Streng Tomi K, Talo Antti, Andersson Karl-Erik, Santti Risto
Department of Anatomy, Institute of Biomedicine, University of Turku, Turku, Finland.
BJU Int. 2005 Nov;96(7):1126-30. doi: 10.1111/j.1464-410X.2005.05811.x.
To explore the effect of different degrees of oestrogenization on male voiding, by treating adult castrated and 5alpha-dihydrotestosterone (DHT)-maintained male mice with different doses of oestrogens, as exposure of male mice to excessive amounts of oestrogens can cause bladder outlet obstruction (BOO); in addition, male mice lacking oestrogen receptor (ER)alpha (ERKO) or ERbeta (BERKO) were studied to assess the importance of ER subtypes.
Castrated, DHT-maintained adult mice were treated with 17beta-oestradiol (E(2); 50 and 250 microg/kg) or oestrone (E(1); 5, 50 and 500 microg/kg) daily for 10 days. Control mice were treated only with the vehicle. BERKO and ERKO mice, and their wild-type littermates used as their controls, remained untreated. Under anaesthesia, the bladder and distal urethra were exposed to record simultaneously the bladder pressure and urinary flow rate from the distal urethra.
E(2)-treated mice showed obstructive voiding, seen as increased bladder pressure, decreased average flow rate and prolonged micturition time. This was also evident when a high dose (500 microg/kg) of E(1) was used. After treatment with a dose of 50 microg/kg, the urodynamic variables were similar to those in the control mice. Surprisingly, after treatment with a low dose (5 microg/kg) all urodynamic variables improved. There was a minor increase in the bladder pressure in BERKO mice; ERKO mice had a significantly lower urinary flow rate.
High doses of oestrogens caused BOO in castrated, DHT-maintained male mice. A small dose of E(1) had a positive effect on voiding, suggesting that oestrogens are needed for normal male voiding. Reduced urinary flow rates in ERKO mice suggest that oestrogen effects on voiding are mediated at least partly via ERalpha.
通过用不同剂量的雌激素处理成年去势及5α - 双氢睾酮（DHT）维持的雄性小鼠，探讨不同程度雌激素化对雄性排尿的影响，因为雄性小鼠暴露于过量雌激素会导致膀胱出口梗阻（BOO）；此外，研究缺乏雌激素受体（ER）α（ERKO）或ERβ（BERKO）的雄性小鼠，以评估ER亚型的重要性。
对去势、DHT维持的成年小鼠每日用17β - 雌二醇（E₂；50和250μg/kg）或雌酮（E₁；5、50和500μg/kg）处理10天。对照小鼠仅用赋形剂处理。BERKO和ERKO小鼠及其作为对照的野生型同窝小鼠未接受处理。在麻醉下，暴露膀胱和尿道远端，同时记录膀胱压力和尿道远端的尿流率。
E₂处理的小鼠出现梗阻性排尿，表现为膀胱压力升高、平均尿流率降低和排尿时间延长。当使用高剂量（500μg/kg）的E₁时，这一现象也很明显。用50μg/kg剂量处理后，尿动力学变量与对照小鼠相似。令人惊讶的是，用低剂量（5μg/kg）处理后，所有尿动力学变量均有所改善。BERKO小鼠的膀胱压力有轻微升高；ERKO小鼠的尿流率明显较低。
高剂量雌激素在去势、DHT维持的雄性小鼠中导致BOO。小剂量的E₁对排尿有积极作用，表明正常雄性排尿需要雌激素。ERKO小鼠尿流率降低表明雌激素对排尿的影响至少部分是通过ERα介导的。
