Levin R M, Longhurst P A, Monson F C, Kato K, Wein A J
Division of Urology, University of Pennsylvania School of Medicine, Philadelphia.
Prostate Suppl. 1990;3:9-26. doi: 10.1002/pros.2990170503.
Bladder outlet obstruction secondary to benign prostatic hyperplasia induces numerous changes in bladder morphology, physiology, and pharmacology. These changes have been studied experimentally in various animal models, and while each species has advantages and disadvantages, it is unclear which is most like man. It has been shown that tissue hypertrophy leading to an increase in tissue mass develops rapidly after bladder outlet obstruction. Ischemia induced by the obstruction results in acute muscle dysfunction. The degree of functional impairment is directly related to the degree of tissue hypertrophy. However, the bladder contractile apparatus appears to have a surprising regenerative ability, such that recovery of bladder function becomes obvious 14 days after obstruction. Urodynamic changes include an increase in urinary frequency and voiding pressure and a decrease in voided volume. Clinically, involuntary bladder contractions are often present. Determination of which of these specific aspects of outlet obstruction the investigator is interested in studying will dictate the selection of the most appropriate animal model.
