Man W K, Saunders J H, Ingoldby C, Spencer J
Gut. 1981 Nov;22(11):923-6. doi: 10.1136/gut.22.11.923.
Measurements were made of the amounts of histamine extracted from patients with peptic ulcer disease and control subjects suffering from various gastrointestinal diseases. Patients with duodenal ulcer, gastric ulcer, or recurrent duodenal ulcer after proximal gastric vagotomy often had less gastric mucosal histamine than did normal controls. Cimetidine therapy increased the amounts of the histamine to above control levels, presumably by suppression of output. It is concluded that endogenous amounts of histamine reflect the pathogenic states in the gastric mucosa of patients with peptic ulcer diseases. Cimetidine, as does vagotomy, increases the amount of gastric mucosal histamine. These findings suggest that the increase in mucosal histamine with cimetidine is not due to activation of histamine methyl transferase, but rather to suppression of histamine output into the gastric juice.
对患有消化性溃疡疾病的患者以及患有各种胃肠道疾病的对照受试者所提取的组胺量进行了测量。十二指肠溃疡、胃溃疡或近端胃迷走神经切断术后复发性十二指肠溃疡的患者，其胃黏膜组胺含量通常低于正常对照组。西咪替丁治疗可使组胺量增加至高于对照水平，推测是通过抑制组胺分泌实现的。得出的结论是，内源性组胺量反映了消化性溃疡疾病患者胃黏膜的致病状态。西咪替丁与迷走神经切断术一样，可增加胃黏膜组胺量。这些发现表明，西咪替丁导致的黏膜组胺增加并非由于组胺甲基转移酶的激活，而是由于抑制了组胺向胃液中的分泌。
