Self-filling blind loops of rat jejunum were used as a model for the blind loop syndrome in humans. Electrical resistance, short circuit current, and unidirectional sodium and chloride fluxes were measured using the Ussing technique. Whereas net fluxes for sodium and chloride did not differ significantly from zero in the blind loop or in the control, unidirectional fluxes of either direction were decreased and electrical resistance was increased, indicating an increase in the tightness of the intestinal wall. Measurements of alternating current impedance and micropuncture experiments revealed that this was due to an increase in epithelial resistance from 9 +/- 1 omega X cm2 (n = 15, results of both methods) to 27 +/- 4 omega X cm2 (n = 15) and in subepithelial resistance from 40 +/- 2 omega X cm2 (n = 15) to 76 +/- 7 omega X cm2 (n = 15). As the ratio of epithelial to subepithelial resistance was similar in the blind loop and in the control, lower transport rates in the blind loop are indicative of impaired epithelial transport function. Subsequently, two different transport systems were characterized. First, the 3-o-methyl-glucose-induced, phlorizin-reversible increase in short circuit current, representing glucose-coupled sodium absorption, showed a 77% decrease in maximum velocity in the blind loop and no change in Km. Second, the chloride-induced, bumetanide-reversible increase in short circuit current in tissues stimulated simultaneously by prostaglandin E1 and theophylline, representing rheogenic chloride secretion, also showed a decrease in maximum velocity (of 83%) and no change in Km. A morphometric analysis revealed that the crypt surface area increased by 100% in the blind loop, whereas the villous surface area was not significantly different between blind loops and controls. We conclude that the jejunal self-filling blind loop is characterized by impaired active ion transport processes and an increase in epithelial and subepithelial resistance.