Kim Khae-Hawn, Jin Long-Hu, Choo Gwoan-Youb, Lee Hun-Jae, Choi Bo-Hwa, Kwak Jiyeon, Yoon Sang-Min, Park Chang-Shin, Lee Tack
Departments of Urology, Gachon University Gil Hospital, Incheon 405-760, Korea.
Departments of Urology, Inha University College of Medicine, Incheon 402-751, Korea.
Int J Mol Sci. 2012;13(4):5048-5059. doi: 10.3390/ijms13045048. Epub 2012 Apr 23.
The involuntary dual control systems of the autonomic nervous system (ANS) in the bladder of awake spontaneously hypertensive rats (SHRs) were investigated through simultaneous registrations of intravesical and intraabdominal pressures to observe detrusor overactivity (DO) objectively as a core symptom of an overactive bladder. SHRs (n = 6) showed the features of overactive bladder syndrome during urodynamic study, especially DO during the filling phase. After injection of the nonselective sympathetic blocking agent labetalol, DO disappeared in 3 of 6 SHRs (50%). DO frequency decreased from 0.98 ± 0.22 min(-1) to 0.28 ± 0.19 min(-1) (p < 0.01), and DO pressure decreased from 3.82 ± 0.57 cm H(2)O to 1.90 ± 0.86 cm H(2)O (p < 0.05). This suggests that the DO originating from the overactive parasympathetic nervous system is attenuated by the nonselective blocking of the sympathetic nervous system. The detailed mechanism behind this result is still not known, but parasympathetic overactivity seems to require overactive sympathetic nervous system activity in a kind of balance between these two systems. These findings are consistent with recent clinical findings suggesting that patients with idiopathic overactive bladder may have ANS dysfunction, particularly a sympathetic dysfunction. The search for newer and better drugs than the current anticholinergic drugs as the mainstay for overactive bladder will be fueled by our research on these sympathetic mechanisms. Further studies of this principle are required.
通过同时记录膀胱内压和腹内压,研究清醒自发性高血压大鼠(SHR)膀胱自主神经系统(ANS)的非自主双重控制系统,以客观观察逼尿肌过度活动(DO),这是膀胱过度活动症的核心症状。在尿动力学研究中,SHR(n = 6)表现出膀胱过度活动症的特征,尤其是在充盈期的DO。注射非选择性交感神经阻滞剂拉贝洛尔后,6只SHR中有3只(50%)的DO消失。DO频率从0.98±0.22次/分钟降至0.28±0.19次/分钟(p<0.01),DO压力从3.82±0.57 cm H₂O降至1.90±0.86 cm H₂O(p<0.05)。这表明起源于副交感神经系统过度活跃的DO通过交感神经系统的非选择性阻断而减弱。该结果背后的详细机制尚不清楚,但副交感神经活动过度似乎需要交感神经系统在这两个系统之间的某种平衡中过度活跃。这些发现与最近的临床发现一致,即特发性膀胱过度活动症患者可能存在ANS功能障碍,尤其是交感神经功能障碍。我们对这些交感神经机制的研究将推动寻找比目前作为膀胱过度活动症主要治疗药物的抗胆碱能药物更新更好的药物。需要对这一原理进行进一步研究。