Gutierrez-Cabano C A
Department of Surgical Pathology II, Faculty of Medical Sciences, National University of Rosario, Argentina.
Acta Gastroenterol Latinoam. 1998;28(2):193-8.
The purpose of this study was to investigate the role played by endogenous prostaglandins, sulfhydryls, gastric motility, fluid volume, and mucus volume retained in the gastric lumen in the protection offered by intragastric amoxicillin against ethanol-induced gastric lesions. It has been demonstrated that intragastric administration of amoxicillin (Amx) dose-dependently protected the rat gastric mucosa from 96% ethanol-induced lesions. The inhibition of the lesions was 28, 41.4, 84.7 and 90% at doses of 50, 100, 200 and 400 mg/kg, respectively. The gastroprotective effect of Amx was significantly reversed by pretreatment with both indomethacin (5 mg/kg, subcutaneously), a cyclooxygenase inhibitors, and iodoacetamide (100 mg/kgm subcutaneously), a sulfhydryl blocker. Gastric motility was measured by a balloon method. There was not any significant differences between Amx (50-400 mg/kg)-induced and spontaneous motility with regard to both amplitudes and frequently of gastric contraction. One milliliter of 96% ethanol produced hemorrhagic bandlike lesions in the corpus mucosa with the occurrence of a complete inhibition of the amplitude and frequency of gastric contraction. This inhibition of gastric motility caused by ethanol was not modified by pretreatment of Amx (400 mg/kg) alone, indomethacin plus Amx or iodoacetamide plus Amx. In addition, there was a significant increase in the mucus volume retained in the gastric lumen for Amx (200 and 400 mg/kg) at 30 min after its administration. We conclude that the intragastric Amx prospective effect against 96% eathanol-induced mucosal lesions may be mediated by endogenous prostaglandins, sulfhydryl compounds of the gastric mucosa, an increase in mucus volume retained in the gastric lumen at the time when ethanol is administered, and is not associated with the gastric motor activity.
本研究的目的是调查内源性前列腺素、巯基、胃动力、液体量以及胃腔内留存的黏液量在胃内给予阿莫西林对乙醇诱导的胃损伤的保护作用中所起的作用。已证明胃内给予阿莫西林(Amx)可剂量依赖性地保护大鼠胃黏膜免受96%乙醇诱导的损伤。在剂量分别为50、100、200和400mg/kg时,损伤的抑制率分别为28%、41.4%、84.7%和90%。用环氧化酶抑制剂吲哚美辛(5mg/kg,皮下注射)和巯基阻断剂碘乙酰胺(100mg/kg,皮下注射)预处理后,Amx的胃保护作用均被显著逆转。通过气囊法测量胃动力。就胃收缩的幅度和频率而言,Amx(50 - 400mg/kg)诱导的胃动力与自发胃动力之间没有任何显著差异。1毫升96%乙醇在胃体黏膜产生出血性带状损伤,并完全抑制胃收缩的幅度和频率。乙醇引起的这种胃动力抑制不受单独用Amx(400mg/kg)预处理、吲哚美辛加Amx或碘乙酰胺加Amx的影响。此外,在给予Amx(200和400mg/kg)后30分钟,胃腔内留存的黏液量显著增加。我们得出结论,胃内给予Amx对96%乙醇诱导的黏膜损伤的保护作用可能由内源性前列腺素、胃黏膜的巯基化合物、在给予乙醇时胃腔内留存的黏液量增加介导,且与胃运动活性无关。