A critical role of gastric mucosal ascorbic acid in the progression of acute gastric mucosal lesions induced by compound 48／80 in rats

AIM: To study the role of gastric mucosal ascorbic acid (AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats. METHODS: C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats. Oral administration of AA (10, 50 or 100 mg/kg) was performed 0.5 h after C48/80 treatment. Determinations for gastric mucosal lesion severity and blood flow, and assays for gastric mucosal total AA, reduced AA, oxidized AA, vitamin E, thiobarbituric acid reactive substances (TBARS), adherent mucus, nitrite/ nitrate (NOx), non-protein SH (NPSH), and myeloperoxidase (MPO), and serum total AA, reduced AA, oxidized AA, and NOx were conducted 0.5 and 3 h after C48/80 treatment. RESULTS: Gastric mucosal lesions occurred 0.5 h after C48/80 treatment and progressed at 3 h. Gastric mucosal blood flow decreased 0.5 h after C48/80 treatment but the decrease was recovered at 3 h. Gastric mucosal total AA, reduced AA, vitamin E, and adherent mucus concentrations decreased 3 h after C48/80 treatment. Gastric mucosal oxidized AA concentration remained unchanged after C48/80 treatment. Gastric mucosal NPSH concentration decreased 0.5 h after C48/80 treatment, but the decrease was recovered at 3 h. Gastric mucosal TBARS concentration and MPO activity increased 0.5 h after C48/80 treatment and further increased at 3 h. Serum total AA and reduced AA concentrations increased 0.5 h after C48/80 treatment and further increased at 3 h, while serum oxidized AA concentration increased at 0.5 h. Serum and gastric mucosal NOx concentrations increased 3 h after C48/80 treatment. AA administration to C48/80-treated rats at 0.5 h after the treatment prevented the gastric mucosal lesion progression and the changes in gastric mucosal total AA, reduced AA, vitamin E, adherent mucus, NOx, and TBARS concentrations and MPO activity and serum NOx concentration found at 3 h after the treatment dose-dependently. The AA administration to C48/80-treated rats caused further increases in serum total AA and reduced AA concentrations at 3 h after the treatment dose-dependently. CONCLUSION: Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.     

胃损伤术后上消化道大出血2例报告

例1.男,36岁。于2005-08-27因多发性骨折由外院转入我院骨科。3年前曾行胃大部切除术,BillrothⅠ式吻合。入院次日出现精神差、烦躁、贫血,左下肺呼吸音消失。胸部X线平片报告:左肺挫伤并血气胸,转入胸外科。急行胸部CT检查,提示左膈肌破裂,膈疝形成。     

环形胰腺引起十二指肠瘀滞症1例

<正>患者,男,50岁,因恶心呕吐1周于2013年5月14日入院,主要表现为进食后约20分钟至半小时腹部不适、恶心,呕吐胃内容物,吐后缓解。空腹状态下无恶心呕吐。入院查体:生命体征正常,心肺未见异常,全腹尚软,剑突下压痛,无明显     

木香槟榔丸全方对小鼠肿瘤坏死因子α含量和胃蛋白酶原的影响

目的:观察木香槟榔丸全方对小鼠肿瘤坏死因子α(TNF-α)和胃蛋白酶原(PG)的影响,探讨木香槟榔丸全方对小鼠酒精性胃损伤的防治作用。方法:小鼠60只随机分为空白对照组(A组)12只、模型对照组(B组)24只、木香槟榔丸干预组(C组)24只。常规饲料喂养,A组灌胃生理盐水,B组灌胃56°白酒和生理盐水,C组灌胃56°白酒和木香槟榔丸全方冲剂,每24 h 1次,持续1周。每日观察记录小鼠的摄食、饮水量及体重,实验结束时检测小鼠胃匀浆中胃蛋白酶原(PGⅠ、PGⅡ)浓度及血中肿瘤坏死因子(TNF-α)浓度。结果:A组小鼠几乎无躁动,进食饮水如常,行动灵活,体重增长在正常范围内,毛发明亮且有光泽;B组小鼠明显不安烦躁,少进食,毛发几乎无光泽,呈灰黄色,排干样便,处死后发现其胃部出现明显胀气、出血倾向;C组小鼠毛发润泽度对比B组较好,排软样便。与B组相比,A组和C组PGⅠ的浓度明显较高,PGⅡ的浓度明显降低(P<0.05),TNF-α浓度显著降低(P<0.05)。结论:木香槟榔丸全方对小鼠酒精性胃损伤具有良好的预防和治疗作用。     

黄连吴茱萸药对水提物对乙醇致大鼠胃损伤的保护作用

目的:研究不同配比黄连吴茱萸药对水提物对乙醇致大鼠急性胃损伤的保护作用及其可能的机制。方法:大鼠经腹腔注射6∶1,6∶6,1∶6 3种不同配比的黄连吴茱萸药对水提物后,通过形态测量法测定胃损伤程度;用ex-vivo chamber法测定50%乙醇造成胃损伤前后的胃电压(PD)变化及灌流液pH值和H+含量。结果:与对照组比较,黄连吴茱萸1∶6药对水提物显著降低胃损伤指数,加快PD的恢复,降低胃灌流液pH值和增加H+含量;黄连吴茱萸6∶6降低胃损伤指数。结论:黄连吴茱萸1∶6水提物对50%乙醇造成的大鼠急性胃损伤具有较好的保护作用,显著优于黄连吴茱萸6∶1和6∶6;其机制可能与抑制酸反渗,增强胃黏膜屏障功能有关,提示吴茱萸在介导胃黏膜保护作用中担当着重要的作用。     

危重症急性胃肠损伤与温下法研究

胃肠功能在危重症医学中起着至关重要的作用,胃肠道作为全身炎症反应综合征的触发器和始动器,是脓毒症以及多脏器功能障碍的中心器官,因此胃肠功能受到越来越多的关注和研究。 ESICM针对重症患者的胃肠功能衰竭,提出了急性胃肠损伤的概念,应作为今后研究的基础。本文通过对危重症患者胃肠功能衰竭的中医文献研究,发现虚证和虚实夹杂证的证候表现较为突出,脏腑辨证多定位在脾、胃和肠腑,病理因素以寒、气、虚为主。根据笔者多年的临床经验,中药以温下通腹、救逆固脱为大法,助于改善患者的胃肠功能。故寻求中医药治疗方法或者联合中医药治疗手段,并深入研究其作用机制,是危重症患者胃肠功能研究的优势和可能的突破口。     

单次大剂量电子线照射SD大鼠胃损伤观察

目的 观察成年雄性SD大鼠经单次大剂量电子线照射胃后的损伤变化,为胃癌术中放疗提供动物实验依据。方法 将38只SD大鼠随机分为对照组与实验组,利用专利技术“小动物放射线精确照射试验台”对实验组大鼠胃进行单次6 MeV 20 Gy照射,照射后不同天数评估大鼠一般情况,观察胃的病理损伤及体重变化。结果 SD大鼠胃受照射后14 d时,镜下观察损伤最重,28 d时已逐渐修复伴腺体萎缩,56 d时胃损伤已纤维素性修复。与对照组相比实验组第1周内体重下降(P<0.05),第2周体重开始上升,但幅度低于对照组(P<0.05),第6周时体重与对照组相近(P>0.05)。结论 单次6 MeV电子线 20 Gy照射SD大鼠胃后损伤最重在2周内,但无穿孔发生,8周内可修复恢复完全正常。     

胃Dieulafoy损害大出血2例报告

胃Ｄｉｅｕｌａｆｏｙ损害大出血２例报告广州军区广州总医院（５１００１０）老年三科余中逊消化科黄小让随着急诊内窥镜的普及和内镜下介入治疗的开展，Ｄｉｅｕｌａｆｏｙ损害——一种极少见的引起消化道大出血的病因逐渐被人们认识。现将我院２例报道如下。病例报告例...     

小儿疳疾临床治验

小儿疳疾是指多种原因导致小儿脾胃损伤，运化失常，以致气液耗伤、全身虚弱赢瘦的疾患，疳证若得不到及时合理治疗，常影响小儿正常生长发育，重的出现体质衰竭，继发多种疾病，甚至危及生命。笔者十多年来在临床上观察治疗小儿疳疾200余例，根据临床小儿疳疾多脾虚肝旺的病症特征，采用扶土抑木的治法，结果收到较好疗效。笔者在本文中将十余年治疳经验做了总结分析。     

光动力疗法与微波对正常大鼠胃损伤的研究

目前，光动力疗法（PDT）治疗胃肠道肿瘤报道较多，但有关PDT对组织损伤机制的研究尚少。本文从显微及超微水平比较PDT与微波对大鼠胃损伤的差异，探讨其损伤机制，旨在为胃肠道肿瘤治疗方法的选择和联合应用，提供理论依据。材料和方法光敏剂：血时财衍生物（Hematoporphyinderivative，HPD）由北京制药工业中心提供。光源：美国产氩离子泵染料激光，氩离子输出波长514．5um，DCM染料经滤光片输出波长630um。石英光导纤维直径为30μm。JK-1型多路温度自动测量仪：军事医学科学院放射医学研究所研制。微波内镜治疗仪：合肥产WNZ-B…