Abstract
The lining of the stomach of man is protected from its unique secretion, hydrochloric acid, by a variety of highly specialized characteristics. Foremost is its relative impermeability to hydrogen ions. The gastric surface epithelial cell which forms a continuous integument from the esophagus to the duodenum plays an important role in this barrier function. Disruption of the barrier by injurious agents, sepsis, or shock may lead to severe erosive gastritis when acid is present within the lumen of the stomach. This process is accelerated during periods of low mucosal blood flow. The relationship of the rate of back-diffusion of hydrogen ions to mucosal blood flow appears critical. Factors which (a) inhibit acid secretion, (b) strengthen the barrier to H+ diffusion, or (c) increase mucosal blood flow will protect the stomach from injury. Prostaglandins of the A, E, and F series offer a level of protection in experimental erosive gastritis that is out of proportion to their effect on acid secretion and mucosal perfusion. The secretion or filtration of an alkaline secretion may be an important component of the cytoprotection which follows the topical exposure of gastric mucosa to 16,16-dimethyl (PGE2). The role of mucus release in this situation requires further elucidation.
Résumé
La paroi gastrique de l'homme est protégée contre sa propre sécrétion, l'acide chlorhydrique par plusieurs mécanismes hautement spécialisés. Le plus important est l'imperméabilité relative de la muqueuse aux ions hydrogènes. Les cellules de l'épithélium de surface, qui tapissent en une couche continue tout l'estomac depuis l'oesophage jusqu'au duodénum, jouent un rôle important dans la fonction de cette barrière muqueuse. Toute rupture de la barrière, par des agents délétères, par une infection ou par un état de choc, peut provoquer, si le contenu gastrique est acide, l'apparition d'une gastrite érosive grave. Le développement des lésions est accéléré par toute réduction du débit sanguin dans la muqueuse. La relation entre rétrodiffusion des ions hydrogènes et débit sanguin muqueux semble être un facteur critique. Les facteurs qui (1) inhibent la sécrétion d'acide, (2) renforcent la barrière à la diffusion des ions H+, (3) accroissent le débit sanguin dans la muqueuse, protègent l'estomac contre le développement des lésions. Dans des conditions expérimentales, les prostaglandines de types A, E et F protègent contre la gastrite érosive; cette protection est sans rapport avec leurs effets sur la sécrétion d'acide et la perfusion de la muqueuse. La sécrétion ou la filtration d'une composante alcaline est peut-être un facteur important de la cytoprotection que donne le 16, 16-diméthyl (PGE 2) en application locale. Le rôle du mucus dans ces circonstances est encore mal connu.
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Supported by NIH Grant #5 R01 AM 16233-10.
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Moody, F.G., Zalewsky, C.A. & Larsen, K.R. Cytoprotection of the gastric epithelium. World J. Surg. 5, 153–163 (1981). https://doi.org/10.1007/BF01658278
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DOI: https://doi.org/10.1007/BF01658278