Schröder A, Chichester P, Kogan B A, Longhurst P A, Lieb J, Das A K, Levin R M
Department of Urology, Johannes Gutenberg-University, Mainz, Germany.
J Urol. 2001 Feb;165(2):640-6. doi: 10.1097/00005392-200102000-00087.
Previous studies have shown that the initial reaction of the rabbit bladder to partial bladder outlet obstruction is increased blood flow at day 1 and a return to baseline blood flow at 1 week. Mucosal and muscle blood flow followed this pattern but mucosal blood flow was always 4 to 5-fold greater. In this study we examined the effect of 4 weeks of outlet obstruction on bladder blood flow and correlated it with the severity of bladder contractile dysfunction.
A total of 14 male New Zealand White rabbits underwent partial outlet obstruction creation by standard methods. After 4 weeks the rabbits were anesthetized, and blood flow to the muscle and mucosa was determined by standard fluorescent microsphere technique. A section of each detrusor was used for in vitro contractility studies. Contractile responses to field stimulation, carbachol and potassium chloride were determined. A section of each detrusor tissue was fixed in formalin and used to determine the smooth muscle volume fraction.
Four weeks of partial bladder outlet obstruction caused a significant and variable increase in bladder weight and a decrease in blood flow to bladder muscle without changes in the blood flow to mucosa. There was a clear correlation between the severity of contractile dysfunction, bladder weight and the magnitude of the decrease in blood flow in muscle. The smooth muscle volume fraction remained stable at approximately 40%.
Bladder decompensation was associated with decreased blood flow to bladder smooth muscle. Because compensated obstructed bladders with relatively normal contractile function are also hypertrophied but have normal blood flow, decreased blood flow in decompensated bladders is not simply a response to bladder hypertrophy. From this study we hypothesize that decreased blood flow to bladder smooth muscle is an etiological factor in bladder contractile dysfunction (bladder decompensation) secondary to partial outlet obstruction.
先前的研究表明，兔膀胱对部分膀胱出口梗阻的初始反应是在第1天血流量增加，而在1周时恢复至基线血流量。黏膜和肌肉血流量遵循这一模式，但黏膜血流量始终高出4至5倍。在本研究中，我们检测了4周出口梗阻对膀胱血流量的影响，并将其与膀胱收缩功能障碍的严重程度相关联。
总共14只雄性新西兰白兔通过标准方法接受部分出口梗阻造模。4周后，将兔子麻醉，采用标准荧光微球技术测定肌肉和黏膜的血流量。取各逼尿肌的一部分用于体外收缩性研究。测定对场刺激、卡巴胆碱和氯化钾的收缩反应。将各逼尿肌组织的一部分固定于福尔马林中，用于测定平滑肌体积分数。
4周的部分膀胱出口梗阻导致膀胱重量显著且变化不定地增加，膀胱肌肉血流量减少，而黏膜血流量无变化。收缩功能障碍的严重程度、膀胱重量与肌肉血流量减少幅度之间存在明显相关性。平滑肌体积分数稳定在约40%。
膀胱失代偿与膀胱平滑肌血流量减少相关。由于收缩功能相对正常的代偿性梗阻膀胱也会肥大，但血流量正常，因此失代偿膀胱中血流量减少并非仅仅是对膀胱肥大的反应。从本研究中我们推测，膀胱平滑肌血流量减少是部分出口梗阻继发膀胱收缩功能障碍（膀胱失代偿）的一个病因学因素。
