消化性潰瘍の成因に関する実験的研究--Cysteamine十二指腸潰瘍について
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概要
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The present experimental studies were carried out to clarify the pathogenetic differences between duodenal ulcer (DU) and gastric ulcer (GU) using cysteamine-induced DU model rats. First, a limited number of several gastric inhibitory agents were given to determine whether these agents inhibited DU formation and gastric secretion induced by cysteamine administration. In addition, attempts were made to determine the gastroduodenal mucosal changes in cysteamine treated rats combined with the methods used for induction of experimental GU formation. Secondly, intraduodenal infusion of HCl and pepsin solution was undertaken to observe their respective effects on the duodenal mucosa. The results obtained were as follows; 1) Atropine, cimetidine and somatostatin remarkably inhibited DU formation and gastric acid and pepsin secretions in cysteamine treated rats. In contrast, these agents did not always exert an influence on the increased values of blood gastrin and corticosterone levels arising from cysteamine administration. 2) Scanning electron microscopic findings showed marked degeneration and desquamation of the epithelial columnar cells, constituting duodenal villi, after cysteamine administration. These mucosal lesions were significantly decreased by pretreatment with these gastric inhibitory agents. These findings seemed to be in parallel with the histological findings obtained in the present studies. 3) Acute gastric mucosal lesions induced by cold restraint stress and oral administration of indomethacin were evidently inhibited by cysteamine administration. These phenomena seemed to participate in the increase of neutral mucoprotein and mucin-like glycoprotein M1 fraction induced by cysteamine administration. On the other hand, duodenal mucosal lesions induced by cysteamine administration seemed to be prevented to some degree in rats kept under cold restraint stress conditions, and the prevention mechanism appeared to be related to the increase of Brunner's gland secretion. 4) Local mucosal lesions following the intraduodenal infusion of HCl and pepsin solutions seemed to be similar to those produced by cysteamine administration. From these findings, it was suggested that some abnormalities of the gastric mucosal barrier were mainly involved in the GU formation. On the other hand, it was assumed that the excess secretion of gastric acid and pepsin, disturbance of blood circulation in the duodenal mucosa and marked changes of several humoral factors participated in the formation and development of DU.
- 札幌医科大学の論文
札幌医科大学 | 論文
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