Deng Han, Liao Limin, Li Xing, Liu Qinggang, Wang Xuesheng, Zhou Zhonghan
Department of Urology, China Rehabilitation Research Center, Rehabilitation School of Capital Medical University, Beijing, China.
University of Health and Rehabilitation Sciences, Qingdao, Shandong, China.
Int Neurourol J. 2022 Dec;26(4):288-298. doi: 10.5213/inj.2244162.081. Epub 2022 Dec 30.
To explore the effect of intravesical electrical stimulation (IVES) on urinary adenosine triphosphate (ATP) and nitric oxide (NO) in rats with detrusor underactivity (DU) induced by bilateral pelvic nerve crush (bPNC), and to determine the underlying peripheral mechanism.
Twenty-four female Sprague-Dawley rats were equally divided into 3 groups: sham; bPNC; and IVES. Rats in the IVES group began to receive IVES treatment 10 days after bPNC (20 minutes per day for 14 consecutive days). After the 14th IVES, rat urine was collected and cystometry was performed. The serum creatinine, blood urea nitrogen, and urinary ATP and NO levels were measured, and a routine urinalysis was performed.
The maximum cystometric capacity (MCC), maximum changes in bladder pressure during filling (∆FP), and postvoid residual urine (PVR) in the IVES group were significantly lower than the bPNC group, and the maximum changes in bladder pressure during voiding (∆VP) was significantly higher than the bPNC group. Compared with the sham group, the MCC, ∆FP and PVR were significantly increased, and the maximum voiding pressure (MVP) and ∆VP were significantly decreased in the bPNC group. After bPNC, urinary ATP was significantly decreased, and urinary NO was significantly increased. In IVES-treated rats, urinary ATP was significantly higher than the bPNC group, and NO was significantly lower than the bPNC group. In addition, the ATP-to-NO ratio of the rats in the bPNC group was significantly lower than the sham and IVES groups. Correlation analysis showed that the ATP and NO were not correlated with the MCC, ∆FP, MVP, ∆VP, and PVR.
Promoting the release of urothelial ATP and inhibiting the release of urothelial NO may be one of the peripheral mechanisms underlying IVES in the treatment of DU. Specifically, IVES may shift the balance between excitation and inhibition toward excitation.
探讨膀胱内电刺激（IVES）对双侧盆神经挤压（bPNC）诱导的逼尿肌活动低下（DU）大鼠尿三磷酸腺苷（ATP）和一氧化氮（NO）的影响，并确定其潜在的外周机制。
将24只雌性Sprague-Dawley大鼠平均分为3组：假手术组；bPNC组；IVES组。IVES组大鼠在bPNC后10天开始接受IVES治疗（每天20分钟，连续14天）。第14次IVES后，收集大鼠尿液并进行膀胱测压。测量血清肌酐、血尿素氮、尿ATP和NO水平，并进行尿常规分析。
IVES组的最大膀胱测压容量（MCC）、充盈期膀胱压力最大变化（∆FP）和排尿后残余尿量（PVR）显著低于bPNC组，排尿期膀胱压力最大变化（∆VP）显著高于bPNC组。与假手术组相比，bPNC组的MCC、∆FP和PVR显著增加，最大排尿压力（MVP）和∆VP显著降低。bPNC后，尿ATP显著降低，尿NO显著增加。在接受IVES治疗的大鼠中，尿ATP显著高于bPNC组，NO显著低于bPNC组。此外，bPNC组大鼠的ATP与NO比值显著低于假手术组和IVES组。相关性分析表明，ATP和NO与MCC、∆FP、MVP、∆VP和PVR均无相关性。
促进尿路上皮ATP释放并抑制尿路上皮NO释放可能是IVES治疗DU的外周机制之一。具体而言，IVES可能使兴奋与抑制之间的平衡向兴奋方向转变。
