Antral Ulcers Research Articles

Evidence for the essential role of Helicobacter pylori in gastric ulcer disease.

Helicobacter pylori (H pylori) eradication heals chronic active type B gastritis and dramatically changes the natural history of duodenal ulcer disease. There are few data concerning the role of anti-H pylori treatment in gastric ulcer disease. A total of 83 patients presenting with H pylori positive active gastric ulcer disease were treated with omeprazole and antibiotics (amoxicillin, ciprofloxacin, roxithromycin) in seven different clinical protocols, each of which included the attempt to eradicate H pylori infection and to evaluate the post-therapeutic course of ulcer disease. The overall proportion of H pylori eradication was 67.9% (53 of 78 patients available for follow up). Best results were obtained with two week treatment regimens comprising omeprazole 20 mg twice daily and amoxicillin 500 mg four times a day or 1000 mg twice daily (eradication > 80%). Eradication of H pylori speeds up ulcer healing, with a six week healing rate of 84.9% compared with 60% in patients with persistent H pylori infection (p = 0.0148). In a subgroup of 11 patients with refractory ulcers, H pylori eradication (n = 10) was associated with ulcer healing on continued acid suppression in nine cases. One male patient with chronic antral ulcer did not respond to treatment within the next six months (H pylori and ulcer persistence), and in one female patient a resistant body ulcer was identified as gastric lymphoma. Fifty patients with healed ulcers were followed up for one year. Patients with (n = 32) and without (n = 18) bacterial eradication had similar demographic and clinical characteristics. H pylori eradication was associated with a statistically significant reduction of ulcer recurrences (3.1 v 55.6%, p<0.001). This study concludes that H pylori eradication considerably changes the natural history of H pylori associated gastric ulcer disease. In addition, H pylori eradication speeds up ulcers healing and is associated with healing of previously refractory ulcers. Thus, treatment aimed at bacterial eradication should be considered in all patients with gastric ulcers severe enough to contemplate further treatment options.

O-21 - Adrenergic β3 Agonists Inhibit Antral Ulcer Formation by an enhancement of gastric mucosal blood flow.

O-21 - Adrenergic β3 Agonists Inhibit Antral Ulcer Formation by an enhancement of gastric mucosal blood flow.

Tissue-selective inhibition of prostaglandin synthesis in rat by tepoxalin: Anti-inflammatory without gastropathy?

Background: Inhibition of prostaglandin synthesis is likely a primary mechanism for both the anti-inflammatory and ulcerogenic effects of nonsteroidal anti-inflammatory drugs (NSAIDs). The present study examined the mechanism underlying the ability of a novel anti-inflammatory drug, tepoxalin, to suppress prostaglandin synthesis without inducing gastric mucosal injury. Methods: The effects on prostaglandin synthesis by various tissues of tepoxalin, diclofenac, and indomethacin were examined in vivo and in vitro. These compounds were also studied in two inflammation models. The capacity of indomethacin and tepoxalin to induced antral ulceration in the rabbit was compared. Results: In most tissues, tepoxalin was a weaker inhibitor of prostaglandin synthesis than the two NSAIDs. However, at a site of peripheral inflammation, tepoxalin was comparable with the NSAIDs in suppressing prostaglandin synthesis and in exerting anti-inflammatory effects. Indomethacin induced penetrating antral ulcers in rabbits whereas tepoxalin produced no detectable mucosal injury. Conclusions: The ability of tepoxalin to suppress inflammation without causing gastric mucosal injury appears to be related to its differential suppression of prostaglandin synthesis in various tissues. Compounds that selectively inhibit prostaglandin synthesis at sites of inflammation may represent a class of anti-inflammatory drugs without detrimental effects on the stomach.

Role of superoxide dismutase in mechanism of diethyldithiocarbamate-induced gastric antral ulcer in rats: protective effect of prostaglandin, cimetidine and pirenzepine.

The role of superoxide radicals and the protective effects of superoxide dismutase (SOD), allopurinol, 16,16-dimethyl-prostaglandin E2 (dmPGE2), cimetidine and pirenzepine in diethyldithiocarbamate (DDC)-treated rats were evaluated. Pretreatment with Cu,Zn-SOD (superoxide radical scavenger) 60,000 units/kg, allopurinol (competitive inhibitor of xanthine oxidase) 50 mg/kg, dmPGE2 (prostaglandin analogue) 10 micrograms/kg, cimetidine (H2-receptor antagonist) 10 mg/kg or pirenzepine (selective antimuscarinic drug) 10 mg/kg all significantly reduced the DDC-induced (800 mg/kg) gastric antral ulcer formation in rats. DDC treatment substantially decreases the gastric mucosal Cu,Zn-SOD activity. In this study treatment with DDC and SOD, DDC and dmPGE2, DDC and cimetidine, and DDC and pirenzepine were demonstrated significantly to prevent the decrease of gastric mucosal Cu,Zn-SOD activity. However, allopurinol did not have this effect. The results suggest that SOD and/or superoxide radicals may play an important role in the mechanism of DDC-induced gastric antral ulcer. The protective property against ulcer formation of these drugs studied might be due to the action of SOD in the gastric mucosa.

Characterization of a simple animal model for nonsteroidal anti-inflammatory drug induced antral ulcer.

Most animal models of nonsteroidal anti-inflammatory drug (NSAID) induced gastric injury are characterized by acute, superficial erosions in the corpus region, whereas the clinically significant injury in man is the deep, antral ulcer. The purpose of this study was to characterize a model of NSAID-induced antral ulceration that more closely resembles the type of damage seen in man. Rabbits received indomethacin subcutaneously every 12 h. The progression of ulcer formation was followed by killing groups of animals after one to seven doses of indomethacin. The dose dependency of ulcer formation was assessed by giving indomethacin at doses of 1 to 20 mg/kg. Healing of antral ulcers was determined by examining the stomach at various times after administering the seventh dose of indomethacin (20 mg/kg). The effects of prophylactic treatment with misoprostol or ranitidine on ulcer formation were assessed. Indomethacin administration initially produced superficial erosions in the corpus and antrum, but with time, ulcers became apparent in the antrum. The formation of these ulcers was dependent upon the number of times indomethacin was administered and the dose. Similar ulcers could be induced with a second NSAID, diclofenac. Misoprostol treatment resulted in a significant reduction in the extent of indomethacin-induced antral ulceration, but ranitidine had no effect. Antral ulcers healed progressively following cessation of indomethacin administration and were almost completely resolved by 108 h after the final dose of indomethacin. These results demonstrate that subcutaneous NSAID administration to rabbits is a simple and reproducible method for producing ulcers that bear striking macroscopic resemblance to NSAID-induced antral ulcers in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Effectiveness of Cisapride in Gastric Ulcer Results of a Double-Blind Randomized Trial Versus Ranitidine and Versus Cisapride plus Ranitidine

Among the factors involved in the pathogenesis of gastric ulcer, the reduced clearing capacity of the stomach seems to play an important role. On this basis, cisapride, which improves gastrointestinal motility, enhances gastric emptying, and prevents duodenogastric reflux, may be effective in the treatment of the gastric ulcer. We randomly allocated 60 consecutive patients, with uncomplicated antral gastric ulcer (diameter 5-25 mm), into three groups of treatment: cisapride 20 mg b.i.d. (C), ranitidine 150 mg b.i.d. (R), cisapride 20 mg b.i.d. + ranitidine 150 mg b.i.d. (C+R). Endoscopic examination with biopsy specimens was performed on admission, after 4 weeks and (if ulcer not healed) after 8 weeks of therapy. Three patients were lost to follow-up (two in C and one in C+R), and three were withdrawn, due to malignant ulcer (one case in R) or to side effects (one case of diarrhea in C, one case of headache in C+R). Healing rates at 4 weeks were 41.1% in C, 52.6% in R, and 50.0% in C+R; at 8 weeks they were 88.2% in C, 89.4% in R, and 94.4% in C+R. Though the lack of a placebo arm makes final considerations difficult, the results were similar in all three groups, with no evident differences. In conclusion, therapy with cisapride appears as effective as H2-blocker alone or combined treatments in healing benign gastric ulcer.

Pepsinogen C gene polymorphisms associated with gastric body ulcer.

This study was aimed to investigate the association of restriction fragment length polymorphisms (RFLPs) for pepsinogen genes with peptic ulcer disease. Eighty unrelated controls, 61 patients with gastric ulcer, and 57 patients with duodenal ulcer were studied. No genetic polymorphisms for pepsinogen A were detected by EcoRI digestion in Japanese subjects but a 100 base pairs insertion-deletion RFLP for the pepsinogen C gene was observed. The allele frequencies of the large (3.6 kilobase EcoRI fragment) and the small fragment (3.5 kilobase EcoRI fragment) were 80.6% and 19.4% respectively in controls, 55.4% and 44.6% in patients with gastric body ulcer, 79.4% and 20.6% in patients with gastric angular ulcer, 71.4% and 28.6% in patients with gastric antral ulcer, and 75.4% and 24.6% in patients with duodenal ulcer. The allele frequency of the small fragment was significantly higher in patients with gastric body ulcer than in controls and in patients with gastric angular or antral ulcer. The genotypes which possessed the small fragment were significantly more frequent in patients with gastric body ulcer (78.4%) than in controls (33.8%) and in patients with gastric angular or antral ulcer (37.5%). These results suggest that there is a significant association between the genetic polymorphism at the pepsinogen C gene locus and gastric body ulcer, and that the pepsinogen C RFLP is a useful marker of the genetic predisposition to this disorder. These results also indicate genetic heterogeneity of gastric ulcer disease, and suggest that the pepsinogen C RFLP may be a useful subclinical marker to explain the differences in genetic aetiologies of gastric body ulcer and gastric angular or antral ulcer.

Misoprostol Healed a Benign Nonsteroidal Antiinflammatory Drug-Induced Gastric Ulcer in a Patient with Pentagastrin-Fast Achlorhydria

A patient with rheumatoid arthritis, who also had documented achlorhydria, first had the diagnosis of an antral ulcer made by barium meal in 1980. She did well taking cimetidine intermittently after that, along with various nonsteroidal antiinflammatory drugs (NSAIDs). In 1988, a shallow antral ulcer was found, but the patient did not respond to H2 blockade or to sucralfate. At that time misoprostol therapy was prescribed. Despite the continued use of NSAIDs, the ulcer healed. It has remained healed for the past 3 years.

Endogenously Released DOPA Is Probably Relevant to Nicotine-Induced Increases in Locomotor Activities of Rats

The effects of capsaicin-sensitive nerve degeneration (capsaicin-treatment) on the corpus and the antrum was investigated in the absolute ethanol-induced lesion model in rats. The gastric lesion in the antrum were significantly aggravated by the capsaicin-treatment, while those in the corpus were not affected. To clarify the different susceptibility between the antrum and the corpus, the effects on gastric mucosal blood flow (GMBF), mucus secretion and levels of calcitonin gene-related peptide (CGRP) or substance P (Sub P), were investigated by the hydrogen gas clearance method, histochemical methods and immunohistochemical methods, respectively. The GMBF in the antrum was significantly decreased by the capsaicin-treatment, but that in the corpus was not. Moreover, capsaicin-treatment increased the mucus secretion in the antrum, but not in the corpus. Capsaicin-treatment significantly decreased CGRP- and Sub P-immunoreactive substances in the vascular smooth muscle in the antrum, but not in the corpus. On the 4th day after absolute ethanol, antral ulcers were observed. From the above results, it was suggested that capsaicin-treatment decreased the gastroprotective ability in the antrum to a greater extent than in the corpus and this may be caused by the decrease of GMBF through the decrease of CGRP- and Sub P-immunoreactive substances.

The rat gastric phospholipids: increased in ulcerated mucosa and decreased after healing.

The composition and content of the gastric phospholipids were followed during development and healing of indomethacin-induced chronic, antral ulcers in rats. The individual phospholipids were identified by thin-layer chromatography and quantitatively estimated by spectrophotometric analysis of phosphate. No changes were found in phospholipid composition and content after a 24-hour fast or during the first 24 h after indomethacin was given. The total phospholipid content and the content of lysophosphatidylcholine and phosphatidylcholine were increased on the 5th day, when chronic ulcers were established. After 4 weeks, when the ulcers were healed, the total phospholipid content, and content of phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol, respectively, were decreased, while the content of lysophosphatidylcholine was increased. In conclusion, the composition and content of gastric phospholipids were altered in rats with ulcers as well as in rats with healed ulcers.

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.

Cytomegalovirus infection and gastric emptying.

Gastrointestinal infection due to cytomegalovirus occurs frequently in liver transplant recipients. Upper gastrointestinal cytomegalovirus infection is associated with subjective complaints of nausea, a sense of abdominal fullness, and occasionally emesis and/or dysphagia. In order to determine whether these symptoms reflect a disruption of the normal motility of the stomach, the following study was performed. Eleven individuals who were evaluated for liver transplantation were prospectively recruited and studied as follows: (1) upper gastrointestinal endoscopy with biopsy of the gastric antral mucosa; (2) viral culture of the gastric mucosa; (3) a histologic examination of the gastric mucosa; and (4) a radionuclide gastric emptying study was obtained before and 4-8 weeks following successful liver transplantation. Prior to liver transplantation, none had symptoms of nausea, vomiting, or epigastric fullness. All were culture-negative for cytomegalovirus. All had endoscopic and histologic evidence of portal hypertensive gastropathy but none had antral erosions or ulcers. All demonstrated normal gastric emptying of a liquid meal. Following liver transplantation, 6 remained free of gastric cytomegalovirus while 5 developed a culture-confirmed gastric cytomegalovirus infection. Those that developed a gastric cytomegalovirus infection also had more gastric symptoms, and more gastric histologic abnormalities. Moreover, those with a gastric cytomegalovirus infection demonstrated enhanced gastric retention of a liquid meal (P less than 0.01).

Antiulcer mechanism of action of rebamipide, a novel antiulcer compound, on diethyldithiocarbamate-induced antral gastric ulcers in rats

The mechanism of the inhibitory action of rebamipide, a new mucosal protective drug, was studied using rats with diethyldithiocarbamate-induced gastric antral ulcers. Rebamipide reduced ulcer formation and inhibited the elevation in lipid peroxide concentration in the gastric mucosa. Rebamipide inhibited both luminol- and lucigen-dependent chemiluminescence of neutrophils activated by formyl-methionyl-leucyl-phenylalanine. Rebamipide did not alter the reduction of cytochrome c induced by the xanthine-xanthine oxidase system or the NADPH-dependent micirosomal lipid peroxidation in the liver. These findings suggest that rebamipide prevents diethyldithiocarbamate-induced gastric ulcer formation by inhibiting neutrophil activation.

Peptic Ulcer Disease in Children

Primary duodenal ulcer disease occurs in children of all ages, but is most often seen in those over 10 years. As in the adult, it often pursues a chronic course. Primary gastric ulcer is seen in children under 6 years, is more unusual, and does not tend to recur. Stress ulcers are seen most often in infants and in critically ill children and are asymptomatic until the complications of hemorrhage or perforation appear. Drug-related ulcers are being seen more frequently as the use of nonsteroidal anti-inflammatory agents increases. With the use of new therapeutic agents, management has been simplified and surgical intervention has become a rarity. Helicobacter pylori is now a recognized cause of antral gastritis and ulceration in the child.

Effects of various mucosal protective drugs on diethyldithiocarbamate-induced antral ulcer in rats

This study was designed to determine the effects of exogenous Cu,Zn-superoxide dismutase (SOD) and various mucosal protective agents against antral ulcer induced by diethyldithiocarbamate (DDC), inhibitor of Cu,Zn-SOD. Exogenous Cu,Zn-SOD reduced ulcer formation and prevented a decrease in SOD activity in gastric mucosa. This result indicates that maintenance of mucosal SOD activity is essential to prevent the ulcerogenicity of DDC. Many mucosal protective drugs that increase blood flow, mucus secretion, and endogenous prostaglandin failed to prevent ulcer formation and decrease of mucosal SOD activity. Rebamipide, however, significantly reduced ulcerogenesis and maintained mucosal SOD activity. This suggests that rebamipide has new protective effects on gastric mucosa.

Reduction of the extent of diethyldithiocarbamate-induced antral gastric ulcer by neutrophil depletion in the rat.

Pharmacology & ToxicologyVolume 68, Issue 2 p. 144-145 Reduction of the Extent of Diethyldithiocarbamate-induced Antral Gastric Ulcer by Neutrophil Depletion in the Rat Keiki Ogino, Keiki Ogino Department of Public Health, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorTatsuya Hobara, Tatsuya Hobara Department of Public Health, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorShinji Oka, Shinji Oka First Department of Internal Medicine, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorHironobu Ishiyama, Hironobu Ishiyama Department of Public Health, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorKatuya Yamasaki, Katuya Yamasaki Tokushima Research Institute, Otsuka Pharmaceutical Co. Ltd., Tokushima 771–01, (Japan)Search for more papers by this authorToshimi Kanbe, Toshimi Kanbe Tokushima Research Institute, Otsuka Pharmaceutical Co. Ltd., Tokushima 771–01, (Japan)Search for more papers by this author Keiki Ogino, Keiki Ogino Department of Public Health, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorTatsuya Hobara, Tatsuya Hobara Department of Public Health, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorShinji Oka, Shinji Oka First Department of Internal Medicine, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorHironobu Ishiyama, Hironobu Ishiyama Department of Public Health, Yamaguchi University, School of Medicine, Ube 755, (Japan)Search for more papers by this authorKatuya Yamasaki, Katuya Yamasaki Tokushima Research Institute, Otsuka Pharmaceutical Co. Ltd., Tokushima 771–01, (Japan)Search for more papers by this authorToshimi Kanbe, Toshimi Kanbe Tokushima Research Institute, Otsuka Pharmaceutical Co. Ltd., Tokushima 771–01, (Japan)Search for more papers by this author First published: February 1991 https://doi.org/10.1111/j.1600-0773.1991.tb02053.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume68, Issue2February 1991Pages 144-145 RelatedInformation

A Reliable Method for the Production of Antral Gastric Ulcer by a Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats.

In order to establish a reliable method for the production of gastric antral ulcer in rats, combined treatments with three factors: a vagal stimulant, a mucosal barrier breaker and a necrotizing agent were investigated. By the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (100-400 mg/kg, p.o.) and hydrochloric acid (0.15 and 0.35 N, 0.5-1.5 ml/100 g, p.o.) or ammonia solution (0.5-1.0%, 0.5-1.5 ml/100 g, p.o.), gastric lesions were prominently induced in sites of both the corpus and antrum on day 2. The largest antral ulcer was induced by the combination of 2-DG (200 mg/kg), aspirin (200 mg/kg) and ammonia solution (1%, 10 ml/kg); and the mean antral ulcer index (mm2) was 43.1 +/- 4.4 and the incidence was 100%. The antral ulcer was found to penetrate the muscularis mucosae and still observed on day 21 and day 28 after ulcer induction in a few cases. From these findings, it was indicated that this antral ulcer would be a useful model for studying the etiology and therapy of gastric ulcer disease.

Aggravation by the Capsaicin-Treatment of Gastric Antral Ulcer Induced by the Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats

The effect of capsaicin-sensitive nerve degeneration (capsaicin-treatment) was investigated on the antral ulcer induction by the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (200 mg/kg, p.o.) and 1% ammonia solution (10 ml/kg, p.o.) in male Sprague-Dawley rats. On the 2nd day after ulcer induction, erosive lesions were seen in the corpus, and ulcers penetrating into the muscularis mucosae were also seen in the antrum. In the capsaicin-treated rats, the antral ulcer was significantly aggravated as compared with that in capsaicin non-treated rats, although no difference was noted in the formation of corpus lesions between capsaicin-treated rats and non-treated rats. Acid output was investigated in pylorus ligated rats. 2-DG significantly increased the acid output. A significant increase in acid output was also observed in capsaicin-treated rats, and this increase tended to be augmented by the additional treatment with 2-DG. Atropine sulfate inhibited the significant increase in acid output of the capsaicin-treated rats. In all rats, both capsaicin-treated and pylorus-ligated, 2-DG induced antral ulcers that penetrated into the muscularis mucosae. From the above results, it was suggested that capsaicin-sensitive nerve degeneration modifies the gastroprotective ability in the antral mucosa to a greater extent than in the fundic mucosa, and this aggravation may be caused by activation of the vagus nerve, although the role of acid is not completely excluded.

Aggravation by the Capsaicin-Treatment of Gastric Antral Ulcer Induced by the Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats.

The effect of capsaicin-sensitive nerve degeneration (capsaicin-treatment) was investigated on the antral ulcer induction by the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (200 mg/kg, p.o.) and 1% ammonia solution (10 ml/kg, p.o.) in male Sprague-Dawley rats. On the 2nd day after ulcer induction, erosive lesions were seen in the corpus, and ulcers penetrating into the muscularis mucosae were also seen in the antrum. In the capsaicin-treated rats, the antral ulcer was significantly aggravated as compared with that in capsaicin non-treated rats, although no difference was noted in the formation of corpus lesions between capsaicin-treated rats and non-treated rats. Acid output was investigated in pylorus ligated rats. 2-DG significantly increased the acid output. A significant increase in acid output was also observed in capsaicin-treated rats, and this increase tended to be augmented by the additional treatment with 2-DG. Atropine sulfate inhibited the significant increase in acid output of the capsaicin-treated rats. In all rats, both capsaicin-treated and pylorus-ligated, 2-DG induced antral ulcers that penetrated into the muscularis mucosae. From the above results, it was suggested that capsaicin-sensitive nerve degeneration modifies the gastroprotective ability in the antral mucosa to a greater extent than in the fundic mucosa, and this aggravation may be caused by activation of the vagus nerve, although the role of acid is not completely excluded.

Protection by Acidified Maalox against Indomethacin-Induced Gastric Antral Ulceration in Hamsters

The protective capability of Maalox against indomethacin-induced gastric damage was evaluated in hamsters. The effect of acidification on the gastroprotection provided by Maalox against such damage was also determined. Maalox was ineffective against indomethacin-induced gastric antral ulceration in hamsters. Acidification of this antacid to pHs of 1.5-3.5 resulted in significant (80-90%) gastroprotection against indomethacin. Macroscopic and histologic evidence of binding by acidified Maalox to the hamster antral mucosa was clearly evident. In summary, no correlation exists between acid neutralization and the gastroprotective capability of Maalox against indomethacin in hamsters. The gastroprotection by acidified Maalox against antral ulceration in this species corresponds well with the reported presence of its hexaaquoaluminum cation moiety at a pH below 4. Such gastroprotection may involve binding of this cation to the hamster pyloric antrum thereby protecting the antral mucosa against indomethacin-induced ulceration.