阿托品和山莨菪碱抑制兔胸主动脉收缩的作用机制  

Mechanism of inhibitory effects of atropine and anisodamine on contractions of rabbit thoracic aorta

作　　者：刘书勤[1] 臧伟进[1] 李增利[1] 孙强[1] 于晓江[1] 

机构地区：[1]西安交通大学医学院药理学教研室,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2005年第1期16-18,25,共4页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：西安交通大学自然科学基金资助.

摘　　要：目的　探索阿托品和山莨菪碱扩血管作用机制。方法　离体兔主动脉环张力描记法。结果　内皮完整主动脉环经阿托品或山莨菪碱(1、3μmol/L)预处理 10 min 后, KCl (60、30、20 mmol/L)引起的收缩张力均不改变(P>0.05),但去甲肾上腺素(NA:0.01μmol/L)、组织胺(His:3μmol/L)和5 羟色胺(5 HT:0.1 μmol/L)引起的收缩均明显减弱(P<0.01)。阿托品抑制NA的缩血管作用弱于山莨菪碱(P<0.01), 抑制 His的缩血管作用强于山莨菪碱(P<0.01或<0.05);抑制5 HT的缩血管作用与山莨菪碱相当(P>0.05)。在去内皮血管环后得到相似的结果。结论　阿托品和山莨菪碱可抑制受体介导的家兔主动脉平滑肌收缩,其作用不依赖于血管内皮。Objective To investigate the vasodilative mechanisms of atropine and anisodamine (Ani). Methods Rabbit isolated aortic ring tension recording method was used. Results After 10 minutes of atropine (1, 3μmol/L) or Ani (1, 3μmol/L) pretreatment, the contractive responses of the endothelium-intact aorta to KCl (60, 30 and 20mmol/L) remained unchanged (P>0.05, respectively), but those to noradrenaline (NA: 0.01μmol/L), histamine (His: 3μmol/L), and 5-hydroxytryptamine (5-HT: 0.1μmol/L), significantly reduced (P< 0.01, respectively). Under Ani pretreatment, compared with atropine pretreatment, the NA-induced contractions were significantly weaker (P<0.01, respectively), the His-induced contractions were significantly more powerful (P<0.01 or 0.05), and the 5-HT-induced contractions and the Ani-induced contractions were comparative (P>0.05, respectively). Under atropine or Ani pretreatment, the NA-, His- and 5-HT-elicited contractions in endothelium-denuded aorta were similar to those in endothelium-intact aorta. Conclusion Atropine and Ani can inhibit receptors-mediated constrictions of rabbit aortic vascular smooth muscle cells; the actions are endothelia independent.

关 键 词：阿托品 山莨菪碱 兔主动脉 去甲肾上腺素 组织胺 5-羟色胺 

分 类 号：R972[医药卫生—药品]