Sanders K M, Bauer A J
Am J Physiol. 1982 Mar;242(3):G222-30. doi: 10.1152/ajpgi.1982.242.3.G222.
Ethyl alcohol (EtOH) inhibited spontaneous and acetylcholine (ACh)-induced contractions in a dose-dependent manner (0.1-2.5%). These concentrations also reduce the amplitudes of intracellularly recorded slow waves. The effects of EtOH do not appear to be mediated by adrenergic or prostaglandin mechanisms, nor can they be explained on the basis of hyperosmolarity. At higher concentrations (1-10%), EtOH totally abolished phasic contractile activity and caused tonic contraction. ACh was not able to restore normal phasic contractions to muscles treated with EtOH above 2.5% and, in fact, further enhanced the force of the tonic contraction. The membrane potential response to EtOH above 1% was biphasic; the membrane transiently hyperpolarized and then tonically depolarized. It appears that many of the effects of EtOH on gastric emptying might be due to direct interference by EtOH in the membrane events leading to excitation-contraction coupling in gastric smooth muscle.
乙醇(EtOH)以剂量依赖方式(0.1 - 2.5%)抑制自发性收缩和乙酰胆碱(ACh)诱导的收缩。这些浓度也会降低细胞内记录的慢波幅度。乙醇的作用似乎不是由肾上腺素能或前列腺素机制介导的,也不能用高渗性来解释。在较高浓度(1 - 10%)时,乙醇完全消除了相性收缩活动并引起强直性收缩。乙酰胆碱无法使高于2.5%乙醇处理的肌肉恢复正常相性收缩,实际上,反而进一步增强了强直性收缩的力量。高于1%的乙醇对膜电位的反应是双相的;膜先短暂超极化,然后强直性去极化。乙醇对胃排空的许多影响似乎可能是由于乙醇直接干扰了导致胃平滑肌兴奋 - 收缩偶联的膜事件。