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去势及雄激素替代对大鼠阴茎勃起血流动力学的影响。

Effects of castration and androgen replacement on the hemodynamics of penile erection in the rat.

作者信息

Mills T M, Stopper V S, Wiedmeier V T

机构信息

Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912-3000.

出版信息

Biol Reprod. 1994 Aug;51(2):234-8. doi: 10.1095/biolreprod51.2.234.

DOI:10.1095/biolreprod51.2.234
PMID:7948478
Abstract

Previous studies from this laboratory have demonstrated that penile erection in the rat is androgen dependent: 1 wk after castration, there was a significant decline in the magnitude of the intracavernosal pressure (CCP) response during erection induced by stimulation of the autonomic ganglion controlling penile blood flow. The response was altered by vasoactive drugs and appeared to involve nitric oxide synthesis. These earlier studies, however, did not identify the site of androgenic action or the mechanism by which the androgens act. The findings reported here show that even in long-term-castrated animals (up to 7 wk), there remains a rise in CCP in response to ganglionic stimulation, demonstrating that there is an androgen-independent as well as an androgen-dependent portion of the erectile response. Other results show a linear relationship between systemic blood pressure and CCP during erection, although in castrated animals without androgen replacement, the CCP responds less to changes in the systemic pressure than in intact or testosterone-treated animals. This finding could signify a reduced blood inflow and/or an increased blood outflow during erection in the castrated rats. Further studies partially explained the lower erectile pressure by demonstrating that the rate of outflow from the cavernosal spaces was greater in castrated rats than in animals with normal androgen levels. Taken together, these findings show that androgens act to maintain both the inflow and the outflow of blood from the cavernous spaces during erection.

摘要

该实验室之前的研究表明,大鼠的阴茎勃起依赖雄激素:去势1周后,刺激控制阴茎血流的自主神经节诱导勃起时,海绵体内压(CCP)反应的幅度显著下降。该反应会因血管活性药物而改变,且似乎涉及一氧化氮合成。然而,这些早期研究并未确定雄激素作用的部位或雄激素的作用机制。此处报道的研究结果表明,即使在长期去势的动物(长达7周)中,对神经节刺激仍会出现CCP升高,这表明勃起反应中存在雄激素非依赖部分和雄激素依赖部分。其他结果显示,勃起过程中全身血压与CCP之间存在线性关系,不过在未进行雄激素替代的去势动物中,CCP对全身压力变化的反应比完整动物或接受睾酮治疗的动物要小。这一发现可能意味着去势大鼠勃起时血流量减少和/或血液流出增加。进一步的研究部分解释了勃起压力较低的原因,即去势大鼠海绵体间隙的血液流出速率比雄激素水平正常的动物更快。综上所述,这些研究结果表明,雄激素在勃起过程中起到维持海绵体间隙血液流入和流出的作用。

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