Ogle C W, Cho C H, Tong M C, Koo M W
Eur J Pharmacol. 1985 Jun 19;112(3):399-404. doi: 10.1016/0014-2999(85)90787-3.
The influence of verapamil on stress- or bethanechol-induced gastric effects was investigated in rats. Intraperitoneally injected verapamil (1, 2 or 4 mg/kg), given 30 min beforehand, dose-dependently prevented gastric glandular ulceration, mast cell degranulation and the increased stomach wall contractions evoked by restraint at 4 degrees C for 1 h. Gastric acid secretion, as well as ulceration in both the forestomach and glandular segment, produced by subcutaneously-injected bethanechol (3.2 mg/kg) were also inhibited. It is concluded that decreased amine release from the mast cells, stomach wall relaxation and reduced gastric acid were responsible for the ulcer-antagonising effects of the calcium-entry blocker. The possible antiulcer actions of verapamil are discussed in the light of present knowledge regarding calcium involvement in the various mechanisms thought to contribute to the pathophysiology of stress ulceration in rat stomachs.
在大鼠中研究了维拉帕米对应激或氨甲酰甲胆碱诱导的胃部效应的影响。预先30分钟腹腔注射维拉帕米(1、2或4mg/kg),剂量依赖性地预防了胃腺溃疡、肥大细胞脱颗粒以及4℃约束1小时引起的胃壁收缩增加。皮下注射氨甲酰甲胆碱(3.2mg/kg)引起的胃酸分泌以及前胃和腺部的溃疡也受到抑制。得出的结论是,肥大细胞胺释放减少、胃壁松弛和胃酸减少是钙通道阻滞剂抗溃疡作用的原因。根据目前关于钙参与被认为导致大鼠胃应激性溃疡病理生理学的各种机制的知识,讨论了维拉帕米可能的抗溃疡作用。