Changes in sodium transport in epithelial cells in a rat ileal‐augmented bladder model

Abstract

Objective To investigate changes in the morphology and sodium transport ability of intestinal epithelium diverted to the urinary tract, using an in vitro sodiumbinding benzofuran isophthalate (SBFI) technique, as the effects of long-term urine exposure on the transport of electrolytes through intestine are incompletely understood. Materials and methods Ileal augmentation cystoplasty was conducted in female Sprague-Dawley rats; at 3 and 12 months after surgery the serum concentration of sodium, chloride and potassium were measured. Sodium transport in the ileal epithelial cells diverted to the urinary tract was evaluated using SBFI, as the value of the 340/380 nm excitation ratio measured with fluorescence spectrophotometry. The villous height and the number of villi per ileal length were obtained from haematoxylin and eosin-stained sections. Results After 3 months the mean ( SD ) serum sodium concentrations in normal and augmented rats were 140.4 (2.5) and 140.7 (3.5) mmol/L, respectively; the chloride concentration in normal rats was 97.0 (2.9), and in augmented rats at 3 and 12 months it was 102.4 (2.9) and 99.0 (3.7) mmol/L, respectively. At 3 months, chloride concentrations were significantly higher in augmented than in normal rats ( P < 0.05). The mean ( SD ) 340/380 nm ratio increased by 0.85 (0.09) in the normal ileum, and by 0.73 (0.15) and 0.49 (0.23) in the ileum of augmented rats at 3 and 12 months, respectively; the difference between normal and augmented ileum at 12 months was significant ( P < 0.05). At 12 months the villous height in the augmented ileum, at 227.6 (16.0) m m, was significantly less than in the normal ileum, at 803.4 (66.2) m m ( P < 0.05). However, the number of villi/mm ileum in normal and augmented rats at 12 months was 13.7 (1.5) and 15.0 (0.8), respectively, and not significantly different. Conclusion Sodium transport decreased significantly after long-term exposure to urine; the improvement in metabolic change was probably attributable to alterations of electrolyte transport and atrophic changes of the villus.

Ileocystoplasty in Rats: Metabolic, Renal and Enteropatch Changes in a Mid- and Long-Term Follow-Up

“…Acidosis results because intestinal segments retain their absorptive and secretory properties such as the absorption of ammonium, chloride, potassium and urea as well as the secretion of bicarbonate and sodium [8,10,13] . The frequency and severity of metabolic acidosis are mainly related to the type and length of the intestinal segment used [14] .…”

“…Bladder augmentation predisposes the patient to many adverse events such as infections, bladder stones, hyperchloremic metabolic acidosis and even cancers [8][9][10] . In this regard, an incidence of transitional cell carcinoma of 4-27% is reported and an incidence of proliferative lesions in 36-54% of ileocystoplasty in rats [7,11,12] .…”

Global analysis of gene expression profiles in ileum in a rat bladder augmentation model using cDNA microarrays

“…Recently, various complications associated with urinary diversion have been extensively reported 1,2 . Furthermore, several investigators have performed basic experiments to address these complications 3–5 . For example, Fujisawa et al .…”

“…For example, Fujisawa et al . showed that sodium transport was significantly decreased in the ileal epithelium of a rat bladder augmentation model and concluded that the improvement in metabolic change was probably attributable to alterations of electrolyte transport and atrophic changes of the villus 5 . However, to our knowledge, there has not been a study globally analyzing the effect of the long‐term exposure of the intestinal segment to urine at the molecular level.…”

“…Increased experience with the techniques associated with urinary tract reconstruction has resulted in the growing recognition of possible complications, such as metabolic acidosis, urolithiasis, chronic infection and neoplastic disease 1,2 . Although some recent studies have investigated the mechanism of such events, 3–5 there do not seem to be any studies evaluating the effects of long‐term urine exposure on the global genetic changes in intestinal segments.…”