Healing Process Of Gastric Ulcer Research Articles

Expression of ETS-1 transcription factor in relation to angiogenesis in healing process of gastric ulcer

Expression of ETS-1 transcription factor in relation to angiogenesis in healing process of gastric ulcer

Distribution of extracellular matrix (ECM) proteins in the gastric ulcer healing process: [formula omitted]1, M. Shahin 1, Th. Pohle 1, D. Schuppan 2, E. Foerster 1, and Dept. of Gastroenterology, Free University of Berlin 2, Germany

Distribution of extracellular matrix (ECM) proteins in the gastric ulcer healing process: [formula omitted]1, M. Shahin 1, Th. Pohle 1, D. Schuppan 2, E. Foerster 1, and Dept. of Gastroenterology, Free University of Berlin 2, Germany

Changes in Gastric Function During Healing of Gastric Ulcers

Abstract: To determine changes in pathophysiology during the healing process of gastric ulcers, gastric acid secretion, gastric emptying, fasting gastrin levels (FGL) and the integrated gastrin response (IGR) were studied in normal volunteers and in each stage of gastric ulcers. In a study of patients with gastric ulcers in the lesser curvature of the ventricular angulus including 20 in the active stage, 49 in the healing stage and 11 in the healed (scar) stage, gastric acid secretion (BAO and MAO) and FGL gradually decreased as the patients progressed from the active stage through the healing and healed stages. IGR values did not change, but gastric emptying showed marked prolongation in the active and healing stages although this was alleviated in the healed stage. In 11 of the same gastric ulcer patients who were followed up, gastric acid secretion, especially BAO, was lower in the healed stage than in the active stage. No fixed tendency was seen for gastric emptying and IGR, but FGL showed higher values in the active stage than in the healing stage. These findings indicated that changes in the pathophysiology of the stomach occur during the healing of gastric ulcers, and it was assumed that these changes are closely related to the stage of the ulcer.

ラット実験胃潰ようにおける肉芽新生血管の細胞接着因子発現に関する免疫組織化学的研究

Angiogenesis of the experimental-gastric ulcer was investigated by means of immunohistochemical staining using monoclonal antibodies (MoAbs) related to adhesion molecules. In order to study the regulation of the antigen-expression defined by REC16-11, REC4-1 and ICAM-1, which recognize varieties of endothelial cells, we assessed their expression on the microvasculature in the granulation tissues using a model of acetic acid-induced gastric ulcer in rats. Microvasculature in the deep layer of granulation tissues were stained by REC16-11 within 5 days of the ulcer development. In contrast, REC4-1 and/or ICAM-1 were detected in microvasculature only from 10 days, in parallel with the degree of LFA-1-positive lymphocytic infiltration around REC4-1-positive-vessels. In cases of healed ulcer on 40 days, the distribution of the positive reaction with those MoAbs was similar to the normal rats. In cases of unhealed ulcers at the same period, REC16-11-positive-vessels were observed in all vascular endothelial cells of the granulation tissues. However, REC4-1 and/or ICAM-1-positive-vessels had the same pattern as the cases on 15 days. The cell adhesion molecules were expressed temporary on the endothelial cells of these microvasculature during the development of granulation tissues after gastric ulcer. Based on these results, it was suggested that the antigens related to adhesion molecules on the endothelial cells may play an important role in the healing process of gastric ulcer.

Expression of neural cell adhesion molecule (NCAM) in the healing process of gastric ulcer.

Expression of neural cell adhesion molecule (NCAM) in the healing process of gastric ulcer.

A new method for measurement of blood flow, pH, and transmucosal potential difference in rat gastroduodenal mucosa by endoscopy

A method was developed to measure the mucosal blood flow (BF), mucosal pH (pH), and transmucosal potential difference (PD) in various sites from the oral cavity to the duodenum without surgical operation or damage to the subject rats. These measurements were carried out by using three indicator electrodes, which were attached to the various sites through the suction channel of an endoscope. The hydrogen gas clearance method was used for the measurement of BF. BF values obtained at the fundic, pyloric, and duodenal regions were 119 +/- 17, 69.9 +/- 8.8, and 114 +/- 18 ml/min/100 g (mean +/- SE), respectively. The pH values were lowest at the cardiac portion and the forestomach and highest at the duodenum. PD showed higher values at the stomach and lower values at the pharynx and duodenum. Using this technique, it was possible to measure the BF, pH, and PD repeatedly and safely at various sites in the same rat. Therefore, it was suggested that this method is useful in studying the physiological functions of the stomach and duodenum and the pathogenesis of gastroduodenal ulceration and that this method is applicable to measure the change of the above parameters in the healing process of gastric ulcer in rats.

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

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

Quantification of gastric ulcer healing by endoscopic ultrasonography

We studied and quantified the healing process of gastric ulcers in humans by means of endoscopic ultrasonography. Initially, using the water bath method, we scanned specimens of resected human stomachs with gastric ulcers including 9 open ulcers and 14 ulcer scars. Comparison of histological findings and measurement of the cross-section suggested that the ulcers observed in the ultrasonographic photographs were essentially equivalent to those in histological photographs. By using endoscopic ultrasonography, we then examined 16 patients with active, mainly recurrent, gastric ulcers before and after 2, 4, and 8 weeks of H2 blocker treatment, measuring the length and cross-sectional area of the ulcer in endoscopic ultrasonographic photographs. From measurements of the contraction rate of cross-sectional ulcer area during healing, we observed that the healed ulcers showed a relatively rapid rate of contraction in the first 4 weeks of therapy and the non-healed cases showed a poor contraction rate. Endoscopic ultrasonography is useful for the quantitative estimation of histological changes associated with gastric ulcer healing.

Delayed Healing of Acetic Acid-Induced Gastric Ulcers in Rats by Indomethacin

We examined the mechanism by which repeated administration of indomethacin significantly delays the natural healing of experimental gastric ulcers induced in rats. Gastric ulcers were produced 5 days after injecting 20% acetic acid (0.03 ml) into the submucosal layer of the gastric wall of the antral-oxyntic border. The natural healing of the acetic acid-induced ulcers was extensively delayed by administering indomethacin (1 mg/kg) subcutaneously once daily for 2 or 4 wk. Subcutaneous administration of natural prostaglandin E2 (1 or 3 mg/kg) twice daily for 2 and 4 wk, together with indomethacin, significantly prevented the delay of ulcer healing. Prostaglandin E2 (3 mg/kg) administered twice daily for 2 wk also significantly accelerated the natural healing of the ulcers. A single administration of prostaglandin E2 (1 or 3 mg/kg) significantly reduced histamine-stimulated gastric acid secretion for 4 h in acute fistula rats with 1- or 2-wk-old ulcers, treated with or without daily indomethacin (1 mg/kg). Endogenous prostaglandin E2 levels in the gastric mucosa of normal rats were significantly reduced for at least 12 h after a single or repeated administration of indomethacin (1 mg/kg) for 2 or 4 wk. Gastric mucosal prostaglandin E2 levels in rats with ulcers (5 days after acetic acid injection) were also markedly reduced by indomethacin. This reduction significantly reverted toward control levels after administration of exogenous prostaglandin E2 (3 mg/kg). These results suggest that endogenous prostaglandin E2 plays an important role in the healing process of gastric ulcers.

Effects of Trimoprostil on Healing and Recurrence of Acetic Acid-induced Gastric Ulcer in Rats

Chronic gastric ulcers were produced by injection of 20% acetic acid (0.05 ml) into the submucosal layer of the rat stomach in order to determine the effects of the prostanoid trimoprostil on the healing and recurrence of ulcers. Local injection of acetic acid solution produced large demarcated ulcers in all animals on day 5, which rapidly decreased to reach lowjevels on days 40–80 and then became exacerbated on day 100. The exacerbation of the ulcer is probably recurrence. Trimoprostil was administered ad libitum in drinking water containing 0.1, 0.3 and 1.0 μg/ml (average dose 12.4, 37 and 124 μg/kg/day) for a period of 14 days (day 1–15) to assess its effect on healing and for a period of 40 days (day 60–100) to assess its ability to prevent recurrence. The higher two doses of trimoprostil accelerated the spontaneous healing of the ulcers. Furthermore, trimoprostil, at both doses, prevented the observed recurrence of this type of ulcer. Trimoprostil dose-dependently (30–300 μg/kg, p.o.) inhibited gastric secretion in pylorus-ligated rats. Cimetidine at the antisecretory dose (1 mg/ml, 132 mg/kg/day) failed to affect the healing process of gastric ulcers, but tended to prevent the recurrence of gastric ulcers. Our present study suggests that trimoprostil is a promising antiulcer drug for the treatment of chronic gastric ulcer.

Gastric mucosal blood distribution and its changes in the healing process of gastric ulcer

Changes in gastric mucosal blood volume in the healing process of ulcers were investigated by organ reflectance spectrophotometry performed during endoscopy. Spectra were taken from 24 regions in the stomach in 42 patients with gastric ulcers located at the angle of the stomach. Fifty-one patients with no gastric lesions were used as normal controls. In patients with active gastric ulcers, mucosal blood volume decreased significantly in most regions in the stomach. During the healing process, mucosal blood volume returned to the same levels as those of the controls. On the other hand, mucosal blood volume around the gastric ulcer increased significantly as compared with that of surrounding mucosa at the healing stage. The rise in mucosal blood volume of the ulcer margin at the healing stage (H2 stage) was 33% in cases where gastric ulcers healed within 3 mo, and 2% in cases where the gastric ulcer failed to heal after 3 mo of therapy. It was concluded that the mucosal blood volume changes during the healing process of gastric ulcer and that an increased blood supply to the ulcer margin at the healing stage has a strong effect on the healing periods of ulcer. The reduction of mucosal blood volume at the active stage of the ulcer may also be implicated in the pathogenesis of gastric ulcers.

Studies on the Healing Process of Gastric Ulcer

Studies on the Healing Process of Gastric Ulcer

Effect of gastric regimen on healing process of gastric ulcer

Effect of gastric regimen on healing process of gastric ulcer

A NEW METHOD FOR THE PRODUCTION OF CHRONIC GASTRIC ULCER IN RATS AND THE EFFECT OF SEVERAL DRUGS ON ITS HEALING

Several methods have been reported to produce an experimental chronic ulcer in the rat, such as thermal ulcer by Skoryna et al. (1, 2), clamping-cortisone ulcer by Umebara et al. (3), and methylcholanthrene ulcer by Lauren et al. (4). In these methods thermal and clamping-cortisone ulcers seem to be valuable tools in investigation of the healing process of gastric ulcer, because of the relatively long period of its persistence and closer histologic resemblance to human peptic ulcer. However, both methods include the undesirable procedure such as the incision of glandular portion of stomach in order to perform the thermocautery of the innersurface of stomach in the former method and the consecutive administration of cortisone acetate for 8 days after the gastric operation in the latter. On the other hand, Robert and Selye (5) have reported the method to evoke an ulcer by an injection of formalin solution into the rat stomach wall itself. We also tried the same procedure and found the gastric necrosis corresponding to the injected area. However, the necrotic tissue did not disappear from the stomach wall even 6 days after the operation so that the so-called gastric ulcer was not produced. Then we injected the acetic acid solution, which is well known to injure the gastric mucosa (6) or to evoke inflammation in rat paw in our laboratory (7), into the rat stomach wall and found the definite gastric ulcer having resemblances to the human peptic ulcer at gross and microscopical observation. This paper deals with the studies of the healing process of the produced ulcer and the usefulness for the assay method of the curative drugs of gastric ulcer.

On the significance of tissue contraction in healing process of gastric ulcers

In order to evaluate the significance of the contraction of tissues at the ulcer base in the healing process of gastric ulcers, we made histological studies of ulcer cases which had been followed up radiologically. We could find that there were often ulcer cases, in which niches had evidently diminished in size but histologically no signs of regeneration of mucous epithelium could be found, therefore, in these cases we can consider that the diminishing process of the ulcers occurred only as the result of contraction of tissues as the ulcer base. The contraction of t issues of this kind was sometimes so noticeable, that the area left which required to be covered with regenerated epithelium was very small. Fur thermore we came across a case with linear ulcer scar, which was considered mainly to have resulted from tissue contraction of a round niche as shown in X ray pictures in its initial stage. The results obtained from these cases proved that 1) only by the contraction of granulation tissues ulcers could decrease in size to such an extent that we could expect real healing before long, and that 2) such a contraction of t issues could account for the formation of linear ulcers.