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AIM To determine the effect of glutathione (GSH) on stress gastric mucosal lesion.METHODS The stress gastric mucosal lesion as produced by restraint water-immersion in rats and gastricmucosal lesion, gastric mucosal GSH content, gastric acid secretion and gastric barrier mucus secretion wereexamined. We also observed the effect of GSH on gastric mucosal lesion and the effect of N-ethylmaleimine(NEM) and indomethacin on GSH protection. Comparisons between two groups were made using the Students t test.RESULTS GSH (100 and 200 mg/kg) intraperitoneally protected against stress gastric mucosal lesion(P<0.001 and P<0.001). Restraint water-immersion stress significantly reduced gastric mucosal GSHcontent (P < 0.001), but pretreatment with GSH (100 mg/kg) had no effect on gastric mucosal GSH content(P>0.05). The preinjection of NEM (10 mg/kg, sc.), a sulfhydryl-blocking reagent, or indomethacin(5 mg/kg, im.), a cyclooxygenase inhibitor, had no effect on protection of GSH (P>0.05). GSH(100mg/kg) significantly increased secretion of gastric barrier mucus (P<0.05), but had no effect onsecretion of gastric acid in restraint water-immersed rats (P >0.05).CONCLUSION GSH can inhibit the formation of gastric mucosal lesions induced by restraint water-immersion. The protective effect of GSH was due, in part, to promoting the secretion of gastric barriermucus, but not to suppress the gastric acid secretion. The protection effect of GSH has no relation withgastric mucosal GSH and PGs.
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Previous studies have shown that somatic sensation by acupuncture and visceral nociceptive stimulation can converge in the nucleus tractus solitarii where neurons integrate signals impact-ing on the function of organs. To explore the role of the nucleus tractus solitarii in the protective mechanism of pre-moxibustion on gastric mucosa, nucleus tractus solitarii were damaged in rats and pre-moxibustion treatment at the Zusanli (ST36) point followed. The gastric mucosa was then damaged by the anhydrous ethanol lavage method. Morphological observations, enzyme linked immunosorbent assays, and western immunoblot analyses showed that gastric mucosa surface lesion and the infiltration of inflammatory cells were significantly ameliorated after pre-moxibustion treatment. Furthermore, the gastric mucosal damage index and somatostatin level were reduced, and epidermal growth factor content in the gastric mucosa and heat-shock protein-70 expression were increased. These results were reversed by damage to the nucleus tractus solitarii. These findings suggest that moxibustion pretreatment at the Zusanli point is protective against acute gastric mucosa injury, and nucleus tractus solitarii damage inhibits these responses. Therefore, the nucleus tractus solitarii may be an important area for regulating the signal transduction of the protective effect of pre-moxibustion on gastric mucosa.
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胃黏膜保护剂与急性胃黏膜病变
一、急性胃黏膜病变的概念和发生机制急性胃黏膜病变(acute gastric mucosal lesion,AGML)又称应激性溃疡,是指机体在各类严重创伤、危重疾病、严重心理应激或各类损害胃黏膜的药物(如阿司匹林、乙醇等)作用下所引起的上消化道急性糜烂、溃疡,主要表现为上消化道出血,少数可并发穿孔.
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65岁以上老年患者术后急性胃粘膜病变12例临床分析
急性胃粘膜病变(Acute Gastric Mucosal Lesion, AGML)系机体遭受各种应激性因子作用于胃粘膜发生的急性损害.严重创伤、手术、大面积烧伤、某些药物等均有可能引起AGML.我们自1996~1998年诊治了12例老年患者术后AGML,均采用非手术方法治愈,现分析总结如下.1 临床资料1.1 一般资料男9例,女3例,年龄65~83岁,既往均无胃病史,出血均有手术创伤应激诱因,手术范围:复合性外伤3例,胆管系统手术2例,结肠肿瘤3例,嵌顿性疝肠坏死切除1例,后腹膜肿瘤及胸部手术各1例.
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胃周围血管阻断治疗急性胃粘膜病变大出血
急性胃粘膜病变(Acut gastric mucosal lesion AGML)见于各种危重病例,10%~20%AGML急性大出血需外科手术治疗.近年来我院收治6例AGML急性大出血病人,在药物止血无效后施行胃周围血管阻断术,取得较好的疗效,报道如下.
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应激性胃粘膜损伤的中枢调控机制研究进展
应激性胃粘膜损伤(stress gastric mucosal lesion,SGML)是指机体在严重创伤、烧伤、休克、力竭运动、水浸-束缚以及内脏功能严重受损等多种危重情况下发生的以胃粘膜的出血、溃疡、糜烂为主要特征的应激性病变,是创伤后为常见的内脏并发症之一,对患者有潜在的致命性威胁.目前认为SGML是中枢神经系统保护和胃粘膜的神经递质的平衡状态遭到破坏引起的.中枢神经系统的活动与消化道的功能有密切的关系,机体抗应激的反应首先启动于中枢神经系统,严重引发中枢神经系统功能紊乱,导致一系列变化是发生SGML的重要环节.多年来,国内外学者对其进行了大量的基础和临床研究,迄今其发病机制尤其中枢调控机制尚未明确.鉴于SGML在临床上的重要性,本文就其中枢调控机制予以综述,以期为防治的深入研究提供帮助.
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急性胃黏膜病变与胃黏膜保护研究进展
急性胃黏膜病变(acute gastric mucosal lesion,AGML)是指以胃黏膜糜烂和急性溃疡为特征,且常致急性上消化道出血的疾病.过去曾名为急性糜烂性胃炎和出血性胃炎等,由某些药物和重症伤病应激状态下所引起的急性胃黏膜病变,包括由黏膜糜烂至坏死的病理变化,统称应激性溃疡.祖国医学属"胃脘痛"、"腹痛"、"吐血"、"呕血"、"便血"等范畴.