Gastric emptying in patients with peptic ulcer and normal subjects was studied using the acetaminophen method. The subjects consisted of 15 normal subjects, 52 gastric ulcer patients and 65 duodenal ulcer patients, who were studied in active stage of the ulcer. As an indicator of gastric emptying, the plasma acetaminophen concentration was measured by dye method (diphenylhydrazyl), as mcg/ml, at 45 minutes after ingestion of a high calory pasty test meal (200 ml) with 1.5 gr of acetaminophen. In normal subjects, the plasma acetaminophen concentration was 9.4 +/- 3.6 mcg/ml. In gastric ulcer patients, the concentration was 7.4 +/- 3.2 mcg/ml, which showed significantly delayed gastric emptying (P less than 0.05). In duodenal ulcer patients, the concentration was 11.6+/-3.3 mcg/ml, which suggested significantly rapid gastric emptying (P less than 0.05). In consideration of gastric secretion, gastric ulcer cases with lower acid secretion have more delayed gastric emptying. In duodenal ulcer cases with hypersecretion, gastric emptying is more rapid than normo-and/or hyposecretory cases (P less than 0.005). The delayed gastric emptying may play a role in etiology of gastric ulcer. On the other hand, the rapid gastric emptying with gastric acid hypersecretion may be important in the pathogenesis of duodenal ulcer.

This study was designed to compare the effects of omeprazole and cimetidine on ultrastructural changes in parietal cells of guinea pigs during histamine stimulation. Both omeprazole and cimetidine remarkably inhibited acid secretion induced by histamine stimulation. Omeprazole, however, failed to prevent the morphological transition of parietal cells to an active stage during histamine stimulation, in contrast to cimetidine which inhibited the morphological transition. In addition, it was noticed that administration of omeprazole caused vacuolation in approximately 27% of all parietal cells. This phenomenon was not seen in control animals with histamine stimulation alone and only very rarely in cimetidine treated animals. Ultrastructural findings suggested that vacuoles originated in secretory canaliculi of parietal cells. These results may be the key to explain the difference of the inhibitory mechanism between omeprazole which acts on the final step of intracellular process (so-called proton pump) and cimetidine which acts on the H2-receptor site of plasma membrane.

The VT(+) strain of H. pylori has an inhibitory effect on gastric acid secretion, whereas the VT(-) strain does not. This inhibitory effect was not associated with the response of second messengers. It is speculated that VT produced by H. pylori has a direct action on H(+)-K+ adenosine triphosphatase in parietal cells.

Endoscopy of the upper gastrointestinal tract was performed on 84 patients with end-stage chronic renal failure undergoing hemodialysis. Gastric acid secretion and fasting plasma gastrin levels were also examined in these patients. Hemorrhagic gastritis was most frequently observed (23 cases) followed by erosive gastritis (18 cases). No patients had gastric ulcers. Duodenal ulcers were observed in only two patients. Gastrointestinal bleeding was observed in 15 cases (17.9%). Thirteen of these 15 cases had hemorrhagic gastritis, one of which had a duodenal ulcer as a complication. Fasting plasma gastrin levels (359.6 +/- 336.5 pg/ml) were significantly higher than those of normal subjects (35.2 +/- 37.1 pg/ml), but no acceleration in gastric acid secretion was observed either in the basal condition (BAO 0.8 +/- 0.7 mEq/h) or following tetragastrin stimulation (MAO 9.0 +/- 6.9 mEq/h). Our results were inconsistent with the previous reports that high frequencies of peptic ulcers and increased gastric acid secretion were observed in patients with chronic renal failure. Our data suggest that the defensive factors rather than the aggressive factors of the gastroduodenal mucosa may be involved in chronic renal failure.

Background/Aim: There have been only a few studies on the distribution of calcitonin gene-related peptide (CGRP) in the human stomach, in which it was stated that CGRP fibers are rare in that organ. The aim of the present study was to investigate the immunohistochemical localization of CGRP in the human gastric mucosa obtained by endoscopic biopsy from patients with gastric ulcers. Methods: Immunohistochemistry was carried out according to the indirect immunoperoxidase method using an anti-human CGRP antibody. Biopsies were taken from the ulcer margin in 18 patients (age 37–78, average 57.4 years) and from two endoscopically normal portions (antrum and body) in 7 other patients (age 36–65, average 51.0 years). One biopsy specimen was obtained from each portion. Results: Twelve of the eighteen biopsy specimens from the ulcer margin, 6 of the 7 biopsy specimens from normal portions of the antrum and 3 of the 7 biopsy specimens from normal portions of the body showed CGRP-immunoreactive staining. Intense staining was more marked in the specimens from the ulcer margin compared to those of the normal portions. Conclusions: CGRP immunoreactivity was observed in the human gastric mucosa in considerable abundance, and it is presumed that CGRP might participate in a restoration mechanism of the ulcer.