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.
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