Pendleton R G, Miller D A, Ridley P T
Arch Int Pharmacodyn Ther. 1980 Jan;243(1):37-47.
Desmethylimipramine (DMI) and atropine were compared in a variety of organ system tests in rats and mice involving muscarinic receptor function in order to assess the anticholinergic-like activity of this tricyclic antidepressant drug. DMI was similar to atropine in maximally inhibiting basal gastric acid secretion and markedly protecting against restraint-induced stomach ulceration. It did not, however, substantially increase pupil size, reduce fecal pellet output, inhibit cholinergically induced salivation or specifically antagonize the CNS effects of carbachol and oxotremorine as did atropine. From these data and previous work indicating that DMI acts at a site in the central nervous system to inhibit gastric acid secretion, it is concluded that the biological effects of this drug are not mediated through an atropine-like mechanism.
为评估这种三环类抗抑郁药的类抗胆碱能活性,在大鼠和小鼠的各种涉及毒蕈碱受体功能的器官系统试验中,对去甲丙咪嗪(DMI)和阿托品进行了比较。DMI在最大程度抑制基础胃酸分泌以及显著预防束缚诱导的胃溃疡方面与阿托品相似。然而,它不像阿托品那样能大幅增加瞳孔大小、减少粪便颗粒排出量、抑制胆碱能诱导的唾液分泌或特异性拮抗卡巴胆碱和氧化震颤素的中枢神经系统作用。根据这些数据以及之前表明DMI作用于中枢神经系统某部位以抑制胃酸分泌的研究,得出结论:该药的生物学效应不是通过类似阿托品的机制介导的。