Detrusor overactivity (DO) persists after prostatectomy in 20% to 25% of patients with benign disease. Assuming that nonvoiding contractions (NVCs) can be used as a surrogate for DO in humans, the rat model of obstruction/ deobstruction may allow us to study the pathophysiology of persistent DO after deobstruction. We investigated bladder function, with a special focus on NVCs, in rats by use of a new, modified method of obstruction and deobstruction and compared these results with those obtained by use of the conventional method. Seventy female SpragueDawley rats underwent 1) sham operation (n ϭ 10), 2) obstruction by a modified method (Modif-Obs; n ϭ 12), 3) obstruction/deobstruction by the conventional method (Conv-Obs/Deobs; n ϭ 13), or 4) obstruction/deobstruction by the modified method (Modif-Obs/ Deobs; n ϭ 35). The Modif-Obs/Deobs animals were divided into subgroups with (DOϩ) and without (DOϪ) NVCs. Two weeks after partial urethral obstruction, the animals were deobstructed, and 1 wk later cystometry was performed with recording of intravesical and intra-abdominal pressures. NVCs were shown in all groups: ModifObs (80%), Conv-Obs/Deobs (100%), and Modif-Obs/Deobs (40%). In the Modif-Obs/Deobs group, bladder weight and the muscle-tocollagen ratio were higher in DOϩ than in DOϪ rats. The ModifObs/Deobs group showed no mortality compared with 25% mortality in the Conv-Obs/Deobs group. The modified method may be more adequate for studying persistent DO after deobstruction, because it resulted in pressure/volume-and DO-related parameters similar to those found in the clinical situation. The persistence of DO after deobstruction may partly be due to irreversible changes in the bladder caused during the period of obstruction. urinary bladder; cystometry BENIGN PROSTATIC HYPERPLASIA occurs as part of the aging process in men and affects Ͼ 50% of the male population over 60 yr of age (11). The clinical symptoms of benign prostatic hyperplasia are caused not only by the mass-related increase in urethral resistance but also by pathologic processes in the bladder wall secondary to the bladder outlet obstruction (BOO) (18,26,35,40). In many studies on patients with BOO undergoing surgery for benign prostatic hyperplasia, a significant percentage of patients report persistence of storage (irritative) symptoms, associated with detrusor overactivity (DO) on urodynamic investigation, even if the obstruction was successfully relieved. In fact, DO has been shown to persist after prostatectomy in 20% to 25% of patients treated for benign disease (2,19,29,33).Rats subjected to BOO will develop hyperactive voiding, characterized by increased frequency and nonvoiding contractions (NVCs), which persists after deobstruction in a proportion of the animals (6,20,23,24,27,30). The relations between symptoms, BOO, and bladder function can, for obvious reasons, not be studied in animal models. However, assuming that NVCs can be used as a surrogate parameter for DO in humans, the rat model of obstruction/deobstruction may offer an op...

No abstract

Our findings suggest that the rat model with intravesical PGE2 is inappropriate for observing the effects of some drugs or mechanisms on DO, because only approximately 30% of IVPRs were confirmed as true DO. However, this model of intravesical PGE2 instillation has some advantages for the observation of changes in pressure and volume parameters rather than in DO-related ones.

No abstract