Physiological and morphological characteristics of progressive disruption of the canine gastric mucosal barrier.
The investigation had two major goals: to define the progression of physiological changes associated with disruption of the gastric mucosal barrier to sodium and hydrogen and to identify the morphological correlates of the physiological alterations. Fluxes of ions and water were determined before and after treatment of oxyntic mucosa with graded concentrations of butyric acid using dogs with gastric pouches. Three phases of barrier disruption were characterized: I, acceleration of normal Na+/H+ exchange; II, neutralization of H+; III, exudation of interstitial fluid. Parallel studies assessed morphological damage associated with these phases. In Phase I, cellular bulging into the lumen and dilation of intercellular spaces were evident. Some cellular erosion and extreme intercellular dilation were prominent in Phase II. Phase III was represented by necrotic changes and desquamation. It is concluded that disruption of transport mechanisms occurs sequentially and is closely correlated with morphological signs of progressive damage.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002087:Butyrates / Q000494:pharmacology*; D002712:Chlorides / Q000378:metabolism; D004285:Dogs; D004848:Epithelium / Q000648:ultrastructure; D005071:Evoked Potentials; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006851:Hydrochloric Acid / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D014867:Water / Q000378:metabolism
D002087:Butyrates; D002712:Chlorides; D014867:Water; D001285:Atropine; D012964:Sodium; D006851:Hydrochloric Acid; D011188:Potassium