Experimental models of gastric ulceration and injury

There are inumerable experimental models of gastric mucosal epithelial injury. Many of these currently in wide use can be regarded as unphysiological and severe, rarely encountered in humans. An analysis of more physiological and simple models indicates that little is known of the events that ultimately cause cellular death, even in simple and easily controllable systems. A review of acceptable measures of gastric mucosal injury is presented. It is suggested that studies of subtle physiological injuries at the cellular level are more likely to yield meaningful insights into the causation of gastric mucosal ulceration.

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Endogenous nitric oxide modulates ethanol-induced gastric mucosal injury in rats

Gastroenterology ◽

10.1016/0016-5085(95)90008-x ◽

1995 ◽

Vol 108 (1) ◽

pp. 58-64 ◽

Cited By ~ 63

Author(s):

Eiji Masuda ◽

Sunao Kawano ◽

Kouichi Nagano ◽

Shingo Tsuji ◽

Yoshiyuki Takei ◽

...

Keyword(s):

Nitric Oxide ◽

Mucosal Injury ◽

Gastric Mucosal Injury ◽

Endogenous Nitric Oxide

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Reflux-related gastric mucosal injury is associated with increased mucosal histamine content in humans

Gastroenterology ◽

10.1016/0016-5085(93)90274-g ◽

1993 ◽

Vol 104 (4) ◽

pp. 1057-1063 ◽

Cited By ~ 12

Author(s):

Paolo Bechi ◽

Andrea Amorosi ◽

Roberto Mazzanti ◽

Rosanna Dei ◽

Stefano Bianchi ◽

...

Keyword(s):

Mucosal Injury ◽

Gastric Mucosal Injury ◽

Histamine Content

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ICAM-1 and P-selectin expression in a model of NSAID-induced gastropathy

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.274.2.g246 ◽

1998 ◽

Vol 274 (2) ◽

pp. G246-G252 ◽

Cited By ~ 8

Author(s):

Z. Morise ◽

S. Komatsu ◽

J. W. Fuseler ◽

D. N. Granger ◽

M. Perry ◽

...

Keyword(s):

Endothelial Cell ◽

Critical Role ◽

Mucosal Blood Flow ◽

Gastric Mucosal Blood Flow ◽

Mucosal Injury ◽

Gastric Mucosal Injury ◽

Intercellular Adhesion Molecule ◽

Sprague Dawley ◽

Intercellular Adhesion Molecule 1 ◽

Mucosal Permeability

A growing body of experimental evidence suggests that neutrophilic polymorphonuclear leukocyte (PMN)-endothelial cell interactions play a critical role in the pathophysiology of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy. The objective of this study was to directly determine whether the expression of endothelial cell adhesion molecules is enhanced in a model of NSAID-induced gastropathy. Gastropathy was induced in male Sprague-Dawley rats via oral administration of indomethacin (Indo, 20 mg/kg). Lesion scores, blood-to-lumen clearance of 51Cr-EDTA (mucosal permeability), and histological analysis (epithelial necrosis) were used as indexes of gastric mucosal injury. Gastric mucosal vascular expression of intercellular adhesion molecule 1 (ICAM-1) or P-selectin were determined at 1 and 3 h after Indo administration using the dual radiolabeled monoclonal antibody (MAb) technique. For some experiments, a blocking MAb directed at either ICAM-1 (1A29) or P-selectin (RMP-1) or their isotype-matched controls was injected intravenously 10 min before Indo administration. We found that P-selectin expression was significantly increased at 1 h but not 3 h after Indo administration, whereas ICAM-1 expression was significantly increased at both 1 and 3 h after Indo treatment. The blocking ICAM-1 and P-selectin MAbs both inhibited Indo-induced increases in lesion score, mucosal permeability, and epithelial cell necrosis. However, the Indo-induced gastropathy was not associated with significant PMN infiltration into the gastric mucosal interstitium, nor did Indo reduce gastric mucosal blood flow. We propose that NSAID-induced gastric mucosal injury may be related to the expression of P-selectin and ICAM-1; however, this mucosal injury does not appear to be dependent on the extravasation of inflammatory cells or mucosal ischemia.

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