Flow cytometric analysis of cell proliferation kinetics during duodenal ulcer healing

Cell proliferation in the gastroduodenal mucosa of patients with duodenal ulcers was evaluated using flow cytometry. Forty patients with duodenal ulcers and 12 normal subjects were investigated. Biopsy samples were obtained during endoscopic examination and subjected to DNA analysis by flow cytometry. Thirty patients with duodenal ulcers were healed within 3 months with H₂ blockers (tractable or responsive ulcers), whereas 10 patients did not respond to treatment (intractable ulcers). The percentage of cells at the DNA-synthetic phase, an index of cell proliferation, was constant in the adjacent duodenal mucosa 2cm from ulcer margin and antral mucosa during duodenal ulcer healing. The index at the margin of tractable ulcers was elevated during the active stage (12.9 ± 1.3), peaked during the healing stage (15.4 ± 2.8) and returned to the same level at the scarring stage (10.9 ± 2.0) as normal controls (10.3 ± 1.7). However, the index was not elevated in intractable ulcers (10.3 ± 1.7 in the healing stage) and was smaller than in tractable ulcers. These data indicate that augmented mucosal cell proliferation at the ulcer margin plays an important role in duodenal ulcer healing and intractable ulcers are characterized by an abnormal failure to accelerate DNA synthesis to achieve ulcer repair.     

Influence of Helicobacter pylori infection and cetraxate on gastric mucosal blood flow during healing of endoscopic mucosal resection-induced ulcers

BACKGROUND AND AIM: Helicobacter pylori (H. pylori) infection is known to affect the gastric microcirculation, and cetraxate is reported to accelerate gastric ulcer healing, possibly by augmenting gastric mucosal blood flow (MBF). The aim of this study is to clarify the effect of H. pylori infection and cetraxate on MBF during gastric ulcer healing. METHODS: Forty-two patients who had undergone endoscopic mucosal resection (EMR) were studied. Mucosal blood flow was measured by the use of a laser Doppler flowmeter in the surrounding mucosa and at the ulcer margin, before, 1 day, 1 week and 4 weeks after EMR. Helicobacter pylori infection was confirmed by the use of bacterial culture and histology. After EMR, patients were randomly assigned to receive 30 mg lansoprazole (u.i.d; L-regimen) or 30 mg lansoprazole (u.i.d.) with 200 mg cetraxate (q.i.d; LC-regimen) for 4 weeks. RESULTS: The MBF ratio (MBF at ulcer margin/MBF in surrounding mucosa) 1 week after EMR was significantly lower than that before or 4 weeks after EMR only in H. pylori-positive patients treated with the L-regimen. No such decrease in MBF was observed after 1 week in H. pylori-positive patients treated with the LC-regimen or in H. pylori-negative patients. CONCLUSION: A transient decrease in MBF was detected at the ulcer margin during healing of EMR-induced ulcers in H. pylori-infected patients. Cetraxate seemed to prevent this decrease in MBF.     

S phase cells of regenerative epithelium in the healing process of gastric ulcer determined by an in vitro BrdU-anti BrdU method

In order to investigate the healing process of gastric ulcer, cell proliferation kinetics of the regenerative mucosa over gastric ulcers was studied by an in vitro bromodeoxyuridine (BrdU)-anti BrdU method. In addition, the effect of histamine H2 receptor antagonists on gastric cell kinetics was also studied. The BrdU labeling index (L.I.) at the site ulcer margin, which were determined by the ratio of labeled cells to epithelial cells of gastric mucosa, were significantly higher in cases of endoscopic A to S1 stage ulcer than in cases of the atrophic gastritis served as control. While the mean L.I. of surrounding mucosa, approximately 1 cm apart from the ulcer margin, in the stage A to S1 were also significantly higher than that of control, the value in the stage S2 was almost comparable to the value of control. There were no differences of L.I. between the cases treated with and without H2 receptor antagonists. These results suggest that in the healing process of ulcer not only reserved epithelial cells at the ulcer margin but also the cells apart from the margin participate in mucosal regeneration. And it seems advisable to consider the stage S2 rather than the stage S1 as the most precise healing stage of ulcer. H2 receptor antagonist may not give an influence on proliferative properties of regenerating mucosal epithelium.     

Significance of Helicobacter Pylori Infection in Human Peptic Ulcers

Abstract: Experimental studies have suggested that the continuous administration of 0.02% NH, solution, induced by Helicobacter pylori (H, Pylori), leads to a glandular atrophy of the gastric mucosa, and adversely affects healing of acetic acid ulcers in rats, because of the suppression of cell kinetics of the regenerative epithelial cells and connective tissues at ulcer margins. To visualize the distribution of H. pylori in human gastric mucosa, a phenol red dye spraying endoscopy was performed in 45 patients with gastric ulcers, and 43 patients with duodenal ulcers, who were medicated with a full dose of H₂-blocker until ulcer healing, and with half doses thereafter. In the H. pylori negative cases, 8 (88.9%) of 9 gastric ulcers healed within 3 months after medication, with no relapse discernible up to 6 months after healing of the preceding ulcer. The relapse rate was 25% up to 12 months after ulcer healing. In contrast, only 22 (66.1%) of 36 gastric ulcers healed within 3 months after medication in the H. pylori positive cases. The relapse rate was 12.5% up to 3 months, 30.4% UP to 6 months and 63.6% up to 12 months after ulcer healing. In addition, all 6 duodenal ulcers healed within 2 months after medication in the H. pylori negative cases, with no relapse discernible up to 12 months after healing of the preceding ulcer. In contrast, in the H. pylon positive cases, 20 (53.1%) of 37 duodenal ulcers healed within 2 months, and the relapse rate was 14.3%, 33.3%, and 66.7% up to 3, 6 and 12 months respectively after healing of the preceding ulcer. These data suggest that H. pylori is likely to interfer with ulcer healing, and promotes peptic ulcer relapse.     

Omentum and basic fibroblast growth factor in healing of chronic gastric ulcerations in rats

Omentum was shown to exhibit angiogenic activity, but its role in healing of chronic gastric ulcers is unknown. This study was designed to compare the effects of omentum and basic fibroblast growth factor (bFGF), a potent angiogenic factor, on healing of chronic gastric ulcers in rats. Several series of rats with gastric ulcers were used: series A with intact omentum (control), series B with omentum resected, and series C with omentum placed on the serosal side of the ulcer. Series A–C were divided into four groups treated with vehicle (I); indomethacin (II), an inhibitor of prostaglandin formation, difluoromethylornithine (DFMO) (III); an inhibitor of polyamine biosynthesis or bFGF (IV). Seven days after ulcer induction, the animals were anesthetized, the gastric blood flow (GBF) was determined by laser Doppler flowmetry (LDF), and the ulcer area was measured by planimetry. Biopsy samples of the ulcer margin were taken for determination of the number of capillaries and myofibroblasts in the granulation tissue. Attachment of omentum significantly accelerated ulcer healing, whereas omentectomy delayed this process. LDF revealed the decrease in the GBF at the ulcer margin to 45% and at the ulcer bed to 18% of the value recorded in the intact adjacent mucosa. Attachment of the omentum significantly increased the blood flow at the ulcer margin and increased the number of capillaries and myofibroblasts in the granulation tissue. Indomethacin (1 mg/kg/day) that inhibited mucosal PGE₂ by about 85% delayed significantly ulcer healing without affecting the blood flow in the ulcer area. DFMO (200 mg/kg intraperitoneally) suppressed ODC activity in the mucosa but did not influence the ulcer healing. bFGF given subcutaneously accelerated dose-dependently ulcer healing and stimulated angiogenesis to a similar extent as the attached omentum. We conclude that omentum enhances the ulcer healing in similar way as bFGF and that this effect is accompanied by the increased angiogenesis and blood flow in the ulcer area.     

Distribution of Collagen Types I,III, and IV in Peptic Ulcer and Normal Gastric Mucosa in Man

The quality of peptic ulcer healing does not only mean complete epithelial restitution of the mucosal surface but also adequate repair of the underlying connective tissue. To obtain more information about the metabolism of extracellular matrix proteins in gastric mucosa and submucosa, we investigated biopsy specimens from six patients with antral peptic ulcers and six normal controls by staining of collagen types I, III, and IV with an immunofluorescence technique. In normal mucosa we found a certain amount of collagen types I and III in equal distribution and almost no collagen type IV. In contrast, there was a remarkable increase of collagen types I and III in peptic ulcers predominantly located at the ulcer edges. These results are compatible with the view that extracellular matrix proteins play some part in the ulcer healing process.     

Gastroprotective and ulcer healing effects of nitric oxide-releasing non-steroidal anti-inflammatory drugs

BACKGROUND & AIM: New class of nitric oxide-releasing non-steroidal anti-inflammatory drugs was shown to inhibit cyclooxygenase and prostaglandin generation without causing mucosal damage but whether these agents are capable of affecting gastric mucosal damage induced by strong irritants and healing of chronic gastric ulcers remains to be studied. In this investigation, effects of nitric oxide-releasing aspirin and nitric oxide-releasing naproxen were compared with those of native agents on gastric lesions provoked by 100% ethanol and on healing of chronic acetic acid ulcers. RESULTS: Both, nitric oxide-releasing aspirin and naproxen dose-dependently attenuated ethanol-induced damage and produced a significant rise in gastric blood flow but did not delay healing of gastric ulcers while native aspirin and naproxen had no influence on ethanol-induced gastric damage but significantly prolonged ulcer healing, reduced gastric blood flow and suppressed mucosal generation of prostaglandin E2. The gastroprotective and hyperaemic effects of both nitric oxide-non-steroidal anti-inflammatory drugs were completely abolished by ODQ, an inhibitor of guanylyl cyclase-cGMP system but not influenced by suppression of nitric oxide-synthase with L-NNA. The damaging effects of native acetyl salicylate acid or naproxen were aggravated by acidification of these non-steroidal anti-inflammatory drugs but the exogenous acid added to nitric oxide-acetyl salicylate acid or nitric oxide-naproxen failed to influence their effect. Despite inhibiting of PGE2 generation, both nitric oxide-releasing derivatives and native aspirin and naproxen failed to affect expression of cyclooxygenase-1 mRNA but upregulated the cyclooxygenase-2 mRNA. Concurrent inhibition of cyclooxygenase-2 by selective inhibitor NS-398 which by itself delayed ulcer healing and attenuated the gastric blood flow at ulcer margin, significantly worsened the effects of these nitric oxide-non-steroidal anti-inflammatory drugs and their parent drugs on ulcer healing and the gastric blood flow at the ulcer margin. CONCLUSIONS: 1) Coupling of nitric oxide to aspirin or naproxen attenuates ethanol-induced damage, possibly due to an increase in gastric microcirculation mediated by excessive release and action of nitric oxide that probably compensates for PG deficiency induced by non-steroidal anti-inflammatory drugs; and 2) nitric oxide-non-steroidal anti-inflammatory drug, unlike classic non-steroidal anti-inflammatory drugs, does not affect intact gastric mucosa and fails to delay the healing of pre-existing ulcers.     

Gastric Ulcer Relapse

Abstract: In this review we found that the rate of gastric ulcer relapse reached near! 70% over a 13 year period and was nearly 10% after one year from when they reache the white scar stage. A H2-RA or proton pump inhibiter had a high relapse rate the reason being the fragile re-epithelization of the scar³⁾⁴⁾. Factors involved in gastric ulcer relapse are considered to be the fragile re-epithelization of the ulcer, disturbance c blood flow due to fibrosis underneath the ulcer scar, and etiological factors such a smoking and so on. Endoscopic findings of the ulcer scar can statistically suggest th gastric ulcer relapse rate. The main cause of peptic ulcers, especially duodenal ulce relapse, is strongly related to Helicobacter pylori infection. The causes of gastric ulcer relapse are very complicated and variegated. H. pylori infection contributes to les gastric ulcer relapse than duodenal ulcer relapse. To prevent gastric ulcer relapse, therefore, one should consider the eradication c H. pylori, the endoscopic features of the ulcer scar and etiological factors.     

THE HEALING PROCESS OF GASTRIC ARTIFICIAL ULCERS AFTER ENDOSCOPIC SUBMUCOSAL DISSECTION

Background: Due to the remarkable progress of endoscopic resection techniques, endoscopic submucosal dissection (ESD) has been widely performed for larger mucosal tumors that would result in large arti?cial ulcers. The healing process of peptic ulcers has been previously studied in detail; however, no precise investigation for arti?cial ulcers after ESD has been reported. To con?rm the validity of the treatment from the aspect of wound healing, we aimed to clarify the healing process of large gastric arti?cial ulcers after ESD. Methods: Seventy patients with gastric mucosal tumors treated by ESD were enrolled. The size, location and time of scar formation of the ulcers were reviewed using endoscopic pictures taken from the same view and angle. Follow‐up endoscopy was performed at 1, 4, 8 and 12 weeks after ESD. For postoperative medication, all patients received normal doses of proton pump inhibitors and sucralfate for 8 weeks. Results: The average size of the resected specimen was 34.7 mm (20–90 mm). Irrespective of ulcer size and location, all of the cases healed up to scarring stages within 8 weeks. Conclusions: Gastric arti?cial ulcers after ESD healed within 8 weeks regardless of size and location using normal doses of medication as peptic ulcers. The fact that even giant ulcers after ESD heal within 8 weeks could be helpful information for candidates for ESD and for postoperative management of patients after ESD.     

Effect of Cimetidine on the Regeneration of the Gastric Mucosa around a Peptic Ulcer

Histological changes in gastric ulcers during the healing process with cimetidine treatment were compared with those seen with conventional treatment. Healing time of the ulcers was clearly shortened, and the regeneration of the marginal mucosa of gastric ulcers was strongly stimulated by cimetidine. Heightening of the marginal mucosa resulted from active regeneration of the mucosal cells and made the endoscopic features mimic those of gastric cancer. These results suggest that it is necessary to differentiate clearly peptic ulcer from gastric cancer before beginning treatment of a gastric ulcer with cimetidine.     

Epidermal Growth Factor in Gastric Ulcer Healing by Nocloprost,a Stable Prostaglandin E2 Derivative

Background: The gastroprotective and ulcer-healing properties of prostaglandins, especially in gastric ulcers induced by non-steroidal anti-inflammatory drugs, are well established. Ulcer healing is an active process of filling the mucosal defect with migrating and proliferating epithelial cells combined with angiogenesis in granulation tissue at the ulcer bed. Growth factors, especially epidermal growth factor (EGF) and transforming growth factor alpha (TGFa) are crucial in the regulation of the reconstruction of damaged mucosal structures. Methods: In this double-blind, randomized, prospective study 40 patients with gastric ulcer were treated with nocloprost, a stable prostaglandin E₂ derivative, or with ranitidine. All subjects underwent endoscopy before and after 4 and 8 weeks of anti-ulcer therapy. During endoscopy mucosal biopsies were performed for determination of EGF content in gastric mucosa at the ulcer margin and in the intact mucosa. Additionally, EGF output in saliva and its plasma concentrations were determined in all subjects before and during the treatment. Results: The gastric ulcer healing rate after 4 weeks was significantly higher in patients treated with nocloprost than in those treated with ranitidine (63% versus 39%, respectively). At initial examination the EGF content in the gastric mucosa obtained from the ulcer edge was significantly higher than that in the intact mucosa. There was a significant increase in the EGF content in both the ulcer margin and the intact mucosa in subjects treated with nocloprost but not in patients under treatment with ranitidine. Similarly, patients treated with nocloprost had significantly higher EGF output in saliva and higher EGF concentration in plasma throughout the anti-ulcer therapy. Conclusion: Nocloprost is superior to ranitidine in the treatment of chronic gastric ulcers, and these effects could be due, at least in part, to higher expression and mucosal content of EGF in the ulcer area.     

Reduction in index of oxygen saturation at margin of active duodenal ulcers may lead to slow healing

This study tested the hypothesis that reduced perfusion of a duodenal ulcer margin (ie, the mucosa 1–2 mm from the edge of the ulcer base) is associated with slow healing. Reflectance spectrophotometric measurement of indices of mucosal hemoglobin concentration (IHB) and mucosal hemoglobin oxygen saturation (ISO₂) were obtained endoscopically in 21 patients at the ulcer margin and the adjacent mucosa (ie, the mucosa 1–2 cm from the edge of the ulcer base). In 17 patients with adequate follow-up, stepwise multilinear regression analysis revealed a significantly negative correlation (r=s-0.69, P < 0.05) between ISO₂ at the ulcer margin minus ISO₂ at the adjacent mucosa (ISO)₂ and ulcer healing time. In addition, smoking, being black, and early relapse since the last ulcer attack were found to be associated with increased duration required for healing. The results of this pilot study suggest factors, in addition to smoking, that may have to be considered in future studies concerned with duodenal ulcer healing.This work was supported by the National Institute of Arthritis and Metabolism and Digestive Diseases Grant AM34840, American Society for Gastrointestinal Endoscopy Career Development Award H850208, Veterans Administration Medical Research Funds, and UCLA Academic Senate Grant 4063.     

Reproducible demonstration of blood flow at duodenal ulcer margins by endoscopic reflectance spectrophotometry

Changes in gastrointestinal mucosal blood flow were evaluated by index of oxygen saturation (ISO2) and index of hemoglobin concentration (IHB) measured with a reflectance spectrophotometer. This report examined the reproducibility of endoscopic measurements of ISO2 and IHB. Study 1: The everted stomachs of three anesthetized rats provided hands-on instruction (one teacher and three learners). Six sets of readings were obtained endoscopically (the mean calculated to give the measurement) at each level of gastric mucosal perfusion when gastric blood flow was varied by withdrawing blood from the carotid artery. Study 2: Fourteen duodenal ulcer patients with ulcer bleeding were transfused and stabilized. Two endoscopists (one teacher and one learner) took turns to obtain endoscopic ISO2 and IHB measurements at the margin of the ulcer and at the adjacent normal appearing mucosa. delta ISO2 was calculated as the ulcer margin value minus adjacent mucosa value. In study 1, the correlation coefficients between the ISO2 measurements of the experienced and those of the other three observers were 0.99, 0.97, and 0.97, respectively. In study 2, the correlation coefficients between the ISO2 measurements obtained at the ulcer margin and at the adjacent normal mucosa, and delta ISO2 obtained by the experienced observer and one of the three learners were 0.94, 0.97, and 0.94, respectively. Relative to the adjacent area, 79% of the duodenal ulcers studied had increased (+delta ISO2), and 21% had decreased blood flow (-delta ISO2) at the ulcer margins. IHB measurements were less reproducible, particularly at the ulcer margin. The measurements of ISO2 and delta ISO2 were reproducible in the everted rat stomach and in duodenal ulcer patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quality of ulcer healing influences the relapse of gastric ulcers in humans

The usefulness of dye-contrast endoscopy for the evaluation of the quality of gastric ulcer healing and the prediction of relapse was investigated. Sixty consenting patients whose ulcers healed during 3 months of treatment underwent endoscopy for the identification of the pattern of mucosal regeneration. Patients were monitored for relapses for up to 18 months after antiulcer therapy had ended. The pattern of regeneration was flat in 24 patients, nodular in 25 and intermediate in 11. Internal hypoechoic areas seen by endoscopic ultrasonography were less common and histological maturity was better in the patient group with the flat pattern compared with the patient group with the nodular pattern of mucosal regeneration. Prostaglandin E, synthesis was highest in the group with the flat pattern of mucosal regeneration and the relapse rate was lowest in this group. We conclude that the evaluation of the quality of ulcer healing is possible and that findings in individuals may aid the prediction of relapse for particular patients.     

粘膜功能恢复与消化性溃疡愈合的关系

粘膜形态学、组织学以及功能学的恢复有助于提高消化性溃疡的愈合质量,减少溃疡复发。文章就溃疡粘膜的成熟度即粘膜功能的恢复与消化性溃疡愈合质量之间的关系作一综述。     

Influences of Helicobacter pylori on gastric angiogenesis and ulcer healing in mice

BACKGROUND AND AIMS: Helicobacter pylori infection is associated with peptic ulcers; however, it is unclear whether the bacterium delays ulcer healing. We investigated the influence of H. pylori on ulcer healing in mice. We also examined the influence of H. pylori infection on angiogenesis. METHODS: An acetic acid ulcer was made in male BALB/c mice. Three days later (day 0), the animals were inoculated with H. pylori SS1 strain. The healing process of the ulcer was examined macroscopically and microscopically on days 0, 6 and 9. The index of angiogenesis was also determined using carmine dye injection. RESULTS: On day 0, angiogenesis began at the ulcer margin while the mucosal epithelia had not yet regenerated. On days 6 and 9, angiogenesis and epithelial regeneration developed and ulcer size reduced. These phenomena were significantly suppressed in mice infected with H. pylori. CONCLUSION: Helicobacter pylori infection significantly suppressed angiogenesis and delayed ulcer healing. These results indicate that H. pylori plays an important role in ulcer healing.     

Mouse model of gastric infection with cytotoxin-expressing strain of Helicobacter pylori in studying of pathogenesis of chronic gastric ulcer

Abstract Helicobacter pylori is a major risk factor for peptic ulcer, but studies on the role of H. pylori infection in gastric pathology are limited due to lack of convenient models resembling H. pylori infection in humans. We studied the effects of inoculation of conventional BALB/c mice with a toxigenic (cytotoxin associated gene A (cagA)+ and vacuolating cytotoxin gene A (vacA+) H. pylori strain on the course of healing of gastric ulcers. Following inoculation of toxigenic H. pylori or vehicle, gastric ulcers were produced in mice, which were then killed either at day 0 or after 2, 4, 7, 14 or 28 days and ulcer area and gastric blood flow (GBF) were determined. Gastric secretions from mice with chronic gastric fistulae were studied before and after inoculation with toxigenic H. pylori or vehicle (saline). The area (7 mm²) of ulcers in control mice decreased gradually and disappeared almost completely after 14 or 28 days. The ulcers in H. pylori-infected mice were present at all test days, showing a larger area than in vehicle control animals. The GBF in control mice rose gradually with decreasing ulcer size, being significantly higher at the ulcer margin than the ulcer crater. In contrast, the GBF in H. pylori-infected mice was significantly lower at the ulcer area than that in the vehicle controls but, again, the GBF at the ulcer margin was always higher than at the ulcer crater. Gastric acid output was reduced by more than 50% immediately after H. pylori inoculation and was accompanied by a significant increase in plasma gastrin release and a fall in gastric luminal somatostatin content. These secretory changes persisted at all test days. Oedema/congestion of surface epithelium appeared after 7 days and mucosal inflammatory infiltration appeared after 14 days, to further increase after 28 days, upon the induction of ulcer. Plasma interleukin (IL)-Iß and IL-12 were significantly elevated above the initial values compared with controls. Conventional mice with gastric ulcers can be successfully infected with an H. pylori strain expressing cagA and vacA cytotoxin and this infection markedly delays healing of the ulcers, probably due to the fall in GBF in the ulcer area, mucosal inflammation, cytokine release and impairment of the gastrin-somatostatin link.     

Nonsteroidal anti-inflammatory drugs and peptic ulcer disease

Evidence has accumulated that nonsteroidal anti-inflammatory drugs (NSAIDs) cause clinically important gastroduodenal ulcers. The pathogenesis, which involves the impairment of mucosal resistance to injury in an acid-peptic environment, is multifactorial and controversial. Ulcers caused by NSAIDs can occur either in mucosa inflamed because of infection with Helicobacter pylori or in histologically normal mucosa. The use of these drugs has been linked to an unexpectedly high incidence of ulcer complications, and a history of peptic ulcer disease is common in such cases. Nonsteroidal anti-inflammatory drugs thus appear both to exacerbate an underlying peptic diathesis and to cause de novo ulcers. The association between the use of these drugs and ulcer complications is supported by ulcer prevalence data from cross-sectional studies, and by data from case-controlled and cohort studies, and from randomized, experimental trials. Drug-induced gastric ulcers have been prevented by misoprostol, but not by H2 blocker therapy. Several therapies have been reported to promote ulcer healing despite continued use of NSAIDs, but adequate controlled trials have not been done. Small gastric and duodenal ulcers readily heal, whereas larger gastric ulcers require vigorous and prolonged therapy. The relative efficacies of various therapies in preventing ulcers, healing ulcers, or preventing complications remain to be established.     

七方胃痛胶囊对大鼠乙酸胃溃疡愈合质量的影响

[目的]观察七方胃痛胶囊对大鼠实验性胃溃疡愈合质量(QOUH)的影响.[方法]予冰醋酸注射制作大鼠胃溃疡模型后,随机分为5组:分别予0.85%氯化钠液、雷尼替丁胶囊、七方胃痛胶囊(小、中、大3个剂量),连续灌胃14 d,处死大鼠,制作病理切片,予苏木精-伊红染色和黏液组织化学染色,在光镜下观察溃疡指数、再生黏膜厚度、黏膜肌层缺损宽度、表面黏液厚度、再生组织结构.[结果]七方胃痛胶囊能增加再生黏膜厚度及表面黏液厚度,减少再生黏膜肌层缺损宽度(P＜0.01),有量效关系(P＜0.01),能明显改善再生组织结构.[结论]七方胃痛胶囊能改善再生组织结构,从而提高QOUH,达到抗溃疡复发的作用.