1990 Fiscal Year Final Research Report Summary
Experimental and Clinical Studies on Pathophysiology and Treatment of Peptic Ulcer Disease
| Project/Area Number |
01440055
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | The Jikei University School of Medicine |
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Principal Investigator |
AOKI Teruaki The Jikei University School of Medicine Second Department of Surgery, Chief Professor, 医学部・第2外科俊教室, 教授 (20056708)
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| Co-Investigator(Kenkyū-buntansha) |
KASHIWAGI Hideyuki The Jikei University School of Medicine Second Department of Surgery, Lecturer, 第2外科学教室, 講師 (40185757)
AKIMOTO Hiroshi The Jikei University School of Medicine Second Department of Surgery, Lecturer, 第2外科学教室, 講師 (20138704)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Cysteamine / Gastrin / Somatostatin / Famotidine / Prostaglandin E / Adrenalin / Duodenal Ulcer / Peptic Ulcer |
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| Research Abstract |
Experimental Studies : In Wistar male rats, cysteamine increased acid secretion stimulated by adrenalin which resembled that in duodenal ulcer patients. And cysteamine induced increase of gastrin secretion and decrease of somatostatin secretion. Adrenalin-stimulated acid secretion seemed to be related to gastrin and somatostatin secretion. Long-term famotidine administration induced hypergastrinemia and increase of antral gastrin-producing cells (G-cells). And pyloric stenosis induced hypergastrinemia, increase of G-cells and somatostatin-producing cells (D-cells). But famotidine administration suppressed the increase of D-cells by pyloric stenosis. Long-term prostaglandin E administration increased D-cell number, which seemed to suppress the hypergastrinemia by long-term famotidine administration.
Clinical studies : Adrenalin drip infusion (40ng/Kg/minx60min.iv) induced increasing acid secretion in peptic ulcer patients. But it decreased acid secretion in healthy volunteers. Duodenal ulcer patients with perforations had higher basal and insulin-stimulated acid output, but patients with pyloric stenosis had higher basal and adrenalin-stimulated gastrin secretion. Adrenalin-stimulated gastrin secretion, which was abolished by propranolol administration, seemed to be related to antral G-cell numbers and adrenalin-stimulated acid secretion. Duodenal ulcer patients with increased adrenalin-stimulated acid secretion (>10mEq/hr) needed vagotomy and antrectomy for cure of ulcer.
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