Urethral afferent nerve activity affects the micturition reflex; Implication for the relationship between stress incontinence and detrusor instability
Urethral afferent nerve activity affects the micturition reflex; Implication for the relationship between stress incontinence and detrusor instability
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DOI：
10.1097/00005392-199907000-00069
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发表时间：
1999-07-01
影响因子：
6.6
通讯作者：
Chancellor, MB
中科院分区：
文献类型：
--
作者：
Jung, SY;Fraser, MO;Chancellor, MB
目的：人们怀疑压力性尿失禁（SUI）和逼尿肌不稳定之间存在因果关系，但从未得到证实。许多患有混合性失禁的女性在 SUI 手术矫正后，逼尿肌不稳定得到了缓解。我们寻求实验支持，刺激尿道传入神经可以诱导或改变反射性逼尿肌收缩。 材料和方法：通过尿烷麻醉的女性 S.D. 的膀胱穹顶插入导管来测量尿道灌注压和等容膀胱压。大鼠（250 至 300 克；n = 12）。导管组件牢固地固定在膀胱颈中，以阻止膀胱和尿道之间的液体通过，而不影响器官的神经供应。外部尿道未插入导尿管。在对照状态下以 0.075 ml 的尿道盐水灌注速度检查反应。每分钟。用静脉注射金环蛇毒素（0.1 毫克/千克）阻断横纹括约肌活动后，给予尿道内药物。结果：停止尿道盐水输注导致约 50% 的研究动物 (n = 12) 排尿频率显着降低。尿道内注射利多卡因 (1%)，距离 0.075 英里。每分钟导致尿道灌注压略有下降，但逼尿肌收缩幅度没有变化。然而，尿道内注射利多卡因导致膀胱收缩频率显着降低 (45%) (n = 5)。停止利多卡因输注后 30 分钟，排尿频率恢复至基线。尿道内输注一氧化氮 (NO) 供体（S-亚硝基-N-乙酰青霉胺 [SNAP] (2 mM) 或硝普钠 (1 mM)）立即使尿道灌注压降低 30% 至 37% (n = 5)。还观察到膀胱收缩频率降低 45% 至 75% (n = 5)，这与利多卡因后观察到的情况相似。NO 供体均未改变尿道灌注压的幅度。结论：这些结果表明，在麻醉大鼠中，通过尿道灌注激活尿道传入神经可以调节排尿反射，因此，在压力性尿失禁患者中，尿液漏入近端尿道可能会刺激尿道传入神经并促进排尿反射，这意味着压力性尿失禁可以诱发和/或增加逼尿肌不稳定。通过手术或盆底运动矫正混合性尿失禁患者的压力性尿失禁可以解决逼尿肌不稳定的问题。
Purpose: A causative relationship between stress urinary incontinence (SUI) and detrusor instability has been suspected but never proven. Many women with mixed incontinence have resolution of detrusor instability after surgical correction of SUI. We sought experimental support that stimulation of urethral afferent nerves can induce or change reflex detrusor contractions.Materials and Methods: Urethral perfusion pressure and isovolumetric bladder pressure were measured with catheters inserted through the bladder dome in urethane anesthetized female S.D. rats (250 to 300 grams; n = 12). The catheter assembly was seated securely in the bladder neck to block passage of fluid between the bladder and urethra without affecting the nerve supply to the organs. The external urethra was not catheterized. Responses were examined in the control state at a urethral saline perfusion speed of 0.075 ml. per minute. Intraurethral drugs were administered following blockade of striated sphincter activity with intravenous or-bungarotoxin (0.1 mg./kg.).Results: Stopping the urethral saline infusion caused a significant decrease in micturition frequency in approximately 50% of the animals studied (n = 12). Intraurethral lidocaine (1%) infused at 0.075 mi. per minute caused a slight decrease in urethral perfusion pressure but no change in detrusor contraction amplitude. However, intraurethral lidocaine caused a significant (45%) decrease in the bladder contraction frequency (n = 5). The micturition frequency returned to baseline 30 minutes after stopping lidocaine infusion. Intraurethral infusion of nitric oxide (NO) donors (S-nitroso-N-acetylpenicillamine [SNAP] (2 mM) or nitroprusside (1 mM) immediately decreased urethral perfusion pressure by 30 to 37% (n = 5). A 45 to 75% decrease (n = 5) in bladder contraction frequency was also seen, which was similar to that observed following lidocaine. Neither NO donor changed the amplitude of bladder contractions.Conclusions: These results indicate that in the anesthetized rat activation of urethral afferents by urethral perfusion can modulate the micturition reflex. Thus in patients with stress urinary incontinence, leakage of urine into the proximal urethra may stimulate urethral afferents and facilitate voiding reflexes. This implies that stress incontinence can induce and/or increase detrusor instability. These findings have significant implications for the treatment of patients with mixed urge and stress incontinence. Correction of stress incontinence by surgery or pelvic floor exercise in patients with mixed incontinence may resolve the detrusor instability.