Bump R C, Friedman C I
J Urol. 1986 Aug;136(2):508-11. doi: 10.1016/s0022-5347(17)44932-9.
Four female baboons underwent cystometry and simultaneous urethral pressure profilometry (UPP) in a hypoestrogenic castrate state, after estrogen treatment, and after concurrent testosterone and estrogen treatment. Studies were performed under general anesthesia both before and after skeletal muscle paralysis. The results provide objective evidence that estrogen replacement enhances the urethral sphincter mechanism in the castrate female baboon by significantly increasing the paralyzed and nonparalyzed urethral length as well as the paralyzed total UPP area and the paralyzed UPP area to maximum urethral closure pressure (MUCP). The area increases reflected both the increase in functional urethral length as well as increases in mean urethral pressure. Muscle paralysis significantly reduced MUCP in all three hormonal states. The addition of testosterone had no significant effect on the UPP measurements. These findings are discussed in light of conflicting human studies regarding objective evidence for the role of hormonal modulation of urethral function and the role of estrogen therapy for stress urinary incontinence.
四只雌性狒狒在雌激素缺乏的去势状态下、雌激素治疗后以及睾酮和雌激素联合治疗后接受了膀胱测压和同步尿道压力测定（UPP）。在骨骼肌麻痹前后均在全身麻醉下进行研究。结果提供了客观证据，表明雌激素替代通过显著增加麻痹和未麻痹的尿道长度以及麻痹的总UPP面积和麻痹的UPP面积至最大尿道闭合压（MUCP），增强了去势雌性狒狒的尿道括约肌机制。面积增加既反映了功能性尿道长度的增加，也反映了平均尿道压力的增加。在所有三种激素状态下，肌肉麻痹均显著降低了MUCP。添加睾酮对UPP测量无显著影响。鉴于关于激素调节尿道功能的作用以及雌激素治疗压力性尿失禁的作用的人体研究相互矛盾，对这些发现进行了讨论。
