Gutiérrez-Cabano C A
Department of Surgical Pathology II, Faculty of Medical Sciences, National University of Rosario, Argentina.
Dig Dis Sci. 2000 Jan;45(1):105-9. doi: 10.1023/a:1005417612229.
The aim of this study was to investigate the role of alpha2-adrenoceptors in the mechanism of intragastric polyethylene glycol 400 (PEG-400) protection against ethanol-induced gastric mucosal damage. In the injury study, 0.5 hr after subcutaneous control or yohimbine (5 mg/kg), a selective alpha2-adrenoceptor antagonist, rats were treated with intragastric vehicle or PEG-400 (5500 mg/kg). One hour later animals received 96% ethanol (gavage needle), 5 ml/kg, and the rats were killed after another hour. Total lengths of the gastric mucosal lesions were measured by an unbiased observer in a blinded fashion using a binocular magnifier having 5x magnification. In a separate set of experiments, 0.5 hr after subcutaneous control or yohimbine (5 mg/kg) rats received intragastric vehicle or PEG-400 (5500 mg/kg). One hour later gastric mucus volume, gastric juice volume, and gastric acid output in the gastric juice were measured. The protective effect offered by intragastric PEG-400 against ethanol-induced gastric mucosal damage was significantly diminished although not completely abolished by a selective alpha2-adrenoceptor antagonist (yohimbine). Yohimbine also significantly diminished both the basal and PEG-400-stimulated increase in gastric mucus volume. These findings suggest that the protective effect afforded by intragastric PEG-400 against ethanol-induced gastric mucosal damage is partially mediated by alpha2-adrenoceptors, and a mucus-dependent mechanism may be involved.
本研究旨在探讨α2-肾上腺素能受体在胃内给予聚乙二醇400(PEG - 400)预防乙醇诱导的胃黏膜损伤机制中的作用。在损伤研究中,皮下注射对照剂或育亨宾(5 mg/kg,一种选择性α2-肾上腺素能受体拮抗剂)0.5小时后,给大鼠胃内给予赋形剂或PEG - 400(5500 mg/kg)。1小时后,动物经灌胃针给予96%乙醇,5 ml/kg,再过1小时后处死大鼠。由一位公正的观察者使用5倍放大倍数的双目放大镜以盲法测量胃黏膜损伤的总长度。在另一组实验中,皮下注射对照剂或育亨宾(5 mg/kg)0.5小时后,给大鼠胃内给予赋形剂或PEG - 400(5500 mg/kg)。1小时后测量胃黏液量、胃液量以及胃液中的胃酸分泌量。胃内给予PEG - 400对乙醇诱导的胃黏膜损伤的保护作用虽未被选择性α2-肾上腺素能受体拮抗剂(育亨宾)完全消除,但显著减弱。育亨宾还显著降低了基础状态下以及PEG - 400刺激引起的胃黏液量增加。这些发现表明,胃内给予PEG - 400对乙醇诱导的胃黏膜损伤的保护作用部分由α2-肾上腺素能受体介导,且可能涉及一种依赖黏液的机制。