胃炎灵对大鼠胃粘膜保护作用的研究

目的 :探讨胃炎灵对实验大鼠胃粘膜损伤的保护作用及可能机制。方法 :在无水乙醇形成大鼠胃粘膜损伤模型后 ,应用中药胃炎灵治疗并观察胃粘膜病理变化、炎症程度、溃疡指数 (UI)及溃疡面积 ,并检测胃粘膜氨基乙糖及前列腺素 E2 (PGE2 )含量。结果 :治疗组胃粘膜充血、水肿、坏死、炎症程度、UI及溃疡面积较对照组明显减少 (P<0 .0 5 ) ,两组胃粘膜氨基乙糖及 PGE2 对照差异亦有显著性意义 (P<0 .0 5 )。结论 :胃炎灵对胃粘膜有良好的细胞保护作用 ,其机制可能为该药抑制炎症反应 ,提高氨基乙糖含量 ,增加 PGE2 的合成。     

成纤维细胞生长因子与硫糖铝对大鼠实验性胃溃疡的治疗作用

目的　观察碱性成纤维细胞生长因子(bFGF)和硫糖铝联合治疗大鼠实验性胃溃疡的疗效。方法　取32只Sprage Dawley雌性大鼠,平均分为4 组。用bFGF 100 ng·100 g-1·d-1、硫糖铝40 mg·100g-1·d-1、bFGF 100 ng+硫糖铝40 mg·100g-1·d-1、生理盐水1 ml·100 g-1·d-1,分别等容灌胃治疗乙酸诱发的大鼠胃溃疡21 d,观测各组溃疡愈合情况及溃疡周围组织毛细血管增生情况,检测各组胃酸、胃蛋白酶含量。结果　bFGF组对胃酸、胃蛋白酶分泌的影响与生理盐水组相比无差异。bFGF组和硫糖铝组溃疡面积分别为(2.9±0.8) mm2、(3.2±1.1) mm2,明显小于生理盐水组(6.8±1.4) mm2(P<0.05), bFGF+硫糖铝组溃疡面积(2. 0 ±1.1) mm2,小于bFGF组和硫糖铝组(P<0.05)。bFGF组和bFGF+硫糖铝组溃疡边缘组织中毛细血管数分别为(19.7±3.0)、(21.9±4.5)条/每视野,明显多于硫糖铝组(12.2±2.2)条/每视野,生理盐水组(7.0±2.1)条/每视野(P<0.05)。结论　bFGF在不影响胃酸胃蛋白酶分泌情况下明显加速乙酸诱发大鼠胃溃疡的愈合,bFGF+硫糖铝效果更好。bFGF和bFGF+硫糖铝均能明显促进大鼠溃疡周围组织毛细血管增生。     

Response of blood endothelin-1 and nitric oxide activity in duodenal ulcer patients undergoing Helicobacter pylori eradication

AIM: To investigate the effect of Helicobacter pylori eradication on endothelin-1 (ET-1) and nitric oxide (NO) in duodenal ulcer (DU) patients. METHODS: Sixty-six Hpylori-infected active DU patients were consecutively enrolled to receive one-week triple therapy (rabeprazole, amoxicillin and metronidazole) and then one-month rabeprazole therapy. They were asked back to determine ulcer and Hpylori status using endoscopy one month later. Thirty-seven healthy controls (H pylori +/-:17/20) were enrolled for comparison. Blood samples were collected in each visit to measure plasma ET-1 and nitrate/nitrite levels using an enzyme immunoassay kit. RESULTS: Sixty DU patients finished trial per protocol. The ulcer healing and Hpylori-eradication rates were 86.7% and 83.3%, respectively. Plasma ET-1 level in DU patients was higher than that of Hpylori-negative and positive controls (3.59±0.96 vs0.89±0.54 vs0.3±0.2 pg/mL,P<0.01), while nitrate/nitrite levels among them were also significantly different (8.55±0.71 vs5.27±0.68 vs 6.39±0.92 μmol/L, P<0.05). H pylori eradication diminished ET-1 levels (3.64±0.55 vs2.64±0.55 pg/mL, P<0.01) but elevated nitrate/ nitrite level (8.16±0.84 vs11.41±1.42 umol/L,P<0.05). CONCLUSION: Both plasma ET-1 and nitrate/nitrite levels increase in active DU patients. After an effective H pylori eradication, DU healing is associated with diminished blood ET-1 level and elevated nitrate/nitrite level.     

根除幽门螺杆菌对消化性溃疡合并胃炎及胃泌素的影响

目的 :评估胃舒散联合呋喃唑酮、阿莫西林对消化性溃疡 (PU)患者Hp根除的效果及其对溃疡合并胃炎、血清胃泌素(Gas)的影响。方法 :77例Hp阳性十二指肠溃疡组 (DU ,52例 )和胃溃疡组 (GU ,2 5例 )患者 ,均服用胃舒散 2 .0g(含铋 0 .1 2g) ,呋喃唑酮0 .1g,阿莫西林 0 .5g ,各 3次 /d ,2周后再继服胃舒散 4周。治疗前及疗程结束 1月后进行内镜检查并对胃窦、胃体胃炎予以内镜下评分。采用放射免疫法于治疗前及结束 1月、6月后检测胃泌素水平。结果 :DU组与GU组溃疡愈合率分别为 1 0 0 %和 92 % ,Hp根除率分别为 90 .3 %和 84.0 % ,二组比较差异均无显著性 (P >0 .0 5)。将根除Hp的 47例DU和 2 1例GU患者分为 2组 ,治疗前 2组胃窦胃炎的评分差异无显著性 (P >0 .0 5) ;GU组胃体胃炎的评分显著高于DU组 (P <0 .0 0 1 ) ;血浆中胃泌素含量 (DU组 39.4± 1 3 .6pg/ml;GU组38.4± 1 2 .3pg/ml)均显著高于正常对照值 (2 8.5± 1 0 .6pg/ml,P <0 .0 5)。Hp根除 1月后 ,2组患者胃窦胃炎与胃体胃炎的评分均显著下降 ,与治疗前自身比较 ,差异有统计学意义 (均P <0 .0 0 1 )。DU组Hp根除治疗 1月后 ,胃泌素水平显著下降到 32 .7± 1 0 .5pg/ml (P <0 .0 5)。GU组Hp根除 1月后 ,胃泌素水平有所下降 ,但与治疗前相比 ,差     

陈旧性心肌梗塞病人血浆心钠素含量分析

我们测定了43例陈旧性心肌梗塞(OMI)病人和对照组28例的血浆心钠素(ANF)含量变化,分别为32.2.36±46.46 pg/ml、230.26±29.84pg/ml(P>0.05);心功能Ⅲ级者为633.46±163.57pg/ml,较对照组显著升高(P<0.01);左房扩大组和双房扩大组分别为414.49±64.93pg/ml、566.94±262.89pg/ml比心房正常组159.70±15.28pg/ml显著升高(P<0.01);血压升高组比血压正常组明显升高,分别为371.25±73.47 pg/ml、192.75±19.55 pg/ml(P<0.05)。结果表明OMI患者血浆ANF升高,提示该病人可能合并心功能不全,心房扩大或高血压。     

持续正加速度对实验性大鼠胃溃疡愈合质量的影响

目的:探讨正加速度(+Gz)对消化性溃疡模型大鼠的溃疡愈合的影响及其机制.方法:将32只♂SD大鼠随机分为对照组、+5Gz组、+10Gz组、和+10Gz+康复新液组,每组8只.采用乙酸烧灼法建立大鼠胃溃疡模型,造模后3d加速度隔日处理1wk,每次持续5min,共4次.+10Gz+康复新液组同时予以康复新液2mL灌胃1wk,1wk后取其组织及血液标本.运用放射免疫法检测胃黏膜前列腺素E2(prostaglanding E2,PGE2)、血清降钙素基因相关肽(calcitonin gene-related peptide,CGRP),运用硝酸还原酶法检测血清一氧化氮(nitric oxide,NO).结果:随+Gz值增高,光镜下再生黏膜厚度变薄,扩张腺体数目增多.大鼠胃黏膜PGE2含量对照组为6.986pg/mL±0.743pg/mL,+5Gz组为5.147pg/mL±0.652pg/mL,+10Gz组为3.438pg/mL±0.908pg/mL,+10Gz+康复新液组为6.133pg/mL±0.545pg/mL.+10Gz组较+5Gz组和对照组低(P<0.01),并且低于+10Gz+康复新液组(P<0.01).大鼠血清(CGRP)含量对照组为82.583pg/mL±11.788pg/mL,+5Gz组为78.333pg/mL±11.290pg/mL,+10Gz组为62.254pg/mL±15.943pg/mL,+10Gz+康复新液组为78.455pg/mL±12.645pg/mL.+10Gz组较+5Gz组和对照组低(P<0.05),并且较+10Gz+康复新液组低(t=-2.252,P<0.05).大鼠血清NO含量对照组为53.806mol/L±9.272mol/L,+5Gz组为47.783mol/L±2.847mol/L,+10Gz组为44.773mol/L±6.858mol/L,+10Gz+康复新液组为53.853mol/L±7.372mol/L.+10Gz组较+5Gz组和对照组低(P<0.05),并且较+10Gz+康复新液组低(t=-2.551,P<0.05).结论:+Gz条件下,溃疡愈合延迟;康复新液灌胃可减轻胃黏膜的损伤,促进溃疡愈合.     

消化性溃疡患者转化生长因子α、表皮生长因子和前列腺素E_2的关系

目的:研究转化生长因子α(TGFα)在慢性胃粘膜病变患者血液、胃液中的含量变化及其与表皮生长因子(EGF)和前列腺素E_2(PGE_2)的关系,初步探讨TGFα在胃粘膜病变发病过程中的作用。 方法:选择经胃镜和病理组织学检查证实的活动期消化性溃疡(PU)患者44例,其中十二指肠球溃疡(DU)22例,胃溃疡(GU)22例;慢性浅表性胃炎(CSG)患者18例;另选择20例胃镜观察胃粘膜基本正常者作为对照组。胃镜下经活检孔抽取胃液,并采集空腹静脉血,用放免分析法检测胃液、血液中TGFα,EGF,PGE_2的含量。 结果:GU和DU两组的血清TGFα(ng·L~(-1)),EGF(ug·L~(-1))含量均明显低于对照组和CSG组(3.5±1.1,3.4±1.3 vs (5.9±1.6.5.0±1.7,p<0.01;0.3±0.1,0.3±0.1 vs 0.6±0.2,0.5±0.2 p<0.01)。GU和DU血浆PGE_2(ng·L~(-1))含量与对照组和CSG组相比,差异无显著性(24.7±8.4,26.0±8.7 vs 25.2±8.0,20.9±7.7,p<0.05).GU,DU和CSG三组胃液中TGFα(ng·L~(-1)),EGF(ng·L~(-1)),PGE_2(ng·L~(-1))含量均明显低于对照组(1.7±0.7,1.6±0.7,2.1±0.7 vs 2.7±0.8,p<0.05;109±47.121±67.113±48 vs 373±78,p<0.01;15.8±6.6, 14.1±7.3,16.4±6.9 vs 21.9±7.5,p<0.05)。GU组胃液中TGFα与PGE_2间存在直线正相关(r=0.55,p<0.05),GU组     

功能性消化不良昼夜胃内PH变化

本研究应用pH监测系统探讨功能性消化不良(FD,n=12)患者昼夜胃内pH变化,并以健康组(HT,n=9)和十二指肠溃疡(DU,n=10)作为对照。结果表明FD组白天和夜间胃内pH<1的时间分别为27.8±7.0％和12.9±4.4％,与HT组的差别不大(11.4±5.6％,P>0.05,8.3±3.2％,P>0.05),但明显低于DU组(48.8±5.9％,P<0.01,58.5±7.2％,P<0.01);FD组白天胃内pH>3的时间与HT组相近(分别为33.9±7.5％,34.5±8.0％,P>0.05),大于DU组(20.7±3.9％,P<0.01)。33.3％的FD者餐后pH值不上升,高于HT组(7.4％,P<0.05)和DU组(3.3％,P<0.05),FD组夜间pH>4的总时间、所占的％和最长持续时间分别为223.6±45.9min、46.5％和164±41.5min,大于HT组但差别不大(169.7±40.2min、32±6.8％和105.0±22.6min,P值均<0.05),明显大于DU组(57.6±12.0min、10.4±4.3％和44.1±10.0min,P值均<0.05)。本研究表明FD患者并无高酸分泌,因而对FD患者应寻找更合适的治疗。FD患者夜间pH值>4的时间明显延长,提示可能存在十二指肠胃反流,但应作进一步研究。     

潘妥洛克与奥美拉唑治疗十二指肠溃疡的疗效比较

目的:了解潘妥洛克治疗十二指肠溃疡(DU)的疗效和安全性。方法:DU 病人随机分到潘妥洛克组(41例)与奥美拉唑组(41例),分别服相应药物40mg 或20mg,qd,2周。治疗前后行内镜检查和症状评估。结果:潘妥洛克组与奥美拉唑组治疗2周后的:总愈合率分别为75.6%和68.3%,两组总有效率为97.6%与100%,两组间无显著性差异(P>0.05),两组腹痛消失时间(3.1±1.5比3.2±1.6d)无显著差别。结论:2周常规剂量,潘妥洛克愈合溃疡和缓解症状。     

冠心病患者血浆神经肽Y水平的临床观察

选择符合WHO诊断标准的急性心肌梗塞(AMI)21例,心绞痛(AP)19例,应用放射免疫法动态观察血浆神经肽Y(NPY)含量变化,并以21例正常人作对照.结果显示:对照组NPY水平为 75.1±30.4Pg/ml,AMI组发病第1天NPY含量达峰值,为136.7±66.5pg/ml,显著高于正常组(P<0.05).发病第3天开始下降,第1周末趋于正常,为77.4±48.4pg/ml,与正常组比较无显著差异.AP组于心绞痛发作期NPY含量为159.3±98.5pg/ml,亦显著高于对照组(P<0.05);经治疗2周症状缓解后复查血浆NPY含量下降至118.9±54.3pg/ml,前后比较有显著差异(P<0.05).冠心病伴高血压者血浆NPY含量为186.9±103.1Pg/ml,显著高于不伴高血压者(111.7±45.5pg/ml,P<0.01);既往有吸烟史的冠心病患者,血浆NPY含量为181.8±193.1pg/ml,显著高于无吸烟史者(122.0±65.6pg/ml,P<0.05).提示:NPY水平在冠心病发病初期显著升高,其升高可能由于心肌缺血急性期交感神经兴奋性提高、释放活性增强所致,而高血压及吸烟可能也产生对NPY释放的影响.NPY参与了冠心病的发病机理及病理生理过程.     

Duodenal ulcer in China

The author visited China in 1981 and 1984 and obtained data comparing the incidence of duodenal ulcer in the rice eating districts of the south with the incidence in the wheat, maize and millet eating areas of the north. The evidence suggested a higher prevalence of duodenal ulcer in the rice eating areas than in the wheat eating areas, and a low prevalence in association with millet eating. However, the differences were less marked than between similar rice and wheat eating areas of India. It is suggested that the lower prevalence of duodenal ulcer in the wheat eating areas of north India compared with the rice eating areas of south India may be due in part to the mucosal protective effect of wheat bran in the unrefined wheat that is used in making chappatis. In China white refined flour is used in the making of steamed bread with the loss of any protective effect of wheat bran.     

嗜酸乳杆菌合生元对非甾体抗炎药引起的大鼠胃黏膜损伤的保护作用

背景：非甾体抗炎药（NSAID）引起的胃黏膜损伤已成为目前最常见的药物相关并发症，防治NSAID引起的胃黏膜损伤是重要的研究课题。目的：研究由嗜酸乳杆菌和低聚异麦芽糖配制成的合生元对NSAID引起的大鼠胃黏膜损伤的保护作用。方法：将80只Sprague—Dawley大鼠随机分为高、中、低剂量实验组、模型对照组和正常对照组。实验组分别给予不同剂量的嗜酸乳杆菌合生元灌胃30天，模型对照组以0．9％NaCl溶液灌胃。30天后以吲哚美辛诱导大鼠胃黏膜损伤，检测各组大鼠的胃黏膜溃疡指数（UI）和组织病理学变化。结果：不同剂量实验组大鼠的胃黏膜损伤情况均明显轻于模型对照组，黏膜充血程度减轻，UI显著减低（P〈0．05），组织病理学表现明显改善。结论：嗜酸乳杆菌合生元对胃黏膜具有一定保护作用，可减轻NSAID引起的大鼠胃黏膜损伤。     

Effect of oral epidermal growth factor on mucosal healing in rats with duodenal ulcer

AIM: To investigate the effect of epidermal growth factor (EGF) on mucosal healing in rats with duodenal ulcer.METHODS: Male Sprague-Dawley rats were randomly divided into sham operation without EGF, sham operation with EGF, duodenal ulcer without EGF, or duodenal ulcer with EGF groups. Additionally, normal rats without operation served as the control group. Duodenal ulcer was induced in rats by 300 mL/L acetic acid. Rats with EGF were orally administered at a dose of 60 μg/kg/day in drinking water on the next day of operation (day 1). Healing of duodenal ulcer was detected by haematoxylin and eosin staining. Cell growth of damaged mucosa was determined by the contents of nucleic acids and proteins. The level of EGF in duodenal mucosa was measured by ELISA.RESULTS: The pathological results showed that duodenal ulcer rats with EGF improved mucosal healing compared with those without EGF after day 5. Duodenal ulcer rats with EGF significantly increased duodenal DNA content compared with those without EGF on day 15 (6.44±0.54mg/g VS 1.45±0.52 mg/g mucosa, P＜0.05). Duodenal RNA and protein contents did not differ between duodenal ulcer rats with and without EGF during the experimental period.Sham operation and duodenal ulcer rats with EGF significantly increased duodenal mucosal EGF content compared with those without EGF on day 5 (76.0±13.7 ng/g VS 35.7±12.9ng/g mucosa in sham operation rats, and 68.3±10.9 ng/gVS 28.3±9.2 ng/g mucosa in duodenal ulcer rats, P＜0.05).CONCLUSION: Oral EGF can promote mucosal healing of the rats with duodenal ulcer by stimulating mucosal proliferation accompanied by an increase in mucosal EGF content.     

Effect of cell proliferation on healing of gastric and duodenal ulcers in rats

The healing of acetic acid-induced gastric and duodenal ulcers was examined together with the biochemical indices of growth in gastric and duodenal mucosa in the following three groups of rats: (a) chow-fed, (b) fed an isocaloric liquid diet, (c) fed the liquid diet plus pentagastrin injections (250 micrograms/kg, 3 times/day). Animals received the diet regimen for 10 days from 1 day after induction of ulcer (day 0). Following the feeding regimens, serum gastrin levels, oxyntic gland mucosal DNA synthesis, and gastric secretory function were significantly lowered in the rats fed liquid diets. DNA synthesis in the duodenal mucosa was not different from the pre-ulcer levels. Pentagastrin significantly restored the DNA synthetic and gastric secretory activity of the liquid diet-fed rats toward the levels in the chow-fed group. In the latter group, a significant increase in DNA synthesis and levels of serum gastrin was found at day 6 (after 5 days feeding), which corresponded with a rapid, spontaneous healing of ulcers. Feeding rats liquid diet significantly delayed the healing of gastric, but not duodenal ulcers. Repeated administration of pentagastrin accelerated gastric ulcer healing in the liquid diet group toward the rate observed in the chow-fed group, but had no effect on the healing of duodenal ulcers. These results indicate that cell proliferation is an important factor in the healing of gastric ulcers.     

Enzyme Immunoassay of Gastric Luminal Prostaglandin E2 in Duodenal Ulcer Disease

A highly sensitive enzyme immunoassay was used to determine gastric juice prostaglandin E2 (PGE2) levels in control subjects with or without gastritis and in both active or inactive duodenal ulcer patients. Mean pentagastrin-stimulated PGE2 concentration was significantly lower in patients with duodenal ulcer than in control subjects considered as a whole group (with or without gastritis). However, no such difference was found between duodenal ulcer patients and controls showing histologically normal gastric mucosa. On the other hand, controls with chronic superficial gastritis had PGE2 levels significantly higher than those of histologically normal subjects and duodenal ulcer patients. Therefore, it seems unlikely that an absolute gastric PGE2 deficiency is involved in the pathogenesis of duodenal ulcer disease. However, the possibility that PGE2 synthesis could be deficient in relation to the prevailing level of mucosal inflammation cannot be excluded.     

Influence of gender difference and gastritis on gastric ulcer formation in rats

BACKGROUND: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. METHODS: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E(2) (PGE(2)) level were also determined. RESULTS: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE(2) level was higher in female rats with acute gastritis. Both mucus and PGE(2) were increased during ulcer healing in both genders. CONCLUSIONS: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE(2) not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach.     

Duodenal and antral mucosal prostaglandin E2 synthesis in a study of normal subjects and all stages of duodenal ulcer disease treated by H2 receptor antagonists.

We tested the hypothesis that the production of prostaglandin E2 (PGE2) is impaired in duodenal ulcer disease and affected by treatment and healing. This was investigated by a study of maximal PGE2 synthesis rates in duodenal and antral mucosal biopsies obtained at endoscopy. The patients were divided into three groups. Group (a): endoscopically normal controls (n = 56); group (b): treatment controls (non-DU disease: gastric ulcer or oesophagitis treated by histamine H2 receptor antagonists) (n = 41); and group (c): patients with DU disease (n = 183) further subdivided into group (c1) active ulcer not on treatment (n = 47), (c2) treated active ulcer (n = 35), (c3) healed ulcer on treatment (n = 86), and (c4) healed ulcer not on treatment (n = 15). Group (a) synthesised (mean (SD] 106.6 (39.0) pg PGE2/mg wt of tissue from the duodenal bulb and 129.9 (56.9) from the second part of the duodenum. No difference was found between group (a) and (b) at either site. Group (c1) ulcer rim made 49.8 (22.7) and at all stages ulcer rim and scar made less than the control duodenal bulb (p less than 0.02). Uninvolved duodenal bulb form groups (c1) (63.4 (31.0], (c2) (83.6 (38.5], and (c3) (81.5 (31.1], however, also made significantly less than controls (p less than 0.02) and a similar though non-significant trend was seen in group (c4). Biopsies from the second part of the duodenum did not synthesise significantly less than the control group but a similar trend was noticed at each stage of ulcer treatment. Biopsies of control antrum synthesised 124.5 (32.2) but only 93.7 (44.2) in group (cl) (p < 0.005). All stages of duodenal ulcer healing were associated with a decreased capacity to synthesise the major prostaglandin PGE2 at the ulcer site and the uninvolved duodenal bulb and, in acute untreated duodenal ulcer, the uninvolved antrum. This decreased capacity may be the consequence of the disease process itself and not secondary to the treatment, indicating a basic pathophysiological abnormality which may explain the characteristic tendency of the disease to relapse.     

Dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress in rats

AIM: To investigate the dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress (WRS) in rats. METHODS: WRS model of Sprague-Dawley (SD) rats was established. Fifty-six male SD rats were randomly divided into control group, stress group and post-stress group. The stress group was divided into 1, 2 and 4 h stress subgroups. The post-stress group was divided into 24, 48 and 72 h subgroups. The pH value of gastric juice, ulcer index (UI) of gastric mucosa and H , K -ATPase activity of gastric parietal cells were measured. Ultrastructural change of parietal cells was observed under transmission electron microscope (TEM). RESULTS: The pH value of gastric juice decreased time-dependently in stress group and increased in post-stress group. The H , K -ATPase activity of gastric parietal cells and the UI of gastric mucosa increased time-dependently in stress group and decreased in post-stress group. Compared to control group, the pH value decreased remarkably (P = 0.0001), the UI and H , K -ATPase activity increased significantly (P = 0.0001, P = 0.0174) in 4 h stress subgroup. UI was positively related with stress time (r = 0.9876, P < 0.01) but negatively with pH value (r = -0.8724, P < 0.05). The parietal cells became active in stress group, especially in 4 h stress subgroup, in which plenty of intracellular canalicular and mitochondria were observed under TEM. In post-stress group, the parietal cells recovered to resting state. CONCOUSION: The acid secretion of parietal cells is consistent with their ultrastructural changes during the development and healing of stress ulcer induced by WRS and the degree of gastric mucosal lesions, suggesting gastric acid play an important role in the development of stress ulcer and is closely related with the recovery of gastric mucosal lesions induced by WRS.     

Simultaneous measurement of in vitro gastroduodenal prostaglandin E2 synthesis and degradation in peptic ulcer disease

The ability of mucosal specimens from the stomach and duodenum to synthesize and degrade prostaglandin E2 has been determined in normal subjects and peptic ulcer patients. Significant reduction in fundic PGE2 synthesis capacity was observed in gastric ulcer patients. There was also significant reduction in the PGE2 degradation capacity of antral, fundic, and duodenal mucosal specimens in gastric ulcer patients. Patients with gastritis showed significant elevation of both antral and fundic PGE2 synthesis capacity compared with normal but no alteration in PGE2 degradation. No differences were observed in PGE2 synthesis and degradation rates in patients with duodenal ulcer. The results argue in favour of an association between impairment of PGE2 metabolism in the mucosa of patients with gastric but not duodenal ulceration.