外源性给予阿片类药物可导致雌性大鼠体内的尿道固有括约肌收缩。

Exogenously administered opioids contract the female rat intrinsic urethral sphincter in vivo.

机构信息

Department of Clinical and Experimental Physiology, Medical University of Warsaw, Warsaw, Poland.

出版信息

Neurourol Urodyn. 2010 Jun;29(5):777-82. doi: 10.1002/nau.20822.

DOI:10.1002/nau.20822

PMID:19899147

Abstract

BACKGROUND AND OBJECTIVE

Previous studies have reported immunoreactive opioid nerve fibers in the detrusor and lower urinary tract sphincters. However, there is a paucity of in vivo studies demonstrating the direct effect of endogenous opioids in these structures. In the present study, we investigated the contractile actions of intra-arterially administered exogenous Dynorphin-A, Met-enkephalin, Leu-enkephalin, morphine, and the opioid antagonist naltrexone on the female rat intrinsic urethral sphincter in vivo.

METHODS

Intraurethral pressure was recorded by a catheter placed at the maximum pressure zone of the intrinsic urethral sphincter in anesthetized female Sprague-Dawley rats. The effects of different opioids were studied and expressed as means and as percentages of pressure change (cmH(2)O) of the baseline intraurethral pressure.

RESULTS

Dynorphin-A, Met-enkephalin, and Leu-enkephalin evoked rapid, long-lasting contractile effects on the female rat urethra. The greatest intraurethral pressure increase was evoked by Dynorphin-A (89.2 +/- 15.3%). For Met-enkephalin, intraurethral pressure increased by 70.2 +/- 21.8% and for Leu-enkephalin, the pressure increase was 60.6 +/- 20%. Morphine, however, evoked inconsistent intraurethral pressure changes, increasing the urethral pressure in three subjects and lowering the pressure in the remaining six subjects. The opioid antagonist naltrexone reduced the intraurethral pressure by a mean of -19.0 +/- 5.8%.

CONCLUSION

Results of the present study suggest that endogenous opioids by their contractile action on the intrinsic urethral sphincter may play a role in the control of continence in rats, additional to cholinergic and noradrenergic pathways.

摘要

背景与目的

先前的研究已经报道了在逼尿肌和下尿路括约肌中存在免疫反应性阿片神经纤维。然而，目前还缺乏体内研究来证明内源性阿片在这些结构中的直接作用。在本研究中，我们研究了经动脉给予外源性强啡肽-A、甲硫氨酸-脑啡肽、亮氨酸-脑啡肽、吗啡和阿片受体拮抗剂纳洛酮对雌性大鼠内在尿道括约肌的收缩作用。

方法

在麻醉的 Sprague-Dawley 雌性大鼠的内在尿道括约肌最大压力区放置导管，记录尿道内压。研究了不同阿片类药物的作用，并以压力变化（cmH2O）的平均值和基线尿道内压的百分比表示。

结果

强啡肽-A、甲硫氨酸-脑啡肽和亮氨酸-脑啡肽对雌性大鼠尿道产生快速、持久的收缩作用。强啡肽-A 引起的尿道内压增加最大（89.2 +/- 15.3%）。对于甲硫氨酸-脑啡肽，尿道内压增加 70.2 +/- 21.8%，对于亮氨酸-脑啡肽，压力增加 60.6 +/- 20%。然而，吗啡引起的尿道内压变化不一致，在 3 名受试者中增加了尿道内压，在其余 6 名受试者中降低了尿道内压。阿片受体拮抗剂纳洛酮使尿道内压平均降低 19.0 +/- 5.8%。