阿托品和山莨菪碱抑制兔胸主动脉收缩的作用机制

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。

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

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.