Establishing and monitoring of urethral sphincter deficiency in a large animal model.

Abstract

Different methods for induction and monitoring of urethral sphincter deficiency were explored in a large animal model. Sphincter deficiency was established in female pigs by dilatation and cauterization, and amount and frequencies of voiding were monitored andexplored by pad test. Sphincteric closure pressures were recorded prior to and immediately after treatment of each animal, and on day 21 by two techniques: standard urethral pressure profilometry (s-UPP) and high-definition urethral pressure profilometry (HD-UPP). Tissue samples of the urethrae were analyzed by histochemistry (AZAN- and Sirius Red staining) and by immunohistochemistry detecting desmin and fast-myosin to depict muscular tissues. After 3weeks of observation animals treated by dilatation plus electrocautery presented with sphincter deficiency: measurements by both, s-UPP and HD-UPP demonstrated the maximal closure pressure reduced to baseline levels and a diminished area under the curve. Histological analyses documented, that dilatation yielded a pitted connective tissue and cauterization lead to muscle damage. Animals treated by either dilatation only or proximal injury only recovered within 3weeks. By pad test no significant differences between untreated and treated animals or between the differently treated groups were recorded. Significant urethral sphincter deficiency can be induced in female pigs by a combination of urethral dilatation and distal electrocautery. Sphincter deficiency can be measured by standard and high-definition urethral pressure profilometry. It was maintained over 21days after induction and correlated with visible changes in the tissue structure of the distal urethra.