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慢性低剂量和高剂量乙醇摄入对兔海绵体平滑肌松弛和阴茎一氧化氮合酶的影响。

Effects of chronic low- and high-dose ethanol intake on the nitrergic relaxations of corpus cavernosum and penile nitric oxide synthase in the rabbit.

机构信息

Department of Histology and Embryology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey.

出版信息

Int J Impot Res. 2012 Sep;24(5):185-90. doi: 10.1038/ijir.2012.14. Epub 2012 May 10.

DOI:10.1038/ijir.2012.14
PMID:22573232
Abstract

Epidemiological evidence showed that chronic ethanol consumption is a major risk factor in the development of impotence. The present study investigated the effects of carbachol-, electrical field stimulation (EFS)-, sodium nitroprusside (SNP)- and papaverine-induced relaxant responses in the isolated corpus cavernosum tissues from rabbits submitted to an 12-week course of chronic low (5% v/v) or high ethanol intake (30% v/v). Increased carbachol- and EFS-induced relaxant responses but not SNP and papaverine, were observed in low ethanol-fed rabbits compared with controls. However, impaired carbachol- and EFS-induced relaxant responses were observed in high ethanol-fed rabbits compared with control rabbits. There were no significant differences in SNP- and papaverine-induced relaxant responses between control and high ethanol-fed rabbits. In addition, decreased neuronal nitric oxide synthase (nNOS) and endothelial NOS (eNOS) immunoreactivity in penile tissue were found in high ethanol-fed rabbits, but increased the immunoreactivity in low ethanol-fed group, compared with control group. These results suggest that alterations in nitric oxide (NO) production within the cavernous tissue in the high ethanol-fed rabbits are, at least in part, responsible for the erectile dysfunction.

摘要

流行病学证据表明,慢性乙醇摄入是导致勃起功能障碍的一个主要危险因素。本研究旨在探讨慢性低浓度(5% v/v)或高浓度乙醇摄入(30% v/v) 12 周后,兔离体海绵体组织中乙酰胆碱、电刺激(EFS)、硝普钠(SNP)和罂粟碱诱导的舒张反应的变化。与对照组相比,低乙醇喂养组的兔对乙酰胆碱和 EFS 诱导的舒张反应增加,但对 SNP 和罂粟碱诱导的舒张反应受损。与对照组相比,高乙醇喂养组的兔对 SNP 和罂粟碱诱导的舒张反应无明显差异。此外,与对照组相比,高乙醇喂养组的阴茎组织中神经元型一氧化氮合酶(nNOS)和内皮型一氧化氮合酶(eNOS)免疫反应性降低,但在低乙醇喂养组中增加。这些结果表明,高乙醇喂养组海绵体组织中一氧化氮(NO)生成的改变至少部分导致了勃起功能障碍。

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