PurposeWe investigated bladder function, with special focus on initial functional changes, by objective report of decompensated bladder according to the percentage of residual urine volume to bladder capacity in awake, obstructed rats.Materials and MethodsThirty rats were randomly subjected to sham operations (n=10) or partial bladder outlet obstruction (BOO, n=20). Cystometric investigations were performed without anesthesia 1 or 2 weeks after BOO surgery. To reduce the influence of confounding factors in awake cystometry, we used simultaneous recordings of intravesical and intraabdominal pressures. Decompensated bladder was defined as the bladder with more than 20% of residual volume compared with bladder capacity.ResultsCompared with that in sham animals, basal pressure was elevated in both BOO groups. Threshold pressure was higher in the 2 week BOO (p<0.01) group. Compliance was decreased in the 1 week BOO group (p<0.01) and increased in the 2 week BOO group (p<0.001). Bladder capacity was not increased in the 1 week BOO group, but was increased in the 2 week BOO group (p<0.01). Decompensation was found in 62.5% of the 1 week BOO group and in 33.3% of the 2 week BOO group.ConclusionsFrom the earlier phase, the bladders exhibited serial changes in pressure and volume parameters, and decompensated bladders defined by the percentage of residual volume to bladder capacity could be seen. During the later phase, there was an increasing tendency of compensated bladders, accompanied by the bladders being enlarged and more compliant.

PurposeWe investigated bladder function, with a special focus on nonvoiding contractions (NVCs), in awake rats with chronic chemical cystitis and bladder outlet obstruction (BOO) by use of simultaneous registrations of intravesical and intraabdominal pressures. In addition, we tested the effects of tolterodine on the NVCs in these models.MethodsA total of 20 female Sprague-Dawley rats were used in this study. In eight rats, chemical cystitis was induced by intravesical instillation of HCl. Twelve rats were subjected to sham instillations or partial BOO. Four weeks after intravesical instillation or 2 weeks after partial BOO, cystometrograms were obtained by use of simultaneous recording of intravesical and intraabdominal pressure in all unanesthetized, unrestrained rats in metabolic cages.ResultsA total of 17 rats survived. In the rats with acute injury by HCl, 50% showed detrusor overactivity (DO), which was not seen in the sham group. The cystitis group had lower DO pressure without a difference in DO frequency compared with the BOO group. After the administration of tolterodine, the cystitis group showed no difference in DO frequency or pressure, whereas the BOO group showed decreased values for both parameters.ConclusionsOur study showed that toleterodine produced no effect on DO during the filling phase in rats with chronic chemical cystitisbut decreased the frequency and pressure of DO in rats with BOO. Clinically, studies are needed to improve the treatment effect of anticholinergic drugs ininterstitial cystitis patients with overactive bladder.

Purpose: The aim of this study was to investigate the effect of urinary bladder inflammation on bladder function in a rat chemical cystitis model. We also histologically confirmed the effects of inflammation in the detrusor on chronically inflamed bladder in rats. Materials and Methods: A total of 13 female Sprague-Dawley rats were used in this study. In seven rats, intravesical instillation of HCl induced chemical cystitis, and the other rats with intravesical instillation of saline were used as the sham. After 2 weeks, cystometrograms were obtained with additional intraabdominal pressure measurements in all unanesthetized, unrestrained rats in metabolic cages. The rats were killed just after cystometry. The bladders were removed and examined histologically for mast cells and inflammatory changes. Results: The rats with acute injury by HCl showed no differences in pressure parameters, including basal pressure, threshold pressure, and maximum bladder pressure, compared with the sham rats. They showed significantly increased bladder capacity, micturition volume, residual volume, and micturition interval compared with the sham group. They also showed an increased frequency of detrusor overactivity compared with the sham group. The percent of detrusor overactivity was 56.3% among the total intravesical pressure rises above 2 cmH 2 O. The histological findings of the rats with acute injury by HCl were consistent with chemical cystitis. Conclusions:Overlapping patterns of lower urinary tract symptoms and pelvic pain are common disease characteristics among interstitial cystitis patients. The situation in an animal model of interstitial cystitis is similar, as observed in this study by the histologic and awake cystometric examinations. However, the interstitial cystitis model showed detrusor overactivity during the filling phase without a decrease in bladder capacity and micturition intervals, which differs from the characteristics of overactive bladder patients.

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.

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