Ion transport in the experimental short bowel syndrome of the rat

Abstract

The adaptational changes of epithelial ion transport in the short bowel syndrome were studied. Ileal remnants of rats were investigated 8 weeks after 70% proximal small intestinal resection. Pure epithelial resistance measured by impedance analysis decreased from 27 ± 1 to 21 ± 1 Ω · cm2, and polyethylene glycol 4000 fluxes increased from 2.5 ± 0.3 to 3.6 ± 0.3 nmol · h−1 · cm−2, indicating increased permeability of the short bowel. Unidirectional flux measurements in control ileum showed absorptive net fluxes of Na+ and Cl− that were assigned to electroneutral NaCl absorption and a short-circuit current that was accounted for by the residual flux (HCO3− secretion). Neither NaCl absorption nor HCO3− secretion were altered in the short bowel. Also, electrogenic Cl− secretion, defined after maximal stimulation by theophylline and prostaglandin E1 was not changed in the short bowel. In contrast, electrogenic Na+/glucose cotransport increased in Vmax from 2.0 ± 0.3 in controls to 5.0 ± 1.0 μmol · h1 · cm−2 in the short bowel. Tight junction structure was studied by freeze-fracture electron microscopy. The number of horizontal strands was unchanged, whereas tight junction depth was slightly increased in the short bowel. Microvillus area of short bowels was increased by 20% in villus regions. Under the light microscope, villus height was increased by 30%. In conclusion, the short bowel mucosa undergoes adaptive responses to reduced overall absorptive area by increasing glucose-dependent electrogenic Na+ absorption to 250%, which is partly caused by increased villus and microvillus surface area. Electrogenic Cl− and HCO3− secretion and electroneutral NaCl absorption remained unchanged. The decreased epithelial resistance is caused by mucosal surface amplification.