Preventive Effect of Proglumide on Erosive Gastritis in the Rat

The purpose of this study is to determine whether or not proglumide has a preventive effect on the erosive gastritis induced by sodium salt of taurocholic acid (TCA) in the rat. Its effect on the formation of gastric erosions, serum gastrin levels and secretion of acid and pepsin were also studied. The rats were given standard feed containing 0.25% proglumide and water containing 5mM TCA (experimental E group). The control rats were given standard feed and water containing 5mM TCA (TCA group). All rats were killed at the end of the 3 months. The tissue specimens of the resected gastric mucosa were stained with hematoxylin eosin for histopathology and with azan for evaluation of fibrous ploriferation. From microscopic observation of the stained specimens, the following results were obtained. TCA-group showed long mucosal surface injury (erosion), inflammatory cell infiltration, a reduction in the number of parietal cells, a decrease of mucosal thickness, and proliferation of collagenous fiber. In contrast, in the E group, these morphological and morphoquantitative changes were significantly small. The length of erosion and inflammatory cell infiltration were significantly reduced in the E group when compared with the TCA group. Furthermore, mucosal thickness was almost normal and fibrous proliferation was significantly scarce in the E group. Proglumide had an insignificant effect on pH on the mucosa, volume and pH of gastric juice, serum gastrin levels and tetragastrin-induced secretion of acid and pepsin. It is, thus, evident that proglumide has a preventive effect on the induction of erosive gastritis caused by TCA in the rats. Since it is difficult to explain its mechanism for the prevention of gastritis from only the already known facts that it has protective action on gastric mucosa and an inhibitory effect on secretion of acid and pepsin, unknown mechanisms are suspected to be involved

A Galanin-Like Peptide in the Colon of the Golden Hamster

Galanin-like immunoreactive peptide was studied in the colonic wall of the golden hamster using the immunoflurescent technique. Galanin-like immunoreactivity was observed mainly in cell bodies of the myenteric plexus and in fibers in the lamina propria mucosae and in the circular muscle layer. The submucosal plexus and submucosal connective tissue, however, contained very little galanin-like immunoreactive peptide. This peptide appears to be instrinsic mainly to the colon. The presence of the peptide indicates some possible biological roles in the colonic function

Existence of VIP and PHI-Like Immunoreactivities in the Amphibian Gut

The present paper provides the first definitive evidence on the presence and possible co-existence of VIP- and PHI-like peptides in the peripheral nervous system of the amphibian (bullfrog) gut wall. The possibility of co-existence of the peptides suggests that VIP- and PHI-like peptide may be synthesized from the same precursor protein in the amphibian

Gastrin and Somatostatin in Patients with Hyperchlorhydric Duodenal Ulcer

Hormonal and morphological studies were conducted to ascertain the role played by gastrin and somatostatin in the pathophysiology of duodenal ulcer, in particular hyperchlorhydric duodenal ulcer, using 35 patients with duodenal ulcer, of whom 15 were hyperchlorhydric and 20 were normochlorhydric. Twenty normal subjects with normochlorhydria were used as a control. In patients with hyperchlorhydric duodenal ulcer following significant findings were observed: 1. Basal and stimulated hyperchlorhydria, 2. Parietal cell hyperplasia, 3. Basal hypergastrinemia, 4. Increased concentration of gastrin and large number of G cells (G cell hyperplasia) in the antral mucosa. 5. Mucosal concentration of somatostatin and D cells in the antrum was reduced, but the former in patients with hyperchlorhydric duodenal ulcer was not different from that in patients with normoacidic duodenal ulcer. 6. A significant correlation in mucosal concentration was demonstrated between gastrin and somatostatin in control subjects but not in patients with duodenal ulcer. 7. There was a significant correlation in maximal acidity in gastric secretion and mucosal concentration of antral somatostatin in control subjects but not in patients with duodenal ulcer. 8. Concentration of plasma somatostatin in patients with duodenal ulcer was not different from that in control subjects. These findings indicate that gastrin and somatostatin may participate in the pathophysiology of duodenal ulcer, at least in the subgroup of duodenal ulcer associated with hyperchlorhydria, and the subgroup of duodenal ulcer may be an endocrine disorder

ヒトにおける糖尿病およびその治療が胆汁の胆石形成度に及ぼす影響

Bile lipid and bile acid compositions of twenty-five diabetic patients (eight males and seventeen females) were compared with those of twenty normal subjects and twelve non-diabetic patients with cholesterol gallstone. Diabetic patients were grouped into the untreated, insulin-treated and untreated patients with gallstone. The results are as follows. The average molar percentage of cholesterol and incidence of lithogenic bile were higher in all the groups of diabetic patients as well as nondiabetic cholesterol gallstone patients than in normal subjects. However, the incidence of lithogenic bile was distinctly higher in diabetic patients treated with insulin and patients with gallstone as compared with untreated patients. The average molar percentage of phospholipids was significantly higher in diabetic patients untreated and treated with insulin than normal controls but was almost normal in diabetic patients with gallstone and non-diabetic cholesterol gallstone patients. Diabetic patients treated with insulin and those with gallstone tended to have a low molar percentage of chenodeoxycholic acid, which was significant in non-diabetic gallstone patients. These results may indicate that the diabetic patients who fall into gallstone have the bile lipid and bile acid compositions that differ from those of diabetic patients without gallstone and that the insulin administration deteriorates lithogenesity of bile in diabetic patients