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目的 研究阿托品的扩血管作用及机制。方法 以大鼠肠系膜动脉为标本,考察阿托品对去甲肾上腺素(NE)预收缩血管的舒张作用以及血管内皮细胞、血管平滑肌在该效应中的作用。结果 阿托品能显著舒张NE预收缩的完整内皮血管,去内皮后该作用明显降低。L Nω硝基精氨酸甲酯、吲哚美辛、普萘洛尔及格列本脲对阿托品的舒张作用无明显影响。阿托品对KCl的量效曲线及咖啡因缩血管作用均无明显影响,但能浓度依赖性地抑制NE诱导的内钙释放以及经受体操纵性钙通道的外钙内流。结论 阿托品有明显的扩血管作用,其通过抑制受体介导的外钙内流和内钙释放而舒张血管。
Objective To study the vasodilator effect and mechanism of atropine. Methods The rat mesenteric artery was used as a specimen to investigate the effect of atropine on the vasorelaxation of preneoplastic neonate (NE) and the effects of vascular endothelial cells and vascular smooth muscle on this effect. Results atropine can significantly diastolic NE precontracted intact endothelial vessels, the role of endothelium was significantly reduced. L Nω nitro arginine methyl ester, indomethacin, propranolol and glibenclamide had no significant effect on atropine diastolic function. Atropine had no significant effect on the dose-response curve of KCl and caffeine vasoconstrictor, but could inhibit the NE-induced release of Ca2 + and the Ca2 + influx via the Ca2 + channel in a concentration-dependent manner. Conclusions Atropine has a vasodilative effect that vasodilates by inhibiting receptor-mediated calcium influx and intracellular calcium release.