The Role of Bile and Acid in the Production of Esophagitis and the Motor Defect of Esophagitis

Henderson, Robert D.; Mugashe, F; Kn, Jeejeebhoy; Cullen, J; Szczepański, Michał; A, Boszko; Marryatt, G

doi:10.1016/s0003-4975(10)65257-5

Cited by 45 publications

(16 citation statements)

References 10 publications

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“…In our experiment, pancreatic reflux by itself pro duced no esophageal lesion by the 7th post operative day. Nevertheless, total gastrec tomy and bile duct ligation in the rat is of poor physiological value and, on the other hand, the effect of trypsin is reported to be slow and weak in the absence of acid [12], Our results differ from those given by Safaie-Shirazi et al [13] and Henderson et al [5,14], who demonstrated that mucosal ul ceration in the animal developed only when both HCI and bile salts were instilled into the esophagus. Other conditions obviously can create ulceration of the esophageal mucosa, i.e., bile reflux was sufficient in our experi ment to create severe esophagitis [15], Kranendonk et al [6] found contradictory results from ours with identical animal mod els: pancreatic and acid secretions were nec essary to obtain the higher degree of mucosal alterations.…”

Section: Discussioncontrasting

confidence: 86%

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Bile Reflux Esophagitis

Salmon

Hem

1981

Digestion

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This study was designed to determine the relative contribution of acid and/or duodenal contents on development of reflux esophagitis in the rat. Gross and microscopic changes in the esophageal mucosa at 10, 15, 30, and 60 days were recorded in sham-operated animals and in two experimental groups. One study group had a transsection of the esopha-gogastric junction (model I), and the other a total gastrectomy (model II). Bowel continuity was reestablished by esophagojejunal anastomosis. Subgroups of both animal models received either no treatment or cholestyramine or aluminum phosphate for 30 days in drinking water. At 30 days a similar degree of esophagitis was found in the untreated animals of both study models. Cholestyramine improved the degree of esophagitis in model II, whereas aluminum phosphate increased mucosal alterations in model I. At 60 days, 50% of the animals no longer had esophagitis and had regained satisfactory nutritional status. It is concluded that: (1) bile reflux is a major factor in esophagitis; (2) cholestyramine protects against bile reflux, and (3) proper nutritional status is of major importance in mucosal healing.

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Section: Discussioncontrasting

confidence: 86%

“…Photographs and slides were coded randomly. Macroscopic or 'clinical esophagitis' [5,6] was graded at each grade given a number of (+) in order to simplify the statistical analysis. The grading was as follows: Grade I, mild edema (+); grade II, linear ulceration of mucosa (++).…”

Section: Methodsmentioning

confidence: 99%

Bile Reflux Esophagitis

Salmon

Hem

1981

Digestion

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“…Since Helsingen's experiments (1959;1960), many experiments attempting to elucidate the pathogenesis of reflux esophagitis have been performed (Henderson et al, 1972;Siroos et al, 197.5;Salmon and Hem, 1981;Mud et al, 1982;Lehnert et al, 1983). Levrat et al (1962) concluded that reflux esophagitis develops when duodenal contents regurgitate into the esophagus.…”

Section: Referencesmentioning

confidence: 99%

The role of alkaline reflux in esophageal carcinogenesis induced by N‐amyl‐N‐methylnitrosamine in rats

Seto

Kobori

Shimizu

et al. 1991

Intl Journal of Cancer

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It is now accepted that the incidence of esophageal carcinoma is highest in the middle thoracic region. Esophageal carcinoma after gastrectomy, however, has a tendency to develop in the lower thoracic region. These studies suggest a possible correlation between the development of esophageal carcinoma and gastrectomy, i.e., alkaline reflux into the esophagus. To elucidate this correlation, the role of alkaline reflux of duodenal contents in the development of esophageal squamous-cell carcinoma induced by N-amyl-N-methylnitrosamine (AMN) was investigated in Wistar rats. The animals were divided into 3 groups; gastrectomized rats with or without regurgitation of duodenal contents into the esophagus, and control rats without gastrectomy. All received low doses of AMN for 8 weeks and were subsequently killed for pathological examination. Esophageal squamous-cell carcinomas were found only in gastrectomized rats with regurgitation. The carcinomas were found exclusively in areas of reflux esophagitis and were accompanied by severe dysplasia. Our results indicate that alkaline reflux of duodenal contents strongly contributes to the development of esophageal squamous-cell carcinoma.

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“…), and esophageal acid clearance (1,2). The response of the esophageal mucosa to noxious substances and in particular to hydrochloric acid (HCl) has also been investigated (3)(4)(5)(6)(7)(8)(9)(10)(11). However these studies attempted to clarify the mechanism of acid injury to the mucosa by measuring the lumenal disappearance of hydrogen ion (H+), an indirect indicator of tissue damage, and/or by assessing the histology of the injury at one point in time.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of acute acid injury in rabbit esophageal epithelium.

Orlando¹,

Powell²,

Carney³

1981

J. Clin. Invest.

128

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A B S T R A C T To increase our understanding of the pathophysiology of reflux esophagitis, we sought the early sequence of changes in mucosal structure and function in acutely acid-damaged rabbit esophagus. Using a perfused catheter technique esophageal potential difference (PD) profiles were obtained in anesthetized rabbits before, during, and after perfusion of the lower one-half of the esophagus with phosphatebuffered saline or 80 mM HCI-80 mM NaCl. When acid perfusion reduced the lower esophageal PD by 40-50% or 80-100% of the initial values, the esophagus was removed, sectioned, and the mucosa studied with light microscopy, transmission electron microscopy, and Ussing chamber technique for evaluation of sodium and mannitol transport. The earlier stage of acid damage (PD 140-50%) was associated with reduced mucosal resistance from 2,180±+199 to 673±+157 ohm * cm2 and increased passive transport of sodium (0.10+0.06 to 1.82 +0.48 geq/h .cm2) and mannitol (0.008+0.003 to 0.051±0.012 MM/h -cm2) (P < 0.05).There was no significant change in short circuit current (0.35±0.05 to 0.35±0.04) or net sodium transport (0.32±0.06 to 0.37±0.12) at this stage, and the only morphologic finding was dilated intercellular spaces on electron microscopy. The later stage ofacid damage (PDJ80-100%) exhibited a further reduction in resistance to 299±65 ohm cm2 (P < 0.05), a finding now accompanied by a reduction in short circuit current (0.35±0.05 to 0.21±0.04 Aeq/h -cm2) and complete inhibition of net sodium transport (0.32±0.06 to 0.01 ±0.13) (P < 0.05). Morphologic studies at this time revealed cellular necrosis, edema, and vesicle formation in the stratum spinosum. Both gross mucosal changes and transmural necrosis were notably absent. When esophageal perfusion was performed with a combination of acid (80 mM HCG-80 mM NaCl) and pepsin (100 ,ug/ml), the morphologic and physiologic findings were essentially the same as with acid alone; however, the time of perfusion to reach either the 50 or 100%

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The Role of Bile and Acid in the Production of Esophagitis and the Motor Defect of Esophagitis

Cited by 45 publications

References 10 publications

Bile Reflux Esophagitis

Bile Reflux Esophagitis

The role of alkaline reflux in esophageal carcinogenesis induced by N‐amyl‐N‐methylnitrosamine in rats

Pathophysiology of acute acid injury in rabbit esophageal epithelium.

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