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用乙酰毒毛旋花子甙元2.0×10~(-7)mol/L,在绵羊心室浦肯野纤维产生延迟后除极(DAD)为实验模型,观察异丙肾上腺素与氨甲酰胆碱对DAD的影响。异丙肾上腺素1.0—3.0×10~(-8)mol/L能增加DAD幅值,为剂量依赖性,并可诱发出触发型心律失常。氨甲酰胆碱2.0×10~(-6)mol/L单独作用对DAD幅值无影响,然而在异丙肾上腺素增强DAD幅值或产生触发型心律失常后,同样浓度的氨甲酰胆碱能显著地减小DAD幅值以及消除触发型心律失常。但氨甲酰胆碱对由高钙、氨茶碱和组胺等所增加的DAD幅值却无抑制作用。以上结果表明,氨甲酰胆碱能拮抗异丙肾上腺素引起的DAD增强作用,可能与M受体的激活,并继而降低膜上β受体激活时所提高的腺苷酸环化酶活性有关。
The inhibitory effects of isoprenaline and carbachol were observed with deoxynivalenol (2.0 × 10 ~ (-7) mol / L) as a model after delayed depolarization (DAD) in sheep ventricular Purkinje fibers Impact on DAD. Isoprenaline 1.0-3.0 × 10 -8 mol / L can increase the amplitude of DAD, which is dose-dependent and can induce triggered arrhythmia. The effect of carbachol 2.0 × 10 -6 mol / L alone had no effect on the amplitude of DAD. However, after isoproterenol enhanced the amplitude of DAD or triggered arrhythmia, the same concentration of carbachol Alkali can significantly reduce the magnitude of DAD and eliminate trigger arrhythmias. However, carbachol had no inhibitory effect on the amplitude of DAD increased by high calcium, aminophylline and histamine. The above results indicate that carbachol antagonizes the isoproterenol-induced DAD-enhancing effect, which may be related to the activation of M receptor, and then to the decreased adenylate cyclase activity that is increased upon activation of the beta receptor on the membrane .