Abstract:
:Acetic acid-induced pan colitis in rats leads not only to colonic injury but also to a bystander ileal injury, characterized by decreased fluid and electrolyte absorption without associated histological injury or infiltration of inflammatory cells. To examine the nature of this decreased ileal fluid and electrolyte absorption, we measured effect of acetic acid-induced pancolitis on ileal transmural sodium and chloride transport, as well as on ileal permeability to mannitol and inulin on mucosal sheets mounted in Ussing chambers. In addition, ileal tight junctional morphology was assessed by electron microscopy. In colitic animals, ileal serosal-to-mucosal sodium and chloride transmural fluxes were increased (P<0.05); compatible with the observed decrease in net fluid absorption. Mannitol and inulin ileal serosal-to-mucosal and mucosal-to-serosal ileal fluxes were similarly increased (P<0.05), suggesting that an increase in ileal permeability occurred during acetic acid-induced pancolitis. This increase in ileal permeability was not accompanied by changes in tight junctional ultrastructure. These results suggest that: (1) the decrease in ileal fluid and electrolyte absorption seen during acetic acid-induced rat pancolitis occurred in parallel with a rise in both transcellular and paracellular permeability, and (2) the ileal permeability changes were not accompanied by structural changes.
journal_name
Dig Dis Scijournal_title
Digestive diseases and sciencesauthors
Cui N,Madsen KL,Friend DR,Stevenson BR,Fedorak RNdoi
10.1007/BF02093836subject
Has Abstractpub_date
1996-02-01 00:00:00pages
405-11issue
2eissn
0163-2116issn
1573-2568journal_volume
41pub_type
杂志文章abstract::The destruction of the integrity of the gastric epithelial barrier underlies the pathology of many gastric diseases, including gastric tumors. The Helicobacter pylori virulence factor CagA is one of the main destroyers of the gastric epithelial barrier. There are differences among CagA proteins that originate from dif...
journal_title:Digestive diseases and sciences
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