O'Connor L T, Vaughan E D, Felsen D
Department of Urology, James Buchanan Brady Foundation, New York Hospital-Cornell Medical Center, New York 10021, USA.
J Urol. 1997 Aug;158(2):631-5.
Bladder outlet obstruction in man is a common medical disorder that may result from benign prostatic hyperplasia, urethral stricture disease, or congenital anomaly. The functional changes that develop in response to obstruction include detrusor instability, elevated voiding pressures, and the presence of a residual urine. The aim of this study was to document the development of progressive bladder outlet obstruction over time in a rat model using conscious, in vivo urodynamics.
Infravesical bladder outlet obstruction was created in female rats by placing a jeweler's jump ring loosely around the proximal urethra. Gradual development of outlet obstruction was followed urodynamically in awake animals at 3, 7, 14, 21, and 28 days post obstruction using a subcutaneously implanted mediport. For each group n = 5-8 animals.
Animals developed large capacity bladders with increased compliance, a high residual urine volume, and spontaneous activity. Bladder capacity increased from 0.20 + 0.02 ml. to 6.30 + 1.59 ml. at 28 days post obstruction (p < 0.05). Residual volume increased from 0.06 + 0.01 ml. to 5.95 + 1.54 ml. (p < 0.05). Percent void decreases from 72 + 3.7% in sham controls to 6.7 + 2.5% at 28 d (p < 0.05). Voiding pressure increased from 12 + 1.6 mm. Hg in sham animals to a maximum of 42 + 6.1 mm. Hg at 21 d (p < 0.05). Compliance was significantly higher at 28 d when compared to all other time points. 89% of obstructed animals developed bladder instability.
This study provides clear evidence of the progressive change in bladder function which occurs following outlet obstruction. Implantation of a subcutaneous mediport allows in vivo recording of both the filling and voiding phases of micturition in awake animals that have intact neural responses. This is a precise and easily reproducible method for producing obstruction in a small animal which can provide a continuum of tissue and urodynamic data that may be used to further study the pathophysiologic changes underlying bladder outlet obstruction or other models of bladder dysfunction.
男性膀胱出口梗阻是一种常见的医学病症，可能由良性前列腺增生、尿道狭窄疾病或先天性异常引起。因梗阻而发生的功能变化包括逼尿肌不稳定、排尿压力升高以及残余尿的存在。本研究的目的是使用清醒的活体尿动力学方法，记录大鼠模型中膀胱出口梗阻随时间的进展情况。
通过在雌性大鼠近端尿道周围松散地放置一个珠宝匠用的开口环，造成膀胱下出口梗阻。在梗阻后3、7、14、21和28天，使用皮下植入的Mediport对清醒动物进行尿动力学监测，观察出口梗阻的逐渐发展情况。每组n = 5 - 8只动物。
动物出现膀胱容量增大、顺应性增加、残余尿量增多以及自发活动。梗阻后28天，膀胱容量从0.20±0.02毫升增加到6.30±1.59毫升（p < 0.05）。残余尿量从0.06±0.01毫升增加到5.95±1.54毫升（p < 0.05）。排尿百分比从假手术对照组的72±3.7%降至28天时的6.7±2.5%（p < 0.05）。排尿压力从假手术动物的12±1.6毫米汞柱增加到21天时的最高42±6.1毫米汞柱（p < 0.05）。与所有其他时间点相比，28天时的顺应性显著更高。89%的梗阻动物出现膀胱不稳定。
本研究提供了明确证据，证明膀胱出口梗阻后膀胱功能会发生渐进性变化。皮下植入Mediport可在具有完整神经反应的清醒动物体内记录排尿的充盈期和排尿期。这是一种在小动物中产生梗阻的精确且易于重复的方法，可提供一系列组织和尿动力学数据，用于进一步研究膀胱出口梗阻或其他膀胱功能障碍模型的病理生理变化。
