低频强声对大鼠肝脏和脾脏形态学影响

目的探讨低频强声对肝脏及脾脏组织形态学的影响。方法随机将大鼠暴露于频率为103Hz或300Hz的声场中,暴露时间分别为5分钟和10分钟。根据暴露的频率和作用时间,分为4个实验组和对照组。依据暴露后观察时间,每组再分为即刻组、3天组和7天组。依据肝脏、脾脏损伤程度判断标准,对低频强声暴露后及对照组肝脏、脾脏组织病理学进行观察。结果与对照组比较,各实验组光镜下肝脏、脾脏均有不同程度的血管扩张、充血、淤血及组织水肿等改变。结论低频强声可导致肝脏、脾脏损伤。     

+Gz暴露对大鼠胃黏膜损伤及胃液表皮生长因子含量的影响

目的探讨不同+Gz暴露值对大鼠胃黏膜的损伤和胃液EGF含量的影响,探讨高+Gz值暴露后大鼠胃黏膜损伤的可能发生的机制。方法 40只雄性Wistar大鼠随机分成4组:对照组+1Gz值(n=10)、+5 Gz值(n=10)、+10 Gz值组(n=10)、重复暴露组(n=10)。+5 Gz值组、+10 Gz值组各连续暴露5 min,重复暴露组亦为连续暴露:+5 Gz值1.5 min、+10 Gz值2 min、+5Gz值1.5 min。每组下离心机后,光镜下分别观察各组胃黏膜大体损伤程度,用游标卡尺检测胃黏膜损伤指数。放免法检测胃液EGF含量。结果各组胃黏膜损伤的严重程度:重复暴露组>+10Gz暴露组>+5Gz暴露组>对照组。+5Gz暴露组与对照组相比胃黏膜损伤指数无显著差异(P>0.05),另两实验组与对照组比较,差异具有显著统计学意义(P<0.01)。与此同时,各组大鼠胃液EGF含量:重复暴露组<+10Gz暴露组<+5Gz暴露组<对照组。+5Gz暴露组与对照组相比胃液EGF含量无显著差异(P>0.05),另两实验组与对照组比较,具有显著性差异(P<0.01)。结论大鼠在越高水平+Gz值暴露下,胃黏膜受损程度越重,胃液EGF含量越低。高+Gz值暴露造成的急性胃黏膜病变与胃黏膜的保护因子EGF表达下降有关。     

正加速度暴露对大鼠应激性胃黏膜损伤和血浆EGF、CGRP的影响

目的 观察不同正加速度暴露值对大鼠胃黏膜的损伤和胃液EGF含量及降钙素基因相关肽（CGRP）水平的影响,探讨高正加速度值暴露后大鼠胃黏膜损伤的可能发生机制.方法 40只雄性Wistar大鼠随机分成4组：对照组（＋1Gz值,n=10）、＋5Gz值组（n=10）、＋10 Gz值组（n=10）、重复暴露组（n=10）.＋5 Gz值暴露组、＋10 Gz值组均连续暴露5 min;重复暴露组：＋5Gz值下暴露1.5 min,＋10 Gz值连续暴露2 min,＋5 Gz值连续暴露1.5 min.大鼠上机前每只大鼠专用一个固定盒,保证加速度作用的方向.大鼠头朝向离心机轴心,仰面固定于离心机转臂远端,每组10只同时上机.采用梯形正加速度作用曲线,G值增长率1 G/s,由计算机进行加速度程序控制.每组下离心机后,光镜下用游标卡尺检测胃黏膜损伤指数,生化比色法检测血浆EGF和CGRP含量并分析其相互关系.结果 各组胃黏膜损伤指数：重复暴露组＞＋10Gz值组＞＋5Gz值组＞对照组.＋5Gz值组与对照组相比胃黏膜损伤指数差异无统计学意义（P＞0.05）,＋ 10Gz值组、重复暴露组与对照组比较,差异均具有显著统计学意义（P＜0.01）.各组大鼠血浆EGF含量：重复暴露组＜＋10Gz值组＜＋5Gz值组＜对照组.＋5Gz值组与对照组相比血浆EGF含量差异无统计学意义（P＞0.05）,＋ 10Gz值组、重复暴露组与对照组比较,差异具有显著统计学意义（P＜0.01）.各组大鼠血浆CGRP含量：重复暴露组＜＋ 10Gz值组＜＋5Gz值组＜对照组.各实验组与对照组相比血浆CGRP含量差异均具有统计学意义（P＜0.05）.结论 正加速度值暴露对大鼠胃黏膜有损伤作用,在越高正加速度值暴露和正加速度重复暴露下,胃黏膜受损程度越重,血浆EGF和CGRP含量越低.高正加速度值暴露和重复加速度暴露造成大鼠的急性胃黏膜病变与胃黏膜的保护因子EGF和CGRP表达有关.     

十二指肠胃反流对胃黏膜损害的实验性研究

目的：拟通过大鼠实验模型探讨短期十二指肠胃反流(DGR)对胃黏膜的损害及其特点。方法：健康、雄性SD大鼠分成3组：DGR组、结扎幽门组和对照组。手术后3周处死大鼠,观察胃黏膜损害及病理组织学改变、检测胃液pH值、胆红素水平及血清胃泌素水平,透射电镜下观察胃窦黏膜细胞间的紧密连接,测定组织过氧化物酶(MPO)活性。结果：DGR组大鼠胃黏膜可见散在糜烂、溃疡及出血点,而结扎幽门组及对照组胃黏膜光滑。DGR组胃液pH值和胆红素水平明显高于结扎幽门组及对照组,但血清胃泌素水平未见显著升高。短期DGR可引起胃窦黏膜胃小凹增生,没有肠上皮化生及胃黏膜萎缩等。短期DGR炎性细胞浸润不明显,没有导致组织MPO的水平改变,可引起黏膜细胞间的紧密连接受损。结论：DGR短期内可造成胃黏膜损害,表现为胃小凹增生、细胞间紧密连接受损,但炎性细胞浸润不明显,也不引起MPO活性的变化。     

模拟寒区冷暴露环境大鼠胃黏膜内皮素-1与缺氧诱导因子-1α的改变及冬胃颗粒对其影响

[目的]观察模拟寒区冷暴露环境下大鼠胃黏膜内皮素-1（ET-1）与缺氧诱导因子-1α（HIF-1α）改变及冬胃颗粒保护作用。[方法]健康雄性Wistar大鼠40只，随机分为4组：正常组、模型组、冬胃颗粒组、0．9％氯化钠溶液组，每组10只；正常组室温喂养，正常饮食，其他各组均以寒冷暴露法模拟寒区低温[（-10±2）℃]，处理5d，冬胃颗粒组在其过程中给予冬胃颗粒保护。5d后取各组大鼠胃黏膜以免疫组化方法检测其ET-1与HIF-1α表达。[结果]正常组未见异常；模型组及0．9％氯化钠溶液组大鼠冷暴露后出现寒战、蜷缩少动、尾部紫暗等症状，肉眼可见胃黏膜充血水肿与糜烂，光镜下可见有明显损伤；冬胃颗粒组仅表现有轻微的畏寒喜暖、少动等症状，肉眼与镜下仅可见胃黏膜轻微损伤。冬胃颗粒组胃黏膜ET-1与HIF-1α表达明显低于0．9％氯化钠溶液组与模型组，差异有统计学意义（P〈0．05）。[结论]冬胃颗粒可减轻冷暴露大鼠症状，减轻胃黏膜损伤，并使其胃黏膜ET-1与HIF-1α表达减弱。     

正加速度暴露下急性胃黏膜损伤胃组织中MDA、SOD水平的变化

目的:研究正加速度(+Gz)暴露下急性胃黏膜损伤胃组织中氧自由基代谢指标丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)的水平变化,阐明+Gz暴露对胃黏膜损伤的影响,并研究氧自由基在其中的作用,为飞行员胃肠病的防治提供理论依据.方法:30只♂SD大鼠随机分成以下3组:A组为无水乙醇对照组,B组为无水乙醇+5Gz值暴露组,C组为无水乙醇+10Gz值暴露组.每组大鼠各10只,适应性喂养10d后禁食24h,禁水12h,用无水乙醇(0.4mL/100mg)灌胃1h后,A组不受加速度作用,B、C组分别于+5Gz、+10Gz值下连续暴露3min.每组下离心机后立即予戊巴比妥麻醉取大鼠胃组织,观察各组胃黏膜损伤情况及光镜观察组织形态学的改变,按GUTH法及Whittle法计算胃黏膜损伤指数,并用ELISA法检测胃黏膜中MDA、SOD的含量.结果:(1)各组大鼠胃黏膜在肉眼及光镜下观察均有损伤,损伤程度:C组>B组>A组,A组(肉眼11.410±3.742,光镜3.800±1.399),B组肉眼可见胃黏膜充血、水肿,散在出血斑点,光镜下可见急性炎细胞浸润(肉眼23.654±9.678,光镜5.000±1.054),与A组相比差异有统计学意义(P<0.05);C组胃黏膜损伤最重,肉眼可见胃黏膜弥漫性充血、水肿,伴糜烂、大面积出血斑,光镜下可见大部分腺体结构紊乱,组织间质片状充血、糜烂,急性炎细胞浸润(肉眼49.080±10.254,光镜9.400±2.011),与A、B两组相比差异均有统计学意义(P<0.05);(2)与A组相比,B组胃黏膜中MDA含量升高不明显(0.255±0.074vs0.235±0.044),差异无统计学意义(P>0.05),C组胃黏膜中MDA含量明显升高(0.376±0.084vs0.235±0.044),与A、B两组相比差异均有统计学意义(P<0.05);与A组相比,B组胃黏膜中SOD含量下降不明显(10.000±1.067vs10.694±0.965),差异无统计学意义(P>0.05),C组胃黏膜中S O D含量明显下降(8.852±1.001vs10.694±0.965),与A、B两组相比差异均有统计学意义(P<0.05).结论:+Gz值暴露可加重急性胃黏膜损伤,胃组织中MDA、SOD的含量变化说明氧自由基在胃黏膜损伤中起到重要作用.     

寒凝血瘀型胃溃疡大鼠模型的建立及冬胃颗粒保护作用的观察

[目的]建立寒凝血瘀型胃溃疡（GU）大鼠模型,观察冬胃颗粒对其胃黏膜保护作用及胃黏膜微循环血流量与血液流变学的影响。[方法]雄性SD大鼠40只,随机分为4组,正常组,模型组,冬胃颗粒组,0.85%氯化钠组,每组10只。正常组,室温饲养,自由饮食,其余各组用改良寒冷暴露法建立寒凝血瘀型GU大鼠模型,其中冬胃颗粒组造模同时给予冬胃颗粒保护。5 d后观察各组大鼠的胃黏膜损伤指数并测定大鼠胃黏膜微循环血流量及血液流变学各项指标。[结果]正常组大鼠胃黏膜未见损伤,模型组大鼠出现寒战、蜷缩少动、爪尾部紫暗等症状,胃黏膜溃疡指数明显高于正常组,胃黏膜微循环血流量明显少于正常组,血液流变学指标亦较正常组升高,差异有统计学意义（P〈0.01）;冬胃颗粒组仅表现有轻微的畏寒喜暖、少动等症状,其胃黏膜损伤指数低于模型组及0.85%氯化钠组,差异有统计学意义（P〈0.01）,并具有较高的溃疡抑制率,其胃黏膜微循环血流量高于模型组与0.85%氯化钠组,血液流变学各项指标较后者低,差异有统计学意义（P〈0.01）。[结论]用改良寒冷暴露法建立的寒凝血瘀型GU大鼠模型,符合中医证候及GU＂病症结合＂的特点,冬胃颗粒可以保护寒凝血瘀型GU大鼠胃黏膜并改善黏膜微循环与血液流变学指标。     

青年人生理性十二指肠胃反流的相关因素

目的:探讨生理性十二指肠胃反流的反流特点,反流与胃黏膜组织学改变的关系.方法:选取20名青年健康志愿者,分别接受常规胃镜检查,24 h动态胃内pH和胆汁反流监测,HE染色行常规组织病理学检查以及改良Giemsa染色行幽门螺杆菌检查.结果:胃镜与胃黏膜组织检查多为正常黏膜或轻度浅表性炎症,仅2名胃镜下有胆汁反流,6名H pylori阳性.未见溃疡、糜烂、萎缩及肠化生.胆红素监测均有不同程度的十二指肠胃反流,abs>0.14的时间百分比为12.5%±8.8%,短时间反流频率62.8±36.0次、长时间反流频率5.9±3.8次、最长反流时间53.5.0±50.3min,其中立位反流时间显著性长于卧位(P=0.017).胃内pH>4的时间百分比为13.91%±10.1%,与胃内abs>0.14的时间百分比比较无相关性.结论:正常生理条件下均存在生理性十二指肠胃反流,不同个体、不同体位其反流程度不一,但这种反流不引起胃黏膜的病理性改变,也不引起胃内pH的变化.     

小剂量辣椒素对大鼠胃黏膜屏障的影响

目的:给予大鼠不同剂量、不同时期辣椒素(capsaicin,CAP),检测胃黏膜屏障、肝肾组织及血常规、血生化,探讨CAP对胃黏膜屏障的影响及肝肾脏器的安全性.方法:SD大鼠240只,随机分实验组与对照组,实验组分别给予0.1 mg/(kg·d)、1.0 mg/(kg·d)、5.0 mg/(kg·d)CAP饲料,分别于第1、7、14、28天检测血常规、血生化.处死大鼠检测胃黏膜屏障及肝肾组织.结果:各组大鼠状态均良好;大鼠体质量均增加,C组Ⅳ期体质量增加较缓慢,但与对照组D组相比无统计学意义.各组大鼠胃黏膜光滑,未见糜烂出血,Guth评分均为0分.HE染色光镜下观察实验组与对照组大鼠胃黏膜Masude评分无统计学差异(P0.05).血常规、血生化的检测:各实验组与对照组血常规、谷草转氨酶(aspartate transaminase,AST)、谷丙转氨酶(alanine transaminase,ALT)、血肌酐(crea,Cr)检测均无统计学差异.B组、C组血胆固醇(cholesterol,CHOL)及甘油三酯(triglyceride,TG)浓度在Ⅲ、Ⅳ期下降,与D组相比有统计学意义.各实验组大鼠肝肾组织HE染色均未见异常.结论:大鼠摄入CAP 0.1-5mg/(kg·d)饲料,1-28 d对胃黏膜屏障、肝肾组织无损伤,对大鼠血常规、AST、ALT、Cr均无影响.大鼠摄入CAP 1.0-5.0 mg/(kg·d)饲料14-28 d可以调节血脂代谢,降低血脂浓度.     

杏仁核外源性胃动素对大鼠胃运动的调节作用及机制

目的:观察双侧基底内侧杏仁核(BMA)内注射胃动素对大鼠胃运动的影响,并探讨胃动素作用的神经传导通路化测定等方法探讨胃动素作用的神经传导通路．方法:选用成年♂Wistar大鼠40只,进行买验1:双侧BMA注射胃动素(MT,1μg/侧)或生理盐水(NS,0．5μL/例),通过胃内球囊-压力换能器-二道生理记录仪观察胃内压(IGP)和胃运动频率(GMF)的改变(n=14);实验2:膈下迷走神经切断后重复实验1(n=12);实验3:BMA注射MT或NS后60 min,采用免疫荧光法观察下丘脑室旁核(PVN)c-Fos蛋白表达(n=7);实验4:放射免疫法测定正常大鼠各脑区胃动素含量(n=7)．结果:双侧BMA注射胃动素后,大鼠胃运动明显加强,给药10,15,20,25 min后,IGP变化百分率分别为19．7％±6．5％(P=0．023), 62．9％±4．7％(P<0．01),45．1％±7．9％(P<0．01), 29．3％±10．3％(P=0．029)．GMF在给药后15和20 min明显增加,其变化百分率分别为36．7％±8．5％(P<0．01)和19．5％±6．0％(P=0．015)．双侧BMA注射NS后IGP和GMF均未见明显改变．大鼠行膈下迷走神经切断后重复实验1．可观察到胃动素促进胃运动的效应完全被阻断(P>0．05)．双侧BMA注射MT后,PVN内c-Fos阳性细胞数较NS对照组明显增多(53．4±8．9 vs 22．5±5．2,P<0.01),c-Fos蛋白表达增强．正常大鼠下丘脑胃动素含量较高(74．3±19．6 mg／kg),其他脑区内胃动素含量为7．8±2．2→17．3±6．6 mg／kg．结论:基底内侧杏仁核外源性胃动素可加强大鼠胃运动,该效应可能通过杏仁核-下丘脑和脑干-迷走神经通路来完成．     

Effect of environmental hyperthermia on gastrin, somatostatin and motilin in rat ulcerated antral mucosa

AIM: To study the effect of environmental hyperthermia on gastrin, somatostatin and motilin in rat ulcerated antral mucosa.METHODS: Forty-two Wistar rats were equally divided into six groups, according to the room temperature (high and normal) and the treatment (acetic acid, normal saline and no treatment). Levels of gastrin, somatostatin and motilin in rat ulcerated antral mucosa were measured with a radioimmunoassay method.RESULTS: The average temperature and humidity were 32.5℃ and 66.7% for the high temperature group, and 21.1℃ and 49.3% for the normal temperature group,respectively. Gastric ulcer model was successfully induced in rat injected with 0.05 mL acetic acid into the antrum. In rats with gastric ulcers, the levels of gastrin and motilin increased, whereas the somatostatin level declined in antral mucosa, compared with those in rats treated with normal saline and the controls. However, the change extent in the levels of gastrin, motilin and somatostatin in antral mucosa was less in the high temperature group than in the normal temperature group.CONCLUSION: The levels of gastrin, somatostatin and motilin in rat ulcerated antral mucosal tissue remain relatively stable in a high temperature environment, which may relate to the equilibration of the dynamic system.     

十二指肠胃反流对大鼠胃黏膜细胞凋亡及相关细胞因子表达的影响

目的研究十二指肠胃反流(duodenogastric reflux,DGR)对大鼠胃黏膜细胞凋亡及相关细胞因子表达的影响,探讨DGR胃黏膜损伤机制。方法手术组成年SD大鼠10只用于制备和收集十二指肠混合液。DGR模型组和对照组各取SD大鼠8只,前者十二指肠液灌胃,后者生理盐水灌胃。2周后处死大鼠。采用TUNEL技术观察胃黏膜细胞凋亡情况。采用免疫组化方法分析胃黏膜组织TNF-α、ET-1和NOS-2的表达。结果 DGR模型大鼠胃黏膜病理提示造模成功。DGR模型组胃黏膜凋亡细胞在黏膜全层均可见,凋亡指数(AI)显著高于对照组(P<0.05)。DGR模型组大鼠胃黏膜细胞的TNF-α、ET-1和NOS-2的表达均明显高于对照组(P<0.05)。结论细胞凋亡与TNF-α、ET-1和NOS-2等细胞因子表达异常可能参与DGR胃黏膜损伤乃至细胞癌变的发病机制。     

胃溃灵对胃粘膜损伤大鼠胃粘膜分泌的影响

目的 :研究胃溃灵对乙酸引起胃粘膜损伤大鼠胃粘膜分泌的影响。方法 :将 5 0只 SD大鼠制成乙酸胃粘膜损伤模型 ,并随机将大鼠等分为 5组 ,次日起给每组大鼠分别灌服等量生理盐水、大、中、小剂量 ( 12 g/ kg、6g/kg、3 g/ kg)胃溃灵、雷尼替丁 ,10 d后处死大鼠 ,观察大鼠胃粘膜损伤程度。采用阿尔新蓝与胃液中糖蛋白结合的方法 ,分别测定大鼠胃内游离粘液量、胃壁粘液量。结果 :胃溃灵能明显提高大鼠胃内游离粘液、胃壁粘液的分泌量 ,能明显抑制乙酸对大鼠胃粘膜的损伤。结论 :胃粘液分泌量增加可加强对粘膜的屏障作用 ,这是胃溃灵保护胃粘膜损伤的机制之一。     

Vitamin C Concentration in Gastric juice before and after Anti-Helicobacter pylori Treatment

Objectives: To investigate the change of vitamin C concentration (ascorbic and debydroascorbic acid) in gastric juice after anti-Helicobacter pylori treatment, and to relate any observed change to gastric pH, inflammatory compromise of the gastric mucosa, plasma vitamin C concentration, and smoking habits. Methods: Plasma and gastric juice vitamin C, fasting gastric juice pH, gastric bistology, and smoking status were studied in 70 patients with H . pylori-associated gastritis before and after therapy. Results: Gastric juice ascorbic acid increased significantly after H. pylori clearance. For the most part, this change was confined to patients who experienced reduction of gastric pH. It was also related to improvement of the compromise of tbe gastric epithelium, reduction of the proportion of vitamin C composed by debydroascorbic acid, and increase of the gastric juice/plasma vitamin C concentration gradient. Smokers bad lower vitamin C concentrations in plasma and gastric juice before and after H. pylori clearance than nonsmokers. Conclusions: The findings are consistent with a causal association between H. pylori infection and low ascorbic acid levels in gastric juice, and support two mechanisms for this association: increased oxidation and a decreased secretion of ascorbic acid.     

Effects of collagen solution on the prevention of acute gastric mucosa injuryin rats

AIM To investigate the effects of collagen solution on the prevention of acute gastric mucosal injury inrestricted rats inflicted by cooling in low temperature (4℃),METHODS Thirty healthy Wistar rats were randomly divided into normal (N, n = 10),injury (I, n = 10)and prevention (P, n = 10) groups. The rats were fasted for 48 h but free access to water without restrictionand cooling in normal group, fasted for 48 h but free access to water with restriction of rats onto the fixationframe for cooling in 4℃ for 4 h, so to cause stress injury of gastric mucosal membrane in I group and fed with3 mL of collagen solution 30min before injury in P group in addition to the procedures in I grobp. Gastricmucosal potential difference, blood flow volume, content of nitrite (NO2-) and hydrogen ion concentration(H+ ) in gastric juice were determined under aneasthesia at 48 h after fast in N group and at 4 h after injuryin I and P groups to evaluate the degree of injury (injury index).RESULTS Gastric mucosal potential difference was 22.10±5.27 in N group and 11.46±5.25 in I groupwith obvious difference (P<0.01), but 16.98±4.84 in P group which was remarkably improved whencompared to that in I group. Gastric mucosal blood flow volume was 23.65±10.65 in I group and 57.20±11.75 in N group with evident difference (P<0.01), but 37.49±5.87 in P group with sound effects incontrast to that in I group (P<0.01). Gastric injury index was 18.40±8.35 in I group and 7.9±2.13 in Pgroup with significant difference (P<0.01). Hydrogenion concentration in gastric juice was 118.0±41.2mmol/L in N group, 186.9±74.7 mmol/L in I group and 96.4±57.2 mmol/L in P group with prominentdifference (P< 0.01 ) between those in I and P group. Gastric mucosal nitrite concentration was 1.15±0.46in N group, 0.69±0.15 in I group and 1.04±0.44 in P group with obvious differences between N and Igroups (P<0.01) and between I and P group (P<0.01).CONCLUSION Ischemic and hypoxic injury of gastric mucosal due to low blood perfusion during restrictionand cooling injury at 4℃ was supposed to be an important factor in inducing gastric mucosal stress injury. Butcollagen solution could maintain the integrity of gastric mucosal barrier, buffer gastric acid, promotethrombocytic agglutination and ameliorate direct injury to gastric mucosa caused by various factors.     

还原型谷胱甘肽对正加速度暴露下急性胃黏膜损伤大鼠胃黏膜的影响

目的研究还原型谷胱甘肽(GSH)对正加速度(+Gz)暴露下急性胃黏膜损伤大鼠胃黏膜的影响及可能机制。方法 40只雄性SD大鼠随机分成4组:无水乙醇对照组(A组)、+5 Gz值暴露组(B组)、+10 Gz值暴露组(C组)、GSH预处理组(D组),每组10只。D组适应性喂养7 d后,连续3 d腹腔注射GSH。4组均于10 d后禁食24 h,禁水12 h,用无水乙醇灌胃1 h后,A组不受+Gz作用,B组暴露于+5 Gz值3 min,C、D组暴露于+10 Gz值3 min,下离心机后观察各组胃黏膜损伤情况,并检测胃黏膜中丙二醛(MDA)、GSH的含量及谷胱甘肽过氧化物酶(GSH-Px)的活性。结果各组大鼠胃黏膜在肉眼观察均有损伤,损伤程度:+10Gz值暴露组+5 Gz值暴露组无水乙醇对照组GSH预处理组,B组与A组相比差异均有统计学意义(P均0.05),C组分别与A、B两组相比差异均有统计学意义(P0.05);D组胃黏膜损伤最轻,与C组相比差异有显著统计学意义(P0.01)。与A组相比,B组胃黏膜中MDA、GSH含量变化不明显,差异均无统计学意义(P均0.05),GSH-Px活性明显升高,差异有显著统计学意义(P0.01);与A、B两组相比,C组胃黏膜中MDA含量升高明显,GSH含量降低明显,GSH-Px活性明显降低,差异均有统计学意义(P0.05);与C组相比,D组胃黏膜MDA含量明显降低,GSH的含量明显升高,GSH-Px的活性明显升高,差异有统计学意义(P0.05)。结论 GSH对+Gz值暴露引起的急性胃黏膜损伤大鼠的胃黏膜有预防及保护作用,该作用可能是通过增加胃黏膜GSH的含量、GSH-Px的活性及抑制MDA的作用而实现的。     

Does Intragastric Nitrite Concentration Reflect Gastric Carcinogenesis in Japanese Helicobacter pylori-Infected Patients?

Established risk factors for gastric cancer include a diet high in nitrate or nitrite and low in vitamin C and the presence of achlorhydria or hypochlorhydria. The aim of this study was to investigate the relationship between intragastric nitrite concentration and atrophic change of the stomach or gastric carcinogenesis in Japanese Helicobacter pylori-infected patients. Gastric juice pH, nitrite, and total vitamin C concentrations in gastric juice, serum pepsinogen I and II concentrations, and specific Helicobacter pylori antibody were analyzed. Intragastric total vitamin C concentration was decreased by Helicobacter pylori infection of the gastric mucosa and with progression of the atrophic grade. There was a significant positive correlation between atrophic grade and intragastric nitrite concentration. In conclusion, the levels of nitrite in gastric juice play a causal role in the development of cancer in Helicobacter pylori-associated atrophic gastric mucosa.     

Mucosal lesions of the stomach in liver cirrhosis with a special reference to phospholipid metabolism

Gastric mucosal lesions are an inevitable complication in patients with liver cirrhosis. Their etiology, however, is as yet unknown. The present study investigated phospholipid metabolism in the gastric mucosa of rats with cirrhosis induced by carbon tetrachloride. Gastric mucosal lesions were induced by taurocholic acid (TCA) which was given through a gastric tube. Levels of phospholipids, phosphatidylcholine, and disaturated-phosphatidylcholine were found to be markedly reduced at the mucosal surface in the cirrhotic rats, and they were increased in the gastric juice. Metabolism of phospholipids in the gastric mucosa was visualized by 3H-choline autoradiography and the rate of phospholipid metabolism was found to be reduced. These results strongly suggest that mucosal lesions induced by bile regurgitation into the stomach are due to disturbance of phospholipid metabolism in the gastric mucosa.     

Mucosal lesions of the stomach in liver cirrhosis with a special reference to phospholipid metabolism

Gastric mucosal lesions are an inevitable complication in patients with liver cirrhosis. Their etiology, however, is as yet unknown. The present study investigated phospholipid metabolism in the gastric mucosa of rats with cirrhosis induced by carbon tetrachloride. Gastric mucosal lesions were induced by taurocholic acid (TCA) which was given through a gastric tube. Levels of phospholipids, phosphatidylcholine, and disaturated-phosphatidylcholine were found to be markedly reduced at the mucosal surface in the cirrhotic rats, and they were increased in the gastric juice. Metabolism of phospholipids in the gastric mucosa was visualized by³H-choline autoradiography and the rate of phospholipid metabolism was found to be reduced. These results strongly suggest that mucosal lesions induced by bile regurgitation into the stomach are due to disturbance of phospholipid metabolism in the gastric mucosa.