作者: Charles R. Beamon , Carla Mazar , Mohamad W. Salkini , Hardeep S. Phull , Craig V. Comiter
DOI: 10.1111/J.1464-410X.2008.08324.X
关键词:
摘要: OBJECTIVE To investigate if sildenafil citrate can inhibit the functional and structural changes of detrusor in a murine model bladder outlet obstruction (BOO). Phosphodiesterase type 5 (PDE-5) inhibitors have recently been used for treating urinary symptoms associated with prostatic obstruction, but it is unclear whether PDE-5 inhibition acts on urethra or bladder. MATERIALS AND METHODS In 18 male Balb/CAN mice, partial BOO was created mice allowed to survive 6 weeks. Half (nine) were treated oral daily (10 mg/kg) by lavage (BOO + V), half not Six as sham-operated controls received no sildenafil. The assessed urodynamics at baseline after 6 weeks, measurement volume first uninhibited non-voiding contraction (VDO1), capacity (BC), pressure during void (Pdet). At bladders harvested, fixed sectioned, stained haematoxylin eosin (HE results compared those from normal controls. RESULTS BOO had significantly greater BC than control mean (sd) 153 (66) vs 58 (13) µL (P = 0.004). Treatment did alter BC. caused an increase Pdet controls, 25 (7) 12 (5) cm H2O. different treatment median VDO1 percentage lower (20% 53%, P > 0.03) increased 44%, P = 0.04). weight 89 (32) 27 (6) mg (P = 0.001), which decreased treatment, 40 (14) 89 (32) mg (P = 0.013). muscular hypertrophy H&E score 3 2 (P = 0.01) fibrosis trichrome (P = 0.01). BOO + V reduced fibrosis, 1 (P = 0.01). CONCLUSIONS BOO mediates both mouse bladder. weeks BC, overactivity voiding pressure, mediated weight, muscle collagen deposition lamina propria smooth muscle. 6 weeks beginning time prevented without affecting pressures, that otherwise occurred BOO. It appears therefore rather outlet.