Shafik Ahmed, Shafik Ismail A
Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo, Egypt.
World J Urol. 2003 May;20(6):374-7. doi: 10.1007/s00345-002-0309-9. Epub 2003 Apr 4.
A recent study by the senior author demonstrated that striated urethral sphincter contraction effected the inhibition of vesical contraction and suppression of the desire to micturate, an action suggested to be mediated through the "voluntary urinary inhibition reflex". We hypothesized that the effect of pelvic floor muscle (PFM) exercises on the overactive bladder was mediated through this reflex action. The current communication investigates this hypothesis. A total of 28 patients (mean age 44.8+/-10.2 years, 18 men, 10 women) with overactive bladder and 17 healthy volunteers (mean age 42.6+/-9.8 years, 12 men, 5 women) were enrolled in the study. The vesical and posterior urethral pressures were determined before and after vesical filling reached the volume at which urge in control subjects, and involuntary voiding in the patients, occurred. Intra-abdominal pressure was recorded to obtain detrusor pressure readings. The bladder was refilled to the above volume and the subject asked to hold PFM contractions for 10 s during which the vesical and posterior urethral pressures were recorded. In healthy volunteers, the mean detrusor and posterior urethral pressures at urge to void were 30.6+/-4.8 SD and 18.7+/-3.3 cm H(2)O, respectively. On PFM contraction, the detrusor pressure declined to 11.6+/-1.4 cm H(2)O (P<0.01) and urethral pressure increased to 139.8+/-17.4 cm H(2)O (P<0.001). In patients, the mean detrusor and posterior urethral pressure readings when the bladder was filled to the volume which induced involuntary incontinence, were 28.2+/-4.2 and 17.3+/-3.4 cm H(2)O, respectively; on PFM contractions, the detrusor pressure decreased to 10.6+/-2.1 cm H(2)O (P<0.01), while urethral pressure increased to 86.6+/-7.9 cm H(2)O (P<0.001) and voiding did not occur. In conclusion, PFM contractions led to a decline of detrusor and increase of urethral pressures and suppressed the micturition reflex. These contractions appear to induce their effect by preventing internal sphincter relaxation produced by the micturition reflex. Failure of the internal sphincter to relax seems to cause reflex detrusor relaxation, an action presumably mediated through the "voluntary urinary inhibition reflex". The results of the current study encourage the treatment of overactive bladder with PFM contractions.
资深作者最近的一项研究表明,尿道横纹括约肌收缩可抑制膀胱收缩并抑制排尿欲望,这一作用被认为是通过“自主排尿抑制反射”介导的。我们假设盆底肌(PFM)锻炼对膀胱过度活动症的影响是通过这种反射作用介导的。本通讯对这一假设进行了研究。共有28例膀胱过度活动症患者(平均年龄44.8±10.2岁,男性18例,女性10例)和17名健康志愿者(平均年龄42.6±9.8岁,男性12例,女性5例)纳入研究。在膀胱充盈至对照受试者出现排尿冲动、患者出现不自主排尿的体积之前和之后,测定膀胱和后尿道压力。记录腹内压以获得逼尿肌压力读数。将膀胱重新充盈至上述体积,要求受试者进行PFM收缩10秒,在此期间记录膀胱和后尿道压力。在健康志愿者中,排尿冲动时逼尿肌和后尿道的平均压力分别为30.6±4.8标准差和18.7±3.3 cmH₂O。在进行PFM收缩时,逼尿肌压力降至11.6±1.4 cmH₂O(P<0.01),尿道压力升至139.8±17.4 cmH₂O(P<0.001)。在患者中,当膀胱充盈至引起不自主失禁的体积时,逼尿肌和后尿道的平均压力读数分别为28.2±4.2和17.3±3.4 cmH₂O;在进行PFM收缩时,逼尿肌压力降至10.6±2.1 cmH₂O(P<0.01),而尿道压力升至86.6±7.9 cmH₂O(P<0.001),且未发生排尿。总之,PFM收缩导致逼尿肌压力下降和尿道压力升高,并抑制排尿反射。这些收缩似乎是通过防止排尿反射引起的内括约肌松弛来产生作用的。内括约肌未能松弛似乎导致反射性逼尿肌松弛,这一作用大概是通过“自主排尿抑制反射”介导的。本研究结果支持用PFM收缩治疗膀胱过度活动症。