Increased Histidine and Dopa Decarboxylase Activity in the Rat Stomach during Restraint Ulcer Formation

Schauer, A.; Kunze, Ekkehard; Feifel, G.; Permanetter, W.; Fraps, P

doi:10.1159/000197565

Cited by 7 publications

(2 citation statements)

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“…Schauer et al [34] have also tbund a markedly increased histidine decarboxylase activity within 9-11 hours of restraint. Histamine would act both through vascular mechanisms (arteriolar and capillary vasodilation, permeability increase), and through its effect on HCI and pepsinogen secretion.…”

Section: Discussionmentioning

confidence: 93%

“…The role of histamine is suggested by its decreased concentration in the gastric mucosa after restraint-stress and by the increased histidine decarboxylase activity. Schauer et al [34] have also tbund a markedly increased histidine decarboxylase activity within 9-11 hours of restraint. Histamine would act both through vascular mechanisms (arteriolar and capillary vasodilation, permeability increase), and through its effect on HCI and pepsinogen secretion.…”

Section: Discussionmentioning

confidence: 93%

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Restraint‐induced stress ulcer. II. biochemical and ultrastructural studies of gastric mucosa

et al. 1980

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The aim of these studies was to evaluate the light and electron microscopic changes of the gastric mucosa of restrained rats, and to determine if there were correlations between structural changes, histidine decarboxylase activity, histamine content, and gastric secretion.In areas with high-grade mucosal lesions, signs of functional hyperactivity of the oxyntic and chief cells and cytoplasmic degranulation of the enterochromaffin-like cells were observed. These changes were not influenced by vagotomy. The hyperactivity of the chief cells was related to a higher proteolytic activity of the gastric juice and to an increased excretion of uropepsinogen (p < 0.01). The hyperactivity of the oxyntic cells was not accompanied by an increase in total acidity, which could be explained by hydrogen ion back-diffusion through a damaged gastric mucosal barrier. The increase in histidine decarboxylase activity (p < 0.01) and the decrease of histamine content (p < 0.01) in the glandular mucosa of restrained rats, together with the microscopic and ultrastructural observations, suggest that the early microcirculatory changes are due to local alterations in the metabolism of vasoactive amines.Among the mechanisms involved in the pathogenesis of restraint ulcers, special significance has been attributed to acid hypersecretion, damage to the gastric mucosal barrier with H + back-diffusion, andPresented at the XXVIIth Congress of the Socidt6 Internationale de Chirugie, Kyoto, Japan, September 3-8, 1977.Reprint requests: Professor J.L. Balibrea, Department of Surgery, Autonomous University of Barcelona, Bellaterra (Barcelona), Spain. At present, special attention is directed toward the properties of the enterochromaffin cell system, described in the gastric mucosa of the rat by H~kan-son et al. [7], because of its high histidine and dopa decarboxylase activities. The existence of increased histidine decarboxylase activity in the mucosa of restrained rats [8] suggests a role for histamine in the genesis of restraint-induced ulcers, both through its influence on acid and peptic secretions and through microcirculatory effects that might disrupt the gastric mucosal barrier [9].The purpose of the experiments described in this report was to study the effects of restraint stress, in the absence of biliary reflux, on acid and mucus secretion and on proteolytic activity of gastric juice. Histidine decarboxylase and histamine content of the gastric mucosa and the effects of vagotomy on

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 93%