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作 者:吴波[1] 曹红[2] 陈思维[2] 王敏伟[2] 王乃利 姚新生
机构地区:[1]中国医科大学第一临床学院急诊科,沈阳110001 [2]沈阳药科大学药学系,沈阳110015
出 处:《沈阳药科大学学报》2000年第6期447-449,455,共4页Journal of Shenyang Pharmaceutical University
摘 要: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 .The purpose of the paper is to evaluate the effect of the extract of Bulbus Allii macrostemi (EA) on aortic strip′s tension.The fluctuation of the dose-response curves for NE,KCl and CaCl\-2 induced by EA was observed with isolated rabbit aortic strips.The effect of EA on α-adrenoceptor or β-adrenoceptor and influence of EA on the 2 components of NE-evoked contraction were studied.EA inhibited the contractions evoked by CaCl 2,high K\++ or NE in rabbit thoracic aortic strips.EA shifted the dose-response curves of NE,KCl and CaCl 2 to the right,and depressed their maximal responses.EA produced neither α-adrenoceptic blocking nor β-adrenoceptic stimulating effects.EA-induced relaxation on vascular smooth muscle resulted from its antagonistic effect to Ca 2+ and the mode of this antagonism differed from that of Verapamil.EA inhibited both the receptor-operated channel and potential dependent channel.On the contrary,Verapamil inhibited the potential dependent channels only.The mechanism of vasodilatation of EA is related to its antagonistic effect to calcium ion.
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