紫菀乙醇提取物对豚鼠离体气管平滑肌收缩功能的影响

Effects of Alcohol Extract of Aster tataricus L.f.on the Contraction of Guinea Pig Tracheal Smooth Muscle in vitro

本试验旨在研究紫菀乙醇提物对豚鼠离体气管平滑肌收缩功能的影响。采用离体气管恒温灌流的方法,将豚鼠气管制成气管螺旋条,通过BL-420F生物机能实验系统测定其张力的变化,观察紫菀乙醇提物对离体气管平滑肌静息状态下的舒张作用,以及在氯化乙酰胆碱(Ach)、磷酸组胺(His)、CaCl_2条件下和无钙下Ach诱导细胞内钙释放和外钙内流所致两种收缩条件下对离体气管平滑肌张力变化的影响。试验结果显示,低浓度紫菀乙醇提取物(0.002~0.008g/mL)对静息状态下豚鼠离体气管平滑肌具有一定的收缩作用,高浓度(0.008~0.196g/mL)时具有舒张作用;低、中、高3个剂量组均可抑制Ach、His和CaCl_2引起的气管平滑肌收缩强度,使各致痉剂的量效曲线非平行右移并降低最大效应。紫菀乙醇提取物对His的抑制作用强度最大,其次为Ach,最后是CaCl_2,且均呈剂量依赖性。以上结果表明紫菀乙醇提物具有舒张气管平滑肌的作用,其机制可能与抑制豚鼠气管平滑肌M受体、H_1受体和阻断Ca^(2+)通道从而抑制细胞Ca^(2+)内流有关。

The aim of the experiment was to study the effect of alcohol extract of Astertataricus L.f.on the contraction of isolated guinea pig tracheal smooth muscle.The guinea pig tracheal smooth muscle was prepared by isolated tracheal thermostatic perfusion method.The effects of AstertataricusL.f.on tracheal smooth muscle under the resting state and contraction stimulated by acetylcholine（Ach）,histamine（His）,CaCl_2,Ca-2＋release and influx in cells without calcium were measured by BL-420 Fbiological function experiment systems.The results showed that Aster tataricus L.f.could induce the contraction of isolated trachea at resting state at a low concentrations of 0.002 to 0.008g/mL and exerted a relaxation on the isolated trachea when at the higherconcentrations of 0.008 to 0.196g/mL.All of the three concentrations of Aster tataricus L.f.could inhibit the tension stimulated by Ach,His and CaCl_2 which were antispasmodic agents,led to the non-parallelled rightward moving of cumulative concentration-response curve and the decline of maximal responses.The suppressive effect on His was the strongest,followed by Ach and CaCl2,and the suppression could counteract the contraction induced by extracellular Ca-2＋influx significantly,and they were all expressed concentration-dependent manner.These results indicated the alcohol extract of Aster tataricus L.f.could relax tracheal smooth muscle by acting on M-receptor and histamine receptor and blocking Ca-2＋passage,thus inhibiting extracellular Ca-2＋influx.