Ng. Cui et al., INCREASED PERMEABILITY OCCURS IN RAT ILEUM FOLLOWING INDUCTION OF PANCOLITIS, Digestive diseases and sciences, 41(2), 1996, pp. 405-411
Acetic acid-induced pan colitis in rats leads not only to colonic inju
ry but also to a bystander ileal injury, characterized by decreased fl
uid and electrolyte absorption without associated histological injury
or infiltration of inflammatory cells. To examine the nature of this d
ecreased ileal fluid and electrolyte absorption, we measured effect of
acetic acid-induced pancolitis on ileal transmural sodium and chlorid
e transport, as well as on ileal permeability to mannitol and inulin o
n 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 fluxe
s 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 acet
ic acid-induced pancolitis. This increase in ileal permeability was no
t accompanied by changes in tight junctional ultrastructure. These res
ults suggest that: (1) the decrease in ileal fluid and electrolyte abs
orption seen during acetic acid-induced rat pancolitis occurred in par
allel with a rise in both transcellular and paracellular permeability,
and (2) the ileal permeability changes were not accompanied by struct
ural changes.