Role of Intestinal Chyme in the Pathogenesis of Gastric Ulceration Following Experimental Hemorrhagic Shock

Guilbert, Jacques; Bounous, G; Gurd, Fraser N.

doi:10.1097/00005373-196908000-00010

Cited by 35 publications

(9 citation statements)

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“…Hamza and DenBesten [11] have confirmed the observation of Guilbert et al [10] that prevention of pyloric reflux by distal occlusion of the stomach during haemorrhagic shock protects canine gastric muco sa against ulceration. This protective influence was overcome by instilla tion of bile salts into the occluded stomach during shock.…”

Section: Discussionsupporting

confidence: 52%

Role of Pyloric Reflux in Experimental Stress Ulceration during Haemorrhagic Shock

Kivilaakso¹,

Kalima²,

Lempinen³

1975

Eur Surg Res

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The significance of pyloric reflux of bile and duodenal juice in experimental gastric stress ulceration was studied using a swine shock ulcer model. Following a haemorrhagic shock of 3 h duration, nine of the ten control piglets (90%) with normal bile flow have gastric mucosal lesions. None of the five piglets with permanent bile diversion (ligation of common bile duct; cholecystojejunostomy) has gastric lesions. Intragastric instillation of pure bile prior to the shock in piglets with permanent bile diversion induced gastric lesions in only one of the five test animals (20%). If duodenal juice was used instead, four of the six test animals (67%) have lesions. The results indicate that, in the pig, an uninterrupted flow of bile into the duodenum is a prerequisite for the development of gastric mucosal lesions following haemorrhagic shock. They also suggest that duodenal juice containing both bile and pancreatic juice has a stronger ulcerogenic influence on shocked porcine gastric mucosa than bile alone.

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Section: Discussionsupporting

confidence: 52%

Role of Pyloric Reflux in Experimental Stress Ulceration during Haemorrhagic Shock

Kivilaakso¹,

Kalima²,

Lempinen³

1975

Eur Surg Res

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“…This was prevented in our experiments, as was the regurgitation into the stomach of intestinal juice with a high content of lysosomic enzymes as demonstrated by Guilbert et at. [24] in experimental hemorrhagic shock in dogs. The most likely cause of the loss of defensive effectiveness of the gastric mucosal barrier is the loss of mucosal cells.…”

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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“…Sekretionssteigerungen treten regelhaft nur beim neurogenen Cushing-Ulcus oder beim Curling-Ulcus auf [22,43]. Die ulcerogene Wirkung der Gallens~iuren auf die Schleimhaut des oberen Intestinaltraktes ist gut untersucht [ 13,15,20,37]. Die ulcerogene Wirkung der Gallens~iuren auf die Schleimhaut des oberen Intestinaltraktes ist gut untersucht [ 13,15,20,37].…”

Section: J Schleimhautsch~digungunclassified

“…Die Folge ist eine Minderdurchblutung der apikalen Schleimhautareale mit Amputation der DrfisenhSlse. Salzs~iure und Pepsin die Ulcerogenese.GroBe Bedeutung kommt in diesem Zusammenhang auch dem Reflux von Duodeninhalt in den Magen zu[2,13,31,42]. Zusiitzlich l~iSt sich eine Mikrothrombosierung der Gef~iBperipherie unter Schockbedingungen nachweisen, m6glicherweise handelt es sich hierbei um ein sekund~res Ph~inomen der Mikrozirkulationsst6rung.Den Untersuchungen Menguys[26] zufolge bedingt der Sauerstoffmangel eine Verarmung an energiereichen Phosphaten bis hin zum Zusammenbruch des gesamten Schleimhaut-Energiehaushaltes.…”

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Das Stressulcus

Schumpelick

Horatz

1977

Langenbecks Arch Chiv

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Stress ulcer means an acute mucosal lesion of the upper gastrointestinal tract in sick patients, who have not had gastroduodenal ulcer before. Most often stress ulcers follow big operations, burns and different types of shock. Complications as respiratory insufficiency, paralytic ileus or infections favor the ulcer formation. The average age is 53 years, males are more often affected. The main localisation is the proximal stomach, less frequently the lesions are located in the duodenum and terminal oesophagus. The macroscopic type is an erosion or a superficial ulceration, a solitary ulcer is typically situated in the duodenum. From the view of pathogenesis three factors are mainly involved: hydrochlorid acid, a disturbance of microcirculation due to shock and a duodenogastric reflux of bile acids and lysolecithin. Most frequent symptom is upper gastrointestinal bleeding, but more than 50% are symptomless. Medical treatment is successful in 60-70%. The surgical treatment of choise is vagotomy in combination with circular sature or resection. Prevention of shock or respiratory insufficiency, permanent gastric suction, early food administration and intragastral application of antacids and cholestyramin are the essentials of stress ulcer prophylaxis.Key words: Stress ulcer -Acute gastric mucosal lesion (AGML) -Gastric mucosal barrier-shock.Lange Zeit wurde vermutet, dab Stressulcerationen mit einer Hypersekretion ein-

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Role of Intestinal Chyme in the Pathogenesis of Gastric Ulceration Following Experimental Hemorrhagic Shock

Cited by 35 publications

References 0 publications

Role of Pyloric Reflux in Experimental Stress Ulceration during Haemorrhagic Shock

Role of Pyloric Reflux in Experimental Stress Ulceration during Haemorrhagic Shock

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

Das Stressulcus

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