Pinelli A, Colombo R, Trivulzio S, Berti F, Tofanetti O, Caimi B R
Arzneimittelforschung. 1984;34(8):890-4.
In this study 2-guanidinebenzimidazole (GBI) and 1-phenylbiguanide (PBG) appear to be capable of decreasing gastric acid secretion, while the compounds dimethylbiguanide and cyanoguanidine do not. Thus, the antisecretory effect is present when the biguanide groups are associated with lipophilic molecules. GBI and PBG depress gastric acid secretion, even when it has been stimulated by carbamoylcholine (carbachol) or betazole. The antihistamine effects of GBI and PBG on betazole-stimulated gastric acid secretion were confirmed by the inhibitory activity of these compounds on the isolated guinea pig auricle stimulated by histamine. The antimuscarine activity of GBI and PBG on carbachol-stimulated gastric acid secretion in rats is also supported by the way in which these same drugs depress the motility of the duodenum and colon of the anaesthetized cat stimulated by prostigmine. The above mentioned effects of these compounds are also associated with myolytic activity, since they decrease the spontaneous and histamine-stimulated motility of the duodenum and colon. GBI and PBG probably depress gastric acid secretion by interfering with both histamine and acetylcholine receptors and with other sites involved in the secretory process.
在本研究中，2-胍基苯并咪唑（GBI）和1-苯基双胍（PBG）似乎能够减少胃酸分泌，而二甲基双胍和氰基胍则不能。因此，当双胍基团与亲脂性分子结合时，会出现抗分泌作用。GBI和PBG即使在胃酸分泌已被氨甲酰胆碱（卡巴胆碱）或倍他唑刺激的情况下，仍能抑制胃酸分泌。GBI和PBG对倍他唑刺激的胃酸分泌的抗组胺作用，通过这些化合物对组胺刺激的离体豚鼠耳廓的抑制活性得到证实。GBI和PBG对大鼠中卡巴胆碱刺激的胃酸分泌的抗毒蕈碱活性，也得到了同样这些药物抑制麻醉猫由新斯的明刺激的十二指肠和结肠运动的方式的支持。这些化合物的上述作用也与溶肌活性有关，因为它们降低了十二指肠和结肠的自发运动以及组胺刺激的运动。GBI和PBG可能通过干扰组胺和乙酰胆碱受体以及分泌过程中涉及的其他位点来抑制胃酸分泌。
