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猫的胫神经躯体传入轴突长时间刺激后膀胱活动低下。

Bladder underactivity after prolonged stimulation of somatic afferent axons in the tibial nerve in cats.

机构信息

Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania.

Department of Urology, Qianfoshan Hospital, Shandong University, Jinan, P.R. China.

出版信息

Neurourol Urodyn. 2018 Sep;37(7):2121-2127. doi: 10.1002/nau.23577. Epub 2018 Apr 10.

Abstract

AIMS

To establish an animal model of bladder underactivity induced by prolonged and intense stimulation of somatic afferent axons in the tibial nerve.

METHODS

In seven cats under α-chloralose anesthesia, tibial nerve stimulation (TNS) of 30-min duration was repeatedly (3-8 times) applied at 4-6 times threshold (T) intensity for inducing a toe twitch to produce bladder underactivity determined by cystometry. Naloxone (1 mg/kg, i.v.) was administered to examine the role of opioid receptors in TNS-induced bladder underactivity.

RESULTS

After prolonged (1.5-4 h) and intense (4-6T) TNS, a complete suppression of the micturition reflex occurred in six cats and an increase in bladder capacity to about 150% of control and a decrease in the micturition contraction amplitude to 50% of control occurred in one cat. The bladder underactivity was maintained for at least 1-1.5 h. Naloxone reversed the bladder underactivity, but an additional 30-min TNS removed the naloxone effect.

CONCLUSIONS

The results indicate that prolonged and intense activation of somatic afferent axons in the tibial nerve can suppress the central reflex mechanisms controlling micturition. This animal model may be useful for examining the pathophysiology of neurogenic bladder underactivity and for development of new treatments for underactive bladder symptoms.

摘要

目的

建立一种由胫神经躯体传入轴突长时间、高强度刺激引起的膀胱活动低下动物模型。

方法

在 7 只氯醛糖麻醉下的猫中,以 30 分钟的胫神经刺激(TNS),以 4-6 倍阈值(T)强度重复(3-8 次)应用,以产生足搐动,通过膀胱测压法确定膀胱活动低下。静脉注射纳洛酮(1mg/kg)以检查阿片受体在 TNS 诱导的膀胱活动低下中的作用。

结果

在长时间(1.5-4 小时)和高强度(4-6T)TNS 后,6 只猫出现完全抑制排尿反射,1 只猫膀胱容量增加到对照的 150%左右,排尿收缩幅度下降到对照的 50%。膀胱活动低下至少持续 1-1.5 小时。纳洛酮逆转了膀胱活动低下,但额外的 30 分钟 TNS 消除了纳洛酮的作用。

结论

结果表明,胫神经躯体传入轴突的长时间、高强度激活可抑制控制排尿的中枢反射机制。这种动物模型可能有助于研究神经原性膀胱活动低下的病理生理学,并为治疗膀胱活动低下症状开发新的治疗方法。

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