Background. Increased intestinal permeability and translocation of bacteria
and/or bacterial products may cause infection and liver dysfunction in pat
ients with the short bowel syndrome. In previous studies, serum from mice u
ndergoing small bowel resection (SBR) enhanced growth of cultured rat intes
tinal epithelial cells (RIEC-6), implicating a role for a serum factor(s) i
n the enterocyte response to SBR. These experiments tested the hypothesis t
hat epithelial cell permeability is increased following SBR.
Materials and methods. Male Sprague-Dawley rats underwent a 75% SBR or sham
operation. Intestinal permeability in the remnant ileum was determined by
Ussing chambers on Postoperative Day (POD) 3. Additionally, serum was colle
cted on POD 1, 3, and 7 and mesenteric lymph was harvested on POD 3. Once c
onfluent, RIEC-6 cells were incubated for 3 days in media supplemented with
10% fetal bovine serum (FBS; control), 1% FBS, 1% FBS plus 9% Sham serum,
or 1% FBS plus 9% SBR serum or exposed to media with varied concentrations
of SBR or Sham lymph. Monolayer permeability was determined by measuring th
e passage of dextran-rhodamine.
Results. Intestinal permeability was reduced in rats undergoing SBR. Sham s
erum-treated monolayers demonstrated the greatest permeability. Incubation
with SBR serum reduced permeability to near control media. There were no pe
rmeability differences between SBR and Sham lymph-treated monolayers.
Conclusion. The early adaptive response of the remnant intestine after SBR
is associated with reduced permeability. These results suggest an alternati
ve mechanism for the increased bacterial translocation that has been descri
bed following SBR. (C) 2001 Academic Press.