Chai T C, Gemalmaz H, Andersson K E, Tuttle J B, Steers W D
Department of Urology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
J Urol. 1999 May;161(5):1689-93.
Bladder outlet obstruction (BOO) can increase urinary frequency. Even after surgical relief of obstruction, up to 30% of patient are still bothered by irritative voiding symptoms. We tested the hypothesis that deligation of a partial bladder outlet obstruction model mimics this clinical observation.
Female Wistar rats were obstructed for 3 weeks by partial urethral ligation and then were relieved of obstruction by urethral deligation. Measurements of voiding frequency and voided volumes were measured preoperatively, after ligation, and after deligation. Relief of obstruction was confirmed by measuring flow rates through ex vivo perfusion of deligated urethras. Urine osmolality and bladder weights were determined. Awake cystometrograms (CMGs) were performed 3 weeks after deligation to measure bladder function.
Neither sham ligation nor sham deligation altered voiding frequency. Ligation doubled mean voiding frequency (in cc) from 2.01 +/- 0.32 to 3.96 +/- 0.22 per 4 hours (p = 0.0002). Three weeks after deligation, voiding behavior of the animals segregated into 2 groups: 20% had persistent hyperactive voiding frequency (6.67 +/- 1.23 per 4 hours) while 80% normalized voiding frequency (1.53 +/- 0.20 per 4 hours). The difference in voiding frequency in these 2 groups could not be attributed to alterations in urine osmolality, persistence of urethral obstruction, difference in bladder weights or severity of initial obstruction created. Awake CMGs revealed a higher peak micturition pressure and lower voided volume in the hyperactive voiders.
20% of the animals after urethral deligation had persistent hyperactive voiding which parallels clinical observations. Because the CMG data suggested persistent obstruction, yet urethral perfusion and bladder weights indicated no obstruction, we propose that these 20% of animals have a "functional" bladder outlet obstruction and can be used to study mechanisms underlying hyperactive voiding.
膀胱出口梗阻（BOO）可增加尿频。即使在手术解除梗阻后，仍有高达30%的患者受到刺激性排尿症状的困扰。我们检验了这样一个假设，即部分膀胱出口梗阻模型的解除结扎模拟了这一临床观察结果。
雌性Wistar大鼠通过部分尿道结扎梗阻3周，然后通过尿道解除结扎来缓解梗阻。在术前、结扎后和解除结扎后测量排尿频率和排尿量。通过对解除结扎的尿道进行体外灌注测量流速来确认梗阻的缓解情况。测定尿渗透压和膀胱重量。在解除结扎3周后进行清醒膀胱测压（CMG）以测量膀胱功能。
假结扎和假解除结扎均未改变排尿频率。结扎使平均排尿频率（以毫升计）从每4小时2.01±0.32增加一倍至3.96±0.22（p = 0.0002）。解除结扎3周后，动物的排尿行为分为两组：20%的动物排尿频率持续亢进（每4小时6.67±1.23），而80%的动物排尿频率恢复正常（每4小时1.53±0.20）。这两组动物排尿频率的差异不能归因于尿渗透压的改变、尿道梗阻的持续存在、膀胱重量的差异或初始梗阻的严重程度。清醒CMG显示，排尿亢进的动物排尿峰值压力较高，排尿量较低。
尿道解除结扎后20%的动物存在持续的排尿亢进，这与临床观察结果相似。由于CMG数据提示存在持续梗阻，但尿道灌注和膀胱重量表明不存在梗阻，我们提出这20%的动物存在“功能性”膀胱出口梗阻，可用于研究排尿亢进的潜在机制。
