丹参对大鼠乙醇性胃粘膜损伤的保护作用的研究

应用９０只ＳＤ大鼠研究丹参对大鼠乙醇性急性胃粘膜损伤、胃壁结合粘液含量、胃排空运动的影响，以及消炎痛、外源性ＰＧＥ１与这一影响的关系，初步探讨了丹参胃粘膜保护作用的机理。结果表明：丹参水溶液参减轻大鼠惭醇性急性胃粘膜损伤，促进胃壁结合粘液分泌，消炎痛可部分削弱这二个作用，给予外源性ＰＧＥ１可反转消炎痛的抑制作用。提示丹参的保护作用及其促进胃壁结合粘液分泌增加，可能部分是由其刺激内源性前列腺素合成和     

正常胃粘膜屏障血型抗原的表达及其生物学意义

首次应用国产单克隆抗体、ABC法,检测国人胎儿、成人正常胃组织石蜡切片A、B、H、M和N血型抗原(BGA)的定位,结合粘液组化AB(pH 2.5)/PAS染色,判断粘液分泌性质。结果表明:胎儿胃粘膜表面和小凹上皮大部分由粘液细胞组成,BGA表达阳性,分泌混合型粘液;成人胃粘膜表面和小凹上皮完全由粘液细胞组成,BGA表达可分为分泌性(A、B、H)和非分泌性(M、N、A、B)抗原;胃粘液中分泌性抗原主要由表面和小凹上皮粘液细胞分泌。提出BGA为胃粘膜屏障的重要组成,为进一步研究胃疾病提供正常形态学和免疫遗传学对照资料。     

Effect of <Emphasis Type="Italic">Cannabis sativa</Emphasis> extract on gastric acid secretion,oxidative stress and gastric mucosal integrity in rats

Studies were conducted in pylorus-ligated rats to investigate the effect of Cannabis sativa extract on gastric acid secretion, experimental gastric ulcer and on oxidative stress and inflammatory markers in the gastric mucosa. C. sativa (5, 10 and 20 mg/kg, expressed as Δ⁹-tetrahydrocannabinol) was administered subcutaneously daily for 4 weeks prior to pylorus ligation and different treatments. Under basal conditions, pretreatment with cannabis extract at doses of 5 and 10 mg/kg increased gastric acid secretion and induced minimally visible gastric mucosal lesions in the 4 h pylorus-ligated rat. Malondialdehyde and nitric acid concentration increased, while reduced glutathione decreased by cannabis at doses of 5 and 10 mg/kg in gastric mucosa. TNF-α increased by cannabis extract at doses of 5 and 10 mg/kg but decreased following the high dose of 20 mg/kg. On the other hand, the gastric acid secretory responses stimulated by pentagastrin or carbachol (but not histamine) were inhibited in rats pretreated with cannabis extract. Under these conditions, cannabis decreased pepsin content after pentagastrin and carbachol but not histamine stimulation. Cannabis also decreased lipid peroxidation and nitric oxide content, and increased both reduced glutathione and catalase activity in mucosa. Moreover, cannabis decreased mucosal inflammation (level of TNF-α) and the development of gastric mucosal lesions. Cannabis administered for 1 month prior to pylorus-ligation and either acidified aspirin or ethanol (96 %) decreased the development of gastric mucosal damage in a dose-dependent manner, along with reduction in gastric acid output, gastric mucosal oxidative stress and inflammation (TNF-α). Sections of gastric mucosa stained with periodic acid Schiff showed increased mucus secretion by cannabis in basal conditions and after treatment with aspirin or ethanol. Results indicate that: (1) the effect of cannabis differs in basal conditions and after exposure of the gastric mucosa to high acid concentrations or other chemical noxious agents; (2) cannabis administered systemically exerts gastric mucosal protective effects against mucosal damage evoked by stimulation of gastric acid secretion, acidified aspirin or ethanol. These effects of cannabis are likely to involve inhibition of gastric acid and pepsin secretion, increased mucus, decreased oxidative stress and inflammation in gastric mucosa.     

下颔下腺切除对大鼠胃粘膜影响的组织学和组织化学观察

用组织学和组织化学方法，观察了下颌下腺切除对大鼠胃粘膜结构和代谢活动的影响。结果显示，下颌下腺切除术后１０ｄ，胃体和胃窦粘膜均明显薄于对照组（Ｐ＜０．０１）（分别减少１６．６３％和１９．７７％）；壁细胞数量无明显变化。术后１０～２８ｄ，胃粘膜酸性粘液物质有所减少。术后４～２８ｄ，胃粘膜表面粘液细胞和膝上皮细胞Ｆｅｕｌｇｅｎ染色均减弱。术后２～１０ｄ，壁细胞内ＳＤＨ活性增强，至术后２１ｄ恢复正常。术后２ｄ，胃粘膜毛细血管内皮细胞Ｍｇ＋＋－ＡＴＰａｓｅ活性略增强；术后１０～２８ｄ，活性略减弱。胃粘膜表面粘液细胞和晚上皮细胞ＡｃＰ活性在术后４～２１ｄ增强，术后２８ｄ恢复正常。本实验结果提示，下颌下腺的某些生物活性物质是维持胃粘膜正常结构和代谢活动的必需因素，其中表皮生长因子或许更为重要。宁夏医学院组织学胚胎学教研室     

Nitric oxide synthase activity in rat gastric mucosa contributes to mucin synthesis elicited by calcitonin gene-related peptide

The majority of research for the calcitonin gene-related peptide (CGRP) in the stomach has been devoted to the submucosal blood flow, and only slight attention has been paid to its involvement in the gastric epithelial function. In this study, we examined the age-related change in the CGRP-containing nerves and its effects on the mucus metabolism. We compared the immunoreactivity for CGRP in the gastric mucosa of 7-week-old rats (young) to that of 52-week-old animals (middle-aged). The effects of CGRP on the mucin biosynthesis were compared using the stomachs from both young and middle-aged rats. The nitric oxide synthase (NOS) activity was measured in the surface and deep mucosa of the gastric corpus. The density of the CGRP nerve fibers was reduced in both the lamina propria and submucosa of the middle-aged rats compared to the young rats. CGRP stimulated the mucin biosynthesis in the cultured corpus mucosa from the 7-week-old rats, but not from the 52-week-old rats. The total NOS activity of the surface layer in the corpus mucosa was markedly reduced in the middle-aged rats compared to the young rats. These findings demonstrate the age-dependent reduction in the CGRP-induced mucin biosynthesis, as well as in the density of the CGRP fibers in the rat stomach. The decreased NOS activity in the surface layer of the oxyntic mucosa in the aged rats may also be a principal cause for the lack of regulation of the mucin biosynthesis by CGRP.     

Ciliated Cells in the Human Gastric Mucosa Evidence of Metaplastic Change

In the gastric mucosa of Japanese patients, ciliated cells were found in association with intestinal metaplasia. The cells occurred frequently in the pyloric mucosa of nearly half of the cases examined but rarely in the cardiac mucosa of total 12 cases, but never adjacent to the chief cells of gastric glands. The ciliated cells were always found in the basal part of cardiac and pyloric glands, but never in the surface or in the foveolar epithelium. Furthermore, ciliated cells containing a few small mucus granules and simultaneously possessing numerous cilia and basal bodies were noted. Ciliated cells in the gastric mucosa have been found mainly in elderly Japanese patients, but were also observed exceptionally in one Chinese, two Swedes and one American. These ciliated cells are not present in the normal human gastric and intestinal mucosa, and therefore a new term, "ciliated metaplasia", is proposed for their occurrence. Acta Pathol Jpn 40: 98–106, 1990.     

Different effects of two types of H2-receptor antagonists, famotidine and roxatidine, on the mucus barrier of rat gastric mucosa

Compared with the aggressive factors, little attention has been paid to the mucosal defensive factors in ulcer therapy, and the role of the H2-receptor antagonists in gastric mucosal protection has not been well characterized. In the present study, the effects of different types of H2-receptor antagonists (famotidine and roxatidine) on rat gastric mucus cells were investigated using both biochemical and histological methods. Each drug (famotidine, 3 mg/kg; roxatidine, 100 mg/kg) was orally administered to rats by gavage once daily for 7 days. The biosynthesis and tissue content of mucin were compared in the gastric mucosa treated with each drug. Using anti-mucin monoclonal antibodies, the mucin content and immunohistochemical localization were also compared. Both the biosynthesis and the accumulation of gastric mucin were significantly decreased in the famotidine-treated rats, but not in the roxatidine. Both the content and the immunoreactivity of surface mucus cell-derived mucin were reduced by famotidine, while they were maintained in roxatidine-treated rat stomachs. There was no difference between the groups in the content and immunoreactivity of mucous neck cell-derived mucin. H2-receptor antagonists should be classified in relation to gastric surface mucus cell function, raising the possibility of more effective ulcer therapy.     

Specialized metaplastic columnar epithelium in Barrett's esophagus. A comparative transmission electron microscopic study

Barrett's esophagus develops as a complication of regurgitant esophagitis and predisposes patients to the development of dysplasia and esophageal adenocarcinoma. Prior ultrastructural studies have suggested that Barrett's epithelium is a mucous secretory epithelium that shares some morphologic features with the intestine. The origin and development of Barrett's epithelium and the cellular abnormalities accompanying its neoplastic progression are poorly understood. In an attempt to better understand the histogenesis of the mucus-producing cells that predominate in Barrett's epithelium, these cells were studied by transmission electron microscopy and compared with other upper gastrointestinal epithelia: esophageal glands, normal gastric surface, pit, and cardiac gland regions, gastric intestinal metaplasia, and normal jejunal villous tip and crypt regions. A total of 134 mucosal biopsies from the stomach and esophagus of 28 patients with Barrett's esophagus and 37 biopsies from 14 other control patients were studied. Barrett's specialized metaplastic surface cells display a spectrum of ultrastructural features among three main surface columnar epithelial cell types: mucous cells resembling those seen in the normal gastric surface epithelium or resembling mucous neck cells normally seen in the gastric pits; goblet cells similar to those seen in the jejunum; and "pseudoabsorptive" cells with features of both gastric mucous secretory cells and jejunal absorptive cells. Cytoplasmic organelles of Barrett's specialized metaplastic, normal gastric mucous neck, and normal gastric surface mucous epithelial cells, including rough endoplasmic reticulum, glycogen aggregates, Golgi apparatus, and mucous secretory granules, have common ultrastructural features associated with mucus synthesis. The morphologic heterogeneity of Barrett's specialized metaplastic cells and common ultrastructural features associated with normal mucus biosynthesis suggest that they develop from a gastrointestinal stem cell that retains the capacity for a wide range of normal and abnormal differentiation in the esophagus. The identity of this undifferentiated cell, which may reside in normal proximal gastric or esophageal mucosa, remains unknown. However, the gastric mucous neck cell has properties that suggest it could be the progenitor cell for Barrett's esophagus because it is a stem cell that has ultrastructural similarities to Barrett's specialized metaplastic epithelial cells and it is located in intact gastric mucosa adjacent to where Barrett's esophagus forms.     

Mucopolysaccharides of the gastric mucosa in rats after ethanol-induced injury

The experiment was performed in 34 Buffalo rats. After laparotomy 2 ml of 96% ethanol was injected into the stomach for 90 sec. At 15 min, 1 hour, 24 hours and 96 hours mucopolysaccharides of the mucosa of bottom parts of the stomach were analysed histochemically. A direct reaction to concentrated alcohol was massive exfoliation and disintegration of the surface epithelium or abrupt release of the mucus from the superficial epithelial cells, pits and neck leading to a formation of a thick muco-cellular layer of gel precipitating reepithelization. Apart from an increase in the amount of surface mucus significant changes in its composition were found. They included an increase in the amount of sulfo- and sialomucins affecting the level of mucous viscosity. It was also shown that AB+ mucous cells of the neck were, a good marker of proliferative zone; state of the latter affects markedly the rate of regeneration of the damaged gastric mucosa.     

Effect of chronic stress and L-carnitine on rat stomach

BACKGROUND AND AIM: L-Carnitine is an essential cofactor in the mitochondrial transfer of fatty acids, and it is also a scavenger of free radicals in mammalian tissues. The aim of the study was to determine the effect of L-carnitine on chronic restraint stress-induced gastric mucosal injury. METHODS: Wistar rats were applied restraint stress (1 h/day) and L-carnitine (50 mg/kg) for 21 days. The lesion index, prostaglandin E(2) and mucus content, lipid peroxidation, superoxide dismutase, and catalase activity in gastric mucosa were evaluated. RESULTS: Chronic restraint stress increased the lesion index, lipid peroxidation, and superoxide dismutase activity in gastric mucosa, and it decreased prostaglandin E(2) and mucus content. L-Carnitine treatment prevented the stress-induced increase in lesion index, lipid peroxidation and a stress-induced decline in prostaglandin E(2), and mucus content in gastric mucosa, but it increased catalase activity. CONCLUSIONS: L-Carnitine prevents the occurrence of lesion by strengthening the gastric mucosal barrier and by reducing lipid peroxidation against the harmful effects of chronic restraint stress.     

Lectin histochemistry of galactose and N-acetyl-galactosamine glycoconjugates in normal gastric mucosa and gastric cancer and the relationship with ABO and secretor status

The histochemical binding of four lectin-peroxidase conjugates to normal human gastric mucosa and gastric carcinoma is described. The lectins were peanut agglutinin (PNA) which is specific for galactose residues and soy bean agglutinin (SBA), Dolichos biflorus agglutinin (DBA) and Helix pomatia agglutinin (HPA) which are specific for N-acetylgalactosamine. Binding of PNA to surface mucous cells or normal gastric mucosa occurred in non-secretors but not secretors and was independent of ABO blood group at all sites. PNA binding was unrelated to the immunohistochemical demonstration of Thomsen-Friedenreich (T) antigen. DBA and HPA bound selectively to surface mucous cells in normal gastric mucosa from group A secretors but binding at other sites was independent of ABO status. SBA binding showed no relationship with blood group or secretor status. In gastric cancers the major finding was the occurrence of extensive masking of lectin binding sites by sialic acid which was not seen in normal mucosa. Sialic acid masking was most marked with PNA and least marked with DBA. There was no correlation between lectin binding patterns and the stage or differentiation of tumours. Results are consistent with in vitro studies demonstrating increased sialation of membrane glycoproteins following malignant transformation. Difficulties in interpreting the histochemical demonstration of lectin binding in terms of specific glycoconjugates are discussed.     

The cytoprotective effect of prostaglandin E2 on taurocholate-induced erosions in gastric mucosa of the rat. Light microscopic, morphometric and scanning electron microscopic investigations

The morphological changes associated with the cytoprotective effect of prostaglandin E2 (PGE2) following sodium-taurocholate (NaTC) erosive injury in the gastric mucosa were investigated in male rats. A single topic application of NaTC (80 mMol) induced multiple gastric erosions in all animals. Application of 200 micrograms PGE2/kg body weight prior to NaTC treatment led to a significant 90% decrease in the lesion-score in PGE2-protected animals. Light microscopic morphometric studies of the mucus-producing cells in the fundus mucosa were carried out. Within the PGE2-protected animals a significant increase was observed in the length of zones of the mucus-producing cells at the surface and in the foveolae (both PAS-positive and alcian-blue-positive cells). Compared to the NaTC-injured animals, this increase amounted to 8.1% for the PAS-positive, and 6.1% for the alcian-blue-positive zone. Compared to the untreated controls, these values were 4.7% and 3.2% respectively. In the scanning electron microscope we observed a characteristic explosive release of mucus and damage of the cell's surface membranes in the NaTC-treated animals. The PGE2-protected rats showed a predominance of exocytosis of mucus vesicles which formed a characteristic mucus network at the surface membrane. Our investigations suggest that the cytoprotective effect of PGE2 may, in part, be due to an increase in mucus production and to a modification of mucus adherence at the cell membrane.     

Association of Helicobacter pylori with gastritis and peptic ulcer diseases

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.     

Establishment of gastric Campylobacter pylori infection in the neonatal gnotobiotic piglet.

Campylobacter pylori, a gram-negative microaerophilic bacterium, has been implicated in the genesis of human gastritis, dyspepsia, and gastroduodenal ulceration. Previous attempts to reproduce the diseases in conventional laboratory animal species have been unsuccessful. To determine if neonatal gnotobiotic piglets were susceptible to C. pylori, we orally challenged two litters (n = 17) with 10(9) CFU after pretreating them with cimetidine. Controls housed in separate units received nothing or peptone water alone. Piglets were examined 1, 2, 3, and 4 weeks after challenge. Colonization by the bacterium and inflammation of the gastric mucosa persisted throughout the study period. Organisms were revealed by Warthin-Starry silver stain to reside between the mucus layer and the gastric epithelium. Culturing of samples from sites along the gastrointestinal tract revealed that the bacterium colonized essentially only the gastric and proximal duodenal mucosae. Gross pathological changes were restricted to the stomachs of infected piglets and consisted of submucosal edema, increased gastric mucus production, and progressive development of mucosal lymphoid follicles. Microscopic lesions consisted of transient neutrophilic infiltrates followed by diffuse and follicular infiltrations of mononuclear leukocytes into the mucosa and submucosa. Alcian blue-periodic acid-Schiff stains suggested that the infection resulted in the depletion of mucopolysaccharide production by deep gastric glands. These data indicate that gnotobiotic piglets reproduce many of the features of diseases associated with C. pylori in humans.     

Effect of salivary gland stimulation by sialadenotrophic influences on the development of stress ulcers of the stomach in rats

It was demonstrated in experiments on female Wistar rats that transient hypertrophy of the salivary glands (the sialadenotrophic effect) induced by trypsin ingestion or repeated amputation of the lower incisors inhibits the development of stress erosive-ulcerating lesions of the gastric mucosa (GM). Stimulation of the salivary glands by sialadenotrophic effects caused an increase of the depth of the gastric pits and the height of the surface-foveolar epithelium responsible for mucus production, as well as a reduction in the number of parietal cells per unit of area of GM section.     

酪酸梭菌预防小鼠幽门结扎型胃溃疡的机制研究

目的:建立小鼠幽门结扎型胃溃疡(gastric ulcer,GU)模型,观测酪酸梭菌(C.butyricum)对GU的预防作用并探讨其机制。方法:将40只ICR小鼠随机分为假手术组、模型组、奥美拉唑预防给药组和C.butyricum预防给药组。采用小鼠胃幽门结扎的方法建立GU模型,测量各组胃游离黏液量、胃液的p H、胃蛋白酶活性,并做常规HE染色观察胃组织的病理形态学变化,糖原(PAS)染色法观察胃组织糖原含量的变化,采用免疫组化检测胃黏膜组织中Bax、Bcl-2蛋白表达水平。结果:HE及PAS染色结果表明,C.butyricum预防能够显著减轻胃粘膜的损伤,其效果与奥美拉唑相当。与模型组相比,C.butyricum组胃液的p H显著升高(P0.01);胃蛋白酶活性下降(P0.05),但其效果不如奥美拉唑组(P0.01);胃游离黏液量升高(P0.01),糖原染色加深,与奥美拉唑组相比明显增多;Bax蛋白表达量降低(P0.01)但Bcl-2蛋白表达水平显著上调(P0.01)。结论:C.butyricum对小鼠幽门结扎型GU具有较好的预防作用,其机制可能与抑制胃酸分泌、胃蛋白酶活化,尤其是增加胃游离黏液的产生以及诱导bcl-2、抑制bax基因表达有关。     

Protective effect of a cysteine prodrug and antioxidant,L-2-oxothiazolidine-4-carboxylate,against ethanol-induced gastric lesions in rats

Earlier studies have suggested an important role of glutathione (GSH) in cytoprotection against free radicals induced oxidative damage. This study reports gastroprotective effects of a cysteine precursor, L-2-oxothiazolidine-4-carboxylate (OTC), in experimental models of gastric secretion and ulceration. Acid secretion studies (volume and acidity) were undertaken in pylorus-ligated rats whereas the gastric lesions were induced by ethanol. Different groups of animals were treated with OTC (0, 100, 200 and 400 mg/kg). The levels of gastric wall mucus, nonprotein sulfhydryls (NP-SH) and myeloperoxidase (MPO) were measured in the glandular stomach of rats following ethanol-induced gastric lesions. Both medium and high doses of OTC significantly reduced the volume and acidity of gastric secretion in pylorus-ligated rats. Pretreatment with OTC significantly and dose-dependently attenuated the formation of ethanol-induced gastric lesion. OTC significantly protected the gastric mucosa against ethanol-induced depletion of gastric wall mucus, NP-SH and MPO. The gastroprotective effects of OTC may be attributed to its ability to inhibit neutrophils activity and replenish GSH demand.     

Regeneration of the gastric mucosa and reduced secretion after partial removal of the mucosa

Summary Restoration of the gastric mucosa after the removal of its various lenghts was studied in 60 dogs. As shown, gastric mucosa possessed a great restorative ability: in a month after its excision complete reepithelization of the internal surface of the stomach took place. The newly formed mucosa possessed a reduced number of oxyphilic cells.Functional investigations demonstrate that gastric secretion is considerably reduced after the operation. The new gastric mucosa is in good trophic condition.Presented by Active Member, Academy of Medical Sciences, USSR, A. V. Lebedinskii Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 52, No. 11, pp. 115–118, November, 1961     

Spontaneous remission of edema and regranulation of goblet cells in rat tracheae after capsaicin-induced acute inflammation

Previous studies have investigated the short-term effect of capsaicin on edema formation and goblet-cell secretion in the trachea. The present study sought to investigate the long-term effect of a high dose of capsaicin (90 micro g/ml/kg), administered intravenously, on changes in the formation of endothelial gaps among venular endothelial cells, mucosal tissue edema and the secretory activity of goblet cells, including the number and size of goblet cells, and the mucus score and secretory ratio of goblet-cell mucus secretion in the trachea of rats. The tracheal whole mounts with silver staining, those stained with chloroacetate esterase reagent and Alcian blue and tracheal tissue sections stained with Alcian blue and periodic acid-Schiff reagent were used for evaluation. Formation of endothelial gaps occurred a few min after administration of capsaicin, and gaps almost closed within 12 min after capsaicin injection. Five min after capsaicin, the leaky blood vessels were numerous and the subepithelial edema ratio (% of length of edema along the inner circumference of tracheal cross section) was found to be 57.8+/-3.0% ( n=6). The number of Alcian blue-positive goblet cells (1,090+/-220 per mm(2) of mucosal surface) was reduced to half the number of goblet cells in the vehicle-treated rats (2,200+/-230). The mucus score of goblet cell secretion was not changed. The secretory ratio was greatly increased. One day after capsaicin, the edema ratio remained large and the number of Alcian blue-positive goblet cells was also small. The mucus score was also not changed. The secretory ratio was still large. On day 3, the edema ratio remained large, but the number of Alcian blue-positive goblet cells was increased to the level of the controls. The mucus score and secretory ratio returned to the control level. On day 5, the edema ratio was greatly decreased, but it was still significantly larger than that of the controls. The mucus score and secretory ratio remained at the baseline level. Seven days after capsaicin, the edema ratio was similar to the controls. The number of goblet cells was even larger than controls. It is concluded that capsaicin-induced acute inflammation in the rat trachea involves formation of endothelial gaps, extensive plasma extravasation and edema formation, and depletion of goblet-cell secretory granules. Spontaneous gradual remission of edema was accompanied by regranulation of goblet cells with gradual mucogenesis for several days.     

缺血预适应在大鼠肢体缺血再灌注后胃粘膜损伤中的作用

目的:观察肢体缺血再灌注(LIR)对胃粘膜的损伤,探讨肢体缺血再灌注对胃粘膜损伤的作用及其部分机制,以及短暂多次肢体缺血在胃粘膜损伤发生中的作用。方法:按Rosenthal方法复制大鼠LIR模型,观察并测定肢体缺血4h再灌注4h后以及应用缺血预适应干预对胃粘膜损伤的影响:取各组胃粘膜制作切片于光学显微镜和电子显微镜下进行观察,测定各组胃粘膜损伤指数、胃粘膜血流量(GMBF)、胃结合粘液量、胃粘液中磷脂、氨基己糖的含量、血浆和胃组织一氧化氮含量以及胃粘膜一氧化氮合酶(NOS)活性。结果:光学显微镜和电子显微镜观察结果显示大鼠LIR后胃粘膜损伤严重,IPC组各类细胞损伤较LIR组轻;LIR后GMBF及胃结合粘液量、胃粘液中磷脂、氨基己糖的含量均低于对照组,虽然IPC组大部分指标与对照组有差异,但与LIR组对比GMBF及胃结合粘液量、胃粘液中磷脂、氨基己糖的含量均较高于LIR组;LIR组血浆与胃粘膜组织NO含量及NOS活性显著高于对照组,而IPC组血浆与胃粘膜组织NO含量和胃粘膜的NOS活性又显著高于LIR组。结论:肢体缺血再灌注可导致胃粘膜损伤;缺血预适应可减轻肢体缺血再灌注后的胃粘膜损伤。