Zur Pathogenese stressbedingter Magenulcera

Klein, H. J.; Gheorghiu, T; Hübner, G; Eder, M.

doi:10.1007/bf00600670

Cited by 16 publications

(3 citation statements)

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“…The energy deprivation of the mucosa seems to be a consequence of the hypoxia resulting from initial vascular changes. Klein et al [29], employing phase microscopy, found the earliest changes to be constriction of the submucosal arterioles, followed by a stage of capillary stasis resulting finally in mucosal erosion. Our histopathologic observations demonstrated necrosis of the mucosa only in the highest grade lesions.…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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

et al. 1980

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“…Furthermore microcirculatory investigations on the pharmacological action of dopamine on the vessels of the gastric mucosa are lacking. The results communicated to date show that, depending on the dose, dopamine produce both vasodila tation and vasoconstriction in the mesenteric vascular beds through an action on the a-and ^-adrenergic receptors and on specific vascular dopamine receptors [8], It seems not to be excluded, however, that dopamine plays a part in the contractions of the arterioles of the submucosa and muscularis mucosae which can be detected in the early stages of stress electronoptically [22] and by the injection of India ink as well as silicone rubber perfusion techniques [16]. However, in the assessment of a possible pathogenetic mech anisms of dopamine in the formation of erosion, it is difficult to understand that the ulcers are localised exclusively in the glandular part of the stomach while the DDC is localised in the enterochromaffine-like cells of the antrum [2,3,12].…”

Section: Dopa Decarboxylase and Restraint Ulcermentioning

confidence: 99%

“…mucosa and that during the early stages of their development a constriction of the arterioles of the submucosa and muscularis mucosae is to be seen at first [16,22] and later a dilatation of the capillaries of the gastric mucosa [10,11,22] suggests that vascular mechanisms play an important part in the pathogenesis of restraint ulcers. Participation of vasoactive substances is shown by the fact that erosions and ulcers of the gastric mucosa may be in duced by the administration or liberation of biogenic amines such as his tamine [39,44], serotonin [25,29,36], adrenaline and noradrenaline [27,40], The object of the present experiments is to look for a possible relationship between the development of erosions and the activity of histidine decarboxy lase (EC 4.1.1.22) and dopa decarboxylase (EC 4.1.1.26), which produce the powerful vasoactive histamine and dopamine.…”

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confidence: 99%

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

Schauer¹,

Kunze²,

Feifel³

et al. 1974

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The activities of the specific histidine decarboxylase (EC 4.1.1.22) and dopa decarboxylase (EC 4.1.1.26) were determined radiometrically in the glandular portion of the stomach of 250 female rats in restraint stress induced by immobilisation at 2-hour intervals during a period of 2–30 h. After 3 h the histidine decarboxylase showed a continuous increase in activity and attained a maximum of more than twice the activity in the control animals between 9 and 11 h, respectively. The dopa decarboxylase activity was only moderately raised until 11–13 h after the beginning of immobilisation and revealed twice the activity after 13–15 h. Subsequently, the activity of both amino acid decarboxylases decreased and dropped to below the normal level after 21 h. The induction mechanisms and the significance of the increased amounts of histamine and dopamine formed for the vasculature of the gastric mucosa and for the development of erosions are discussed.

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