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本实验以离体兔主动脉条为标本 ,对薤白 (EA)的扩血管机制进行了探讨 .观察了薤白对去甲肾上腺素 (NE)、氯化钾 (KCl)和氯化钙 (CaCl2 )的剂量 效应曲线的影响及主动脉条的α受体及 β受体的作用 .观察了EA对NE引起的兔主动脉条两种收缩成分的影响 .结果表明EA能舒张已为氯化钙、高钾和去甲肾上腺素收缩的兔主动脉条 ,使NE、KCl、CaCl2 的剂量 效应曲线非平行右移 ,最大效应降低 .EA松弛血管平滑肌的作用不依赖于阻断α受体或 β受体 ,而与戊脉安 (Ver)相似 ,是通过阻断钙通道实现的 .但它们阻断钙通道的方式不同 .EA可能无选择性阻断电位依赖性钙通道和受体操纵性钙通道 .因此EA的扩血管机制与其对钙通道阻断作用有关 .
In this study, rabbit aortic strips were used as specimens to investigate the mechanism of vasodilator vasoconstrictor (EA). Observed in vitro with norepinephrine (NE), potassium chloride (KCl) and calcium chloride (CaCl2) The effects of the dose-response curve and the effects of the α-receptor and β-receptor in the aortic strip. The effects of EA on NE-induced contractions in rabbit aortic strips were observed. The results showed that EA was able to relax as calcium chloride, High potassium and norepinephrine contraction of rabbit aortic strips, NE, KCl, CaCl2 dose-response curve is non-parallel to the right, the maximum effect is reduced. EA relaxation of vascular smooth muscle is not dependent on blocking the alpha receptor or beta receptors In vivo, similar to verapamil (Ver), is achieved by blocking calcium channels. However, they block calcium channels in different ways. EA may not selectively block potential-dependent calcium channels and receptor-operated calcium channels. Therefore, the vasodilator mechanism of EA is related to its blocking effect on calcium channels.