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L6-S1脊髓神经刺激可降低环磷酰胺诱导的膀胱炎麻醉大鼠的排尿频率。

L6-S1 spinal nerve stimulation reduces micturition frequency in anaesthetized rats with cyclophosphamide-induced cystitis.

作者信息

Giuliano François A, Denys Pierre, Chartier-Kastler Emmanuel, Alexandre Laurent, Bernabe Jacques

机构信息

Pelvipharm Laboratories, CNRS, Gif-sur-Yvette, AP-HP, Raymond Poincaré Hospital, Garches, France.

出版信息

BJU Int. 2006 Feb;97(2):386-92. doi: 10.1111/j.1464-410X.2005.05914.x.

Abstract

OBJECTIVE

To further investigate the rationale for using spinal nerve stimulation (SNS) for treating bladder overactivity associated with cystitis in a rat model of cyclophosphamide-induced cystitis, as several studies suggested that symptoms associated with chronic cystitis could be treated using stimulation of sacral spinal nerves, but the mechanisms by which it works are unknown.

MATERIALS AND METHODS

Cystitis was induced by i.p. injection of cyclophosphamide 48 h before the experiments in anaesthetized male rats. Neurograms were taken by placing a recording electrode onto the pelvic nerve and a stimulating electrode on either the L6 or S1 ipsilateral spinal nerves. Two selected intensities were then evaluated for SNS in control and cyclophosphamide-treated rats during cystometry.

RESULTS

Cyclophosphamide resulted in significant bladder overactivity. There was no apparent difference in the neurograms generated in response to SNS of the S1 and L6 spinal nerves, and between cyclophosphamide and control rats. Intensities of 200 microA (Adelta-fibre-specific) and 2 mA (Adelta+ C-fibres) were chosen for SNS. Continuous SNS at 200 microA significantly reduced the frequency of voiding and non-voiding contractions in cyclophosphamide-treated rats. SNS at 2 mA resulted in the abolition of voiding contractions, accompanied by continuous leakage of urine.

CONCLUSION

SNS recruiting only Adelta-fibre produced fewer voiding contractions in cyclophosphamide-treated rats, to a level similar to that from the control rats. These results support the ability of SNS to decrease bladder overactivity in a pathophysiological model of chemical irritation of the bladder.

摘要

目的

在环磷酰胺诱导的膀胱炎大鼠模型中,进一步探究使用脊髓神经刺激(SNS)治疗与膀胱炎相关的膀胱过度活动症的理论依据,因为多项研究表明,慢性膀胱炎相关症状可通过刺激骶神经来治疗,但其作用机制尚不清楚。

材料与方法

在实验前48小时,通过腹腔注射环磷酰胺诱导麻醉的雄性大鼠患膀胱炎。将记录电极置于盆神经上,刺激电极置于同侧L6或S1脊髓神经上,记录神经电图。然后在膀胱测压期间,对对照组和环磷酰胺处理组大鼠的SNS评估两种选定强度。

结果

环磷酰胺导致明显的膀胱过度活动。对S1和L6脊髓神经进行SNS时所产生的神经电图,以及环磷酰胺处理组和对照组大鼠之间,均无明显差异。选择200微安(特异性激活Aδ纤维)和2毫安(激活Aδ + C纤维)的强度进行SNS。在环磷酰胺处理的大鼠中,以200微安持续进行SNS可显著降低排尿频率和非排尿收缩频率。以2毫安进行SNS可导致排尿收缩消失,并伴有持续性漏尿。

结论

在环磷酰胺处理的大鼠中,仅募集Aδ纤维的SNS产生的排尿收缩较少,降至与对照组大鼠相似的水平。这些结果支持SNS在膀胱化学刺激病理生理模型中降低膀胱过度活动的能力。

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