Effect of aging on gastric mucosal proliferation in rats treated with aspirin.
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Adaptation, Physiological↗
Biomedical subjects
V Kranz
Publications and source records attributed to V Kranz.
Helicobacter pylori infection does not increase gastric antrum mucosal cell proliferation.
OBJECTIVES: Gastric carcinoma is the world's second most common cancer. Recent studies suggest an association between Helicobacter pylori and gastric carcinoma. The aim of this study was to address the effects of H. pylori infection on gastric antrum mucosal cell proliferation. METHODS: Forty patients undergoing upper endoscopy for standard indications were included in the study. A rapid urease test was used to determine the presence of H. pylori. Epithelial cell proliferation was determined by immunohistochemical techniques utilizing monoclonal antibody to bromodeoxyuridine. RESULTS: There were no significant differences in the number of labeled cells and in the proliferation fraction (p > 0.1) when patients with H. pylori were compared with those without, and when those over the age of 50 were compared to those under 50. The presence of ulcers similarly had no effect (p > 0.1). CONCLUSION: Helicobacter pylori infection does not increase gastric antrum mucosal cell proliferation.
Age Factors↗
P amylase is always greater than S in spot urine of normal subjects. Diagnostic implications.
Single random samples of urine were collected from 50 control subjects; 27 patients with chronic pancreatitis; 19 with acute pancreatitis; 6 with acute on chronic pancreatitis; five in the recovery phase of acute attack; four patients with pseudocysts. Salivary (S) and pancreatic (P) amylase values were measured by cellulose acetate electrophoresis. The P amylase values always exceeded those of S amylase in the control specimens. In acute pancreatitis, both the lower and upper levels of total and P amylase were considerably higher than in the controls, and these high values tended to return to normal during the recovery phase of acute pancreatitis. The S amylase values were often very low or undetectable during the acute phase. Values for P amylase exceeded control values in patients with pseudocysts even in the presence of chronic pancreatitis. In chronic calcific pancreatitis, S amylase was higher than P amylase. We conclude that P amylase is always greater than S amylase in normal urine specimens, and a change in this pattern may be helpful in diagnosing various forms of pancreatitis.
Amylases↗
Effects of the cholecystokinin receptor antagonist L-364,718 on experimental pancreatitis in mice.
The effects of the cholecystokinin receptor antagonist L-364,718 was studied in a model of mild pancreatitis induced in mice by repeated injections of the secretagogue caerulein and in a lethal form of pancreatitis induced by feeding mice an ethionine-supplemented choline-deficient diet. L-364,718 prevented the caerulein-induced rise in serum amylase and pancreatic weight in a dose-dependent manner, the most effective dose being 0.1 mg/kg body wt. L-364,718 also prevented the caerulein-induced pancreatic inflammation as seen by light microscopy. L-364,718 offered no protective effects as determined by changes in serum amylase, pancreatic weight, histology, or mortality in the ethionine-supplemented choline-deficient diet model.
Amylases↗
Prevention of duodenal ulcers in the rat using a combination of ranitidine and sucralphate in subtherapeutic doses.
This study investigated whether ulcer prevention would be greater with the combined use of an acid-inhibiting agent, ranitidine, given together with a mucosal-protective agent, sucralphate. Duodenal ulcers were induced in rats with the secretagogues pentagastrin and bethanechol. Subtherapeutic doses of ranitidine (5 mg/kg/6 hours) and sucralphate (50 mg/6 hour) yielded an ulcer index of 4.0 and 4.1 respectively, not significantly different from the control (untreated) ulcer index of 4.3. Therapeutic doses of ranitidine (20 mg/kg) and sucralphate (200 mg/animal) gave an ulcer index of 0.4 and 0.5 respectively. Subtherapeutic doses of ranitidine and sucralphate given in combination yielded an ulcer index of 0.7. Thus, subtherapeutic doses of ranitidine and sucralphate given in combination had a synergistic effect equal to therapeutic doses of each of these drugs given alone. The therapeutic implications of combined acid inhibiting drugs with mucosal protective drugs is discussed.
Aluminum↗
Prevention of experimental duodenal ulcer in the rat by sucralfate.
We examined the ability of sucralfate to prevent secretagogue induced duodenal ulcer in the rat. Sucralfate was administered orally in dosage schedules of 50 mg, 100 mg or 200 mg before and at 3 and 6 hr after commencing a 24 hr continuous infusion of pentagastrin and bethanechol. The animals were sacrificed at 24 hr and the number and severity of ulcers was scored. Ulcers developed in all 9 control rats, in 8 of 9 on the 50 mg dose, in 4 of 9 on the 100 mg dose, and in only 1 of 9 on the 200 mg dose of sucralfate. We conclude that sucralfate prevents the formation of secretagogue induced duodenal ulcer in the rat.
Aluminum↗