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阴茎纤维化的改善:神话还是现实。

Amelioration of penile fibrosis: myth or reality.

作者信息

El-Sakka Ahmed I, Yassin Aksam A

机构信息

Department of Urology, Suez Canal University, Ismailia, Egypt.

出版信息

J Androl. 2010 Jul-Aug;31(4):324-35. doi: 10.2164/jandrol.109.008730. Epub 2009 Nov 19.

DOI:10.2164/jandrol.109.008730
PMID:19926883
Abstract

Several changes have been reported to occur in the cavernosal tissue and tunica albuginea with aging. The atherosclerosis of the penis that occurs with aging causes a decrease in penile oxygen tension. A reduction in the number of smooth muscle cells (SMCs) has been demonstrated in relation to this change in oxygen tension. Changes in the ratio of penile collagen have also been observed and could explain the decrease in penile elasticity and compliance with aging. Chronic ischemia is therefore associated with fibrosis but also with nitric oxide-cGMP reduction. The sensitivity of the α-adrenoceptors on the SMCs increases with aging. Furthermore, androgen deprivation produces penile tissue atrophy, alterations in dorsal nerve structure, alterations in endothelial morphology, reductions in trabecular SM content, increases in deposition of extracellular matrix, and increases in accumulation of adipocytes in the subtunical region of the corpus cavernosum. All of these modifications can explain the prevalence of erectile dysfunction with aging. The aim of this review is to address the underlying etiology of corporal fibrosis, especially aging, cavernosal nerve damage, androgen deprivation, and tunical fibrosis. Finally, we will address the proposed amelioration and reversal of fibrosis in terms of correcting, at least partially, the relative SMC loss that occurs with aging, diabetes, or cavernosal nerve damage and its impact on prevention of erectile dysfunction-associated cavernosal fibrosis.

摘要

据报道,随着年龄增长,海绵体组织和白膜会发生一些变化。阴茎动脉粥样硬化随着年龄增长而出现,导致阴茎氧张力降低。与这种氧张力变化相关的是,已证实平滑肌细胞(SMC)数量减少。还观察到阴茎胶原蛋白比例的变化,这可以解释随着年龄增长阴茎弹性和顺应性的降低。因此,慢性缺血与纤维化有关,但也与一氧化氮 - 环磷酸鸟苷减少有关。随着年龄增长,SMC上α - 肾上腺素能受体的敏感性增加。此外,雄激素剥夺会导致阴茎组织萎缩、背神经结构改变、内皮形态改变、小梁平滑肌含量减少、细胞外基质沉积增加以及海绵体白膜下区域脂肪细胞积累增加。所有这些改变都可以解释随着年龄增长勃起功能障碍的患病率。本综述的目的是探讨海绵体纤维化的潜在病因,特别是衰老、海绵体神经损伤、雄激素剥夺和白膜纤维化。最后,我们将探讨在至少部分纠正随着衰老、糖尿病或海绵体神经损伤而发生的相对SMC损失方面提出的纤维化改善和逆转方法及其对预防勃起功能障碍相关海绵体纤维化的影响。

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