Inhibitory effects of tibial nerve stimulation on bladder neurophysiology in rats
Inhibitory effects of tibial nerve stimulation on bladder neurophysiology in rats
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DOI：
10.1186/s40064-016-1687-6
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发表时间：
2016-01-15
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影响因子：
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通讯作者：
van Asselt, Els
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作者：
Choudhary, Mahipal;van Mastrigt, Ron;van Asselt, Els
胫神经刺激（TNS）是周围神经调节的一种形式，已被发现对治疗膀胱过度活跃症状有效，副作用比一线药物治疗小。尽管其临床应用广泛，但其潜在的作用机制尚不完全清楚。我们的目的是研究其对膀胱神经生理学的影响，并通过醋酸（AA）滴注模拟过度活动逼尿肌排尿的触发机制。在氨基甲酸乙酯麻醉的雄性Wistar大鼠中，以5 Hz，脉冲宽度200 μ s，幅度约为阈值的3倍刺激胫骨神经30分钟，引起轻微的脚趾运动。在AA诱导的逼尿肌过度活动中，触发排尿收缩的压力（p(3)）在tns前后测量之间没有显着变化。结果发现，TNS通过增加p(3)时膀胱顺应性和膀胱体积显著逆转AA刺激效应，并抑制阈值传入神经活动。压力与传入活动线性关系的斜率在注入AA后增大，刺激后显著减小。除了其众所周知的中枢抑制机制外，本研究还表明，TNS通过外周水平对膀胱传入信号的抑制作用，延迟排尿的发生，从而提高膀胱储存能力。
Tibial nerve stimulation (TNS) is a form of peripheral neuromodulation which has been found effective in treating overactive bladder symptoms, with lesser side effects than first line pharmacotherapy. Despite its widespread clinical use, the underlying mechanism of action is not fully understood. Our aim was to study its effect on the bladder neurophysiology and the trigger mechanism of voiding in the overactive detrusor, simulated by acetic acid (AA) instillation. In urethane anaesthetized male Wistar rats, the tibial nerve was stimulated for 30 min at 5 Hz, pulse width 200 mu s and amplitude approximately three times the threshold to induce a slight toe movement. The pressure at which a voiding contraction was triggered (p(thres)) did not change significantly between the pre-and post-TNS measurements in AA induced detrusor overactivity. It was found that TNS significantly reversed the effects of AA irritation by increasing the bladder compliance and the bladder volume at p(thres), as well as suppressed the threshold afferent nerve activity. The slope of the linear relationship between pressure and the afferent activity increased after AA instillation and decreased significantly after stimulation. In addition to its well-known central inhibitory mechanisms, this study has demonstrated that TNS improves bladder storage capacity by delaying the onset of voiding, via an inhibitory effect on the bladder afferent signaling at the peripheral level.