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阿片受体在猪骶神经调节诱导的膀胱过度活动抑制中的作用:一种可能的作用机制。

Involvement of opioid receptors in inhibition of bladder overactivity induced by sacral neuromodulation in pigs: A possible action mechanism.

作者信息

Li Xing, Liao Limin, Chen Guoqing, Wang Zhaoxia, Deng Han

机构信息

Rehabilitation School of Capital Medical University, Beijing, China.

Department of Urology, China Rehabilitation Research Centre, Beijing, China.

出版信息

Neurourol Urodyn. 2017 Sep;36(7):1742-1748. doi: 10.1002/nau.23187. Epub 2016 Dec 9.

Abstract

AIMS

To determine the role of opioid receptors in the inhibition of bladder overactivity by sacral neuromodulation (SNM) in pigs, and explore the possible mechanism of SNM.

METHODS

Both implant-driven stimulators of the S3 spinal nerve were implanted in seven pigs. Naloxone and tramadol were administered. Multiple cystometrograms were performed to determine the effects of SNM and opioid receptors on the micturition reflex by infusing normal saline (NS) or acetic acid (AA).

RESULTS

AA-induced bladder overactivity significantly reduced the bladder capacity (BC) to 29.9 ± 3.9% of the NS control level (413.1 ± 55.4 mL) (P < 0.01). SNM significantly increased the BC to 39.4 ± 5.5% of the NS control level (P < 0.03). In the absence of SNM, the cumulative dose of naloxone (0.02 and 0.2 mg/kg intravenously) did not significantly change the BC (25.1 ± 3.1% and 20.2 ± 3.1% of the NS control level, respectively) (P > 0.05). In the presence of SNM, both doses of naloxone significantly reduced the BC to 27.2 ± 3.0% and 25.1 ± 2.9% of the NS control level (P < 0.05), respectively. In the absence of SNM, tramadol did not significantly change the BC (31.5 ± 3.9% of the NS control level) (P > 0.05). In the presence of SNM, tramadol significantly increased the BC to 49.1 ± 6.1% of the NS control level (P < 0.01).

CONCLUSIONS

Opioid receptors play a role in inhibition of bladder overactivity during SNM. Combining SNM with tramadol could be a novel treatment modality for overactive bladder.

摘要

目的

确定阿片受体在猪骶神经调节(SNM)抑制膀胱过度活动中的作用,并探讨SNM的可能机制。

方法

将S3脊神经植入式驱动刺激器植入7头猪体内。给予纳洛酮和曲马多。通过输注生理盐水(NS)或醋酸(AA)进行多次膀胱压力容积测定,以确定SNM和阿片受体对排尿反射的影响。

结果

AA诱导的膀胱过度活动显著降低膀胱容量(BC)至NS对照水平(413.1±55.4 mL)的29.9±3.9%(P<0.01)。SNM显著增加BC至NS对照水平的39.4±5.5%(P<0.03)。在无SNM的情况下,纳洛酮累积剂量(静脉注射0.02和0.2 mg/kg)未显著改变BC(分别为NS对照水平的25.1±3.1%和20.2±3.1%)(P>0.05)。在有SNM的情况下,两种剂量的纳洛酮均显著降低BC至NS对照水平的27.2±3.0%和25.1±2.9%(P<0.05)。在无SNM的情况下,曲马多未显著改变BC(NS对照水平的31.5±3.9%)(P>0.05)。在有SNM的情况下,曲马多显著增加BC至NS对照水平的49.1±6.1%(P<0.01)。

结论

阿片受体在SNM抑制膀胱过度活动中起作用。将SNM与曲马多联合使用可能是治疗膀胱过度活动症的一种新方法。

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