Rectal electrolyte transport and mucosal permeability in ulcerative colitis and Crohn's disease.

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Abstract The inflamed rectal stump of 11 patients who had undergone complete colectomy for proximal inflammatory bowel disease was perfused in situ with isotonic sodium chloride solutions or isotonic mixtures of saline, potassium, and bicarbonate. The results were compared with the findings in 6 healthy subjects. Unidirectional fluxes of sodium and the net fluxes of sodium, chloride, potassium, bicarbonate, and water were determined in both groups, whereas estimations of the diffusional permeability coefficient of urea, fructose, 51 Cr-EDTA (ethylene diaminetetra-acetic acid), 57 Co-vitamin B 12 , and 125 I-PVP (polyvinylpyrrolidone) were made in the patients only. The mean absorptive capacity for sodium, chloride, and water was significantly increased in the group of patients, but the electrolyte transfer in one patient, who was in complete remission, did not seem to be different from that of control subjects. The pattern of electrolyte transport in inflammatory bowel disease was the same as that found in the normal rectum and colon. Thus, net water transport was dependent on net sodium absorption, while the bicarbonate secretion balanced the chloride ions absorbed in excess of sodium. Potassium was secreted into the rectal lumen, even when the luminal concentration exceeded that of blood. The mucosa-to-serosa flux of sodium was significantly reduced, but a decreased sodium flux ratio found in patients with active disease was, however, above all due to an increased serosa-to-mucosa flux of sodium suggesting that the defective absorption might be primarily due to the fact that sodium already "pumped" leaks out into the gut lumen. The concept of increased permeability of the epithelium in active disease is supported by the findings of a relatively constant relationship between the diffusional permeability coefficients of the named uncharged hydrophilic solutes and their respective free diffusion coefficients in water.