Arisawa T, Nakazawa S, Asai J, Tsukamoto Y
Second Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Digestion. 1989;43(1-2):87-97. doi: 10.1159/000199866.
Repeated intraperitoneal administration of compound 48/80 to rats produced gastric lesions, a decrease in connective tissue mast cells (CTMCs) and an increase in gastric mucosal mast cells (MMCs). The ratio of MMC to CTMC was significantly correlated with lesion formation. A mast cell stabilizer, MAR-99 (50 mg/kg), prevented lesion formation and changes in the mast cells. Omeprazole (20 or 60 mg/kg) significantly reduced the gastric lesions, but mast cell changes persisted. Cimetidine (50 mg/kg) could not inhibit compound 48/80-induced lesions nor a decrease in CTMCs, but did prevent an increase in MMCs. These facts suggest that in compound 48/80-induced gastric lesions chemical mediators released from CTMCs might be trigger factors, while intraluminal gastric acid might be an aggravating factor. Furthermore, the increase in MMCs might be regulated by histamine released from the CTMCs via H2 receptors and have no causal relation to lesions formation.
对大鼠反复腹腔注射化合物48/80会导致胃损伤,结缔组织肥大细胞(CTMCs)减少,胃黏膜肥大细胞(MMCs)增加。MMC与CTMC的比例与损伤形成显著相关。一种肥大细胞稳定剂MAR-99(50毫克/千克)可预防损伤形成和肥大细胞变化。奥美拉唑(20或60毫克/千克)可显著减轻胃损伤,但肥大细胞变化持续存在。西咪替丁(50毫克/千克)不能抑制化合物48/80诱导的损伤,也不能抑制CTMCs的减少,但可防止MMCs增加。这些事实表明,在化合物48/80诱导的胃损伤中,CTMCs释放的化学介质可能是触发因素,而胃腔内胃酸可能是加重因素。此外,MMCs的增加可能受CTMCs通过H2受体释放的组胺调节,与损伤形成无因果关系。