[Effects of sildenafil on bladder compliance and endothelin-1 in rabbit model of partial bladder outlet obstruction].

Objective: To explore the effects of sildenafil on bladder compliance and endothelin-1 in the rabbit model of partial bladder outlet obstruction.
Methods: A total of 24 adult male New Zealand white rabbits were randomly divided into group A, group B, group C and group D (n = 6 each). The rabbit model of partial bladder outlet obstruction was established in groups C and D while groups A and B underwent a sham operation. Daily sildenafil (10 mg/kg) was dosed to groups B and C by lavage. Daily normal saline was dosed similarly to groups A and D. Bladder urodynamic examinations were conducted in each group at Week 16. Then bladder was isolated and weighed from each group. And ET-1 in bladder tissue was measured by ELISA.
Results: Pressure thresholds for voiding (PT) in A-D groups were (10.6 ± 2.0), (11.6 ± 2.7), (14.0 ± 4.2) and (20.4 ± 6.1) cm H2O respectively. Compared with groups A, B and C, PT in group D was significantly higher (all P < 0.01). Bladder compliance in 4 groups were (2.75 ± 0.51), (2.78 ± 0.46), (4.98 ± 2.15) and (1.22 ± 0.25) ml/cm H2O respectively. Compared with groups A, B and C, bladder compliance was significantly lower in group D (all P < 0.01). Bladder compliance in group C was higher than that in groups A and B (both P < 0.01). The weights of bladder specimens in 4 groups were (5.0 ± 0.4), (4.6 ± 0.4), (8.2 ± 1.3) and (17.9 ± 2.3) g respectively. Compared with groups A and B, the weights of groups C and D were significantly heavier (all P < 0.01). And the weight of group D was much greater than that of group C (P < 0.01). The contents of ET-1 in bladder tissue of 4 groups were (72 ± 19), (69 ± 18), (76 ± 21) and (106 ± 29) pg/g respectively. Compared with groups A, B and C, ET-1 in bladder tissue was significantly higher in group D (all P < 0.05).
Conclusions: Daily sildenafil can effectively alleviate the damage of rabbit bladder compliance from partial bladder outlet obstruction and protect bladder functions. Its mechanism may be related with the down-regulation of ET-1 in bladder tissue of partial bladder outlet obstruction.