the ACh-induced contractures, whereas it increases the TEA-induced responses. Some of these effects of lignocaine may be interpreted in terms of effects on excitation-contraction coupling in muscle.

摘要

研究了利多卡因(0.01 - 100微克·毫升⁻¹)对雏鸡离体双腹肌骨骼肌间接和直接诱发的抽搐收缩幅度以及乙酰胆碱(ACh)(0.1 - 10毫摩尔)和四乙铵(TEA)(1.2 - 12毫摩尔)所产生的挛缩的影响。利多卡因(0.01 - 0.9微克·毫升⁻¹)增加了间接诱发的抽搐收缩幅度。在高浓度(10 - 100微克·毫升⁻¹)时,利多卡因降低或阻断了抽搐张力,并在雏鸡骨骼肌中产生了挛缩。利多卡因还以剂量依赖性方式降低或阻断了直接诱发的抽搐收缩。利多卡因(10微克·毫升⁻¹)降低了ACh诱导的挛缩,而增加了TEA诱导的挛缩。毒扁豆碱(2微克·毫升⁻¹)在低浓度时增强了利多卡因的刺激作用。然而,反复暴露于利多卡因后再给予毒扁豆碱,间接诱发的抽搐收缩既有增加也有减少。得出的结论是,利多卡因在神经肌肉接头处具有双重作用。在低浓度时,利多卡因可能通过抗胆碱酯酶作用增加抽搐张力,而在高浓度时,它降低或阻断抽搐张力,在肌肉中产生挛缩,并降低ACh诱导的挛缩,而增加TEA诱导的反应。利多卡因的这些作用中的一些可能可以从其对肌肉兴奋 - 收缩偶联的影响方面来解释。

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