Murakami Shigetaka, Yoshida Masaki, Masunaga Koichi, Maeda Yoshihiro, Ueda Shoichi
Department of Urology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
BJU Int. 2008 Mar;101(5):633-9. doi: 10.1111/j.1464-410X.2007.07325.x. Epub 2007 Dec 7.
To investigate changes in acetylcholine release from the bladder of rats with partial bladder outlet obstruction (BOO), as partial BOO leads to hypertrophy and an alteration in the contractions of the detrusor smooth muscle, and acetylcholine plays an important role in urinary bladder contractions but there is little available information on acetylcholine release after BOO.
Partial BOO was induced in adult female rats by ligating the proximal urethra over a 1 mm angiocatheter; sham-operated rats served as controls. The rats were killed 2 weeks, 3 and 6 months after induction of BOO. We investigated the contractions induced by carbachol, KCl (80 mm), ATP and electrical-field stimulation (EFS, 2.5-40 Hz), and collected the dialysate obtained from a microdialysis probe inserted into the muscle strips during EFS, and measured the amount of acetylcholine in the dialysate fraction by high-performance liquid chromatography with electro-chemical detection. S-100 immunohistochemical staining of the bladder preparations was used for histological examination in BOO and control rats.
The bladder weight gradually increased after BOO. There were no significant changes in KCl-induced contractions throughout the experimental period in either group. There were no significant changes in carbachol-induced contractions until 3 months after BOO but there was a significant reduction at 6 months. ATP-induced contractions were significantly increased 2 weeks and 3 months after BOO. EFS-induced contractions were gradually reduced after BOO. Acetylcholine release from the bladder strips was not significantly different between the groups until 2 weeks after BOO. However, acetylcholine release in BOO rats was significantly decreased 3-6 months after BOO, being significantly lower than that of the control rats. In the histological study, the number of nerve fibres in the BOO rats was significantly lower than in the control rats.
We suggest that the prolonged BOO caused a decrease in EFS-induced acetylcholine release and the number of nerves in the rat urinary bladder, which might contribute to bladder underactivity in BOO.
探讨部分膀胱出口梗阻（BOO）大鼠膀胱乙酰胆碱释放的变化，因为部分BOO会导致膀胱逼尿肌平滑肌肥大及收缩改变，且乙酰胆碱在膀胱收缩中起重要作用，但关于BOO后乙酰胆碱释放的信息较少。
通过在1毫米血管导管上结扎成年雌性大鼠的近端尿道诱导部分BOO；假手术大鼠作为对照。在诱导BOO后2周、3个月和6个月处死大鼠。我们研究了卡巴胆碱、氯化钾（80毫摩尔）、三磷酸腺苷（ATP）和电场刺激（EFS，2.5 - 40赫兹）诱导的收缩，并在EFS期间收集从插入肌肉条的微透析探针获得的透析液，通过高效液相色谱 - 电化学检测法测量透析液部分中乙酰胆碱的含量。对膀胱标本进行S - 100免疫组织化学染色用于BOO大鼠和对照大鼠的组织学检查。
BOO后膀胱重量逐渐增加。两组在整个实验期间氯化钾诱导的收缩均无显著变化。卡巴胆碱诱导的收缩在BOO后3个月前无显著变化，但在6个月时显著降低。ATP诱导的收缩在BOO后2周和3个月时显著增加。BOO后EFS诱导的收缩逐渐降低。在BOO后2周前，两组膀胱条带中乙酰胆碱的释放无显著差异。然而，BOO大鼠在BOO后3 - 6个月时乙酰胆碱释放显著降低，明显低于对照大鼠。在组织学研究中，BOO大鼠的神经纤维数量显著低于对照大鼠。
我们认为，长期的BOO导致大鼠膀胱中EFS诱导的乙酰胆碱释放减少以及神经数量减少，这可能导致BOO时膀胱活动不足。
