Tostes Rita C, Carneiro Fernando S, Lee Anthony J, Giachini Fernanda R C, Leite Romulo, Osawa Yoichi, Webb R Clinton
University of Sao Paulo, Department of Pharmacology, Sao Paulo, SP, Brazil.
J Sex Med. 2008 Jun;5(6):1284-95. doi: 10.1111/j.1743-6109.2008.00804.x. Epub 2008 Mar 4.
Thirty million men in the United States suffer from erectile dysfunction (ED) and this number is expected to double by 2025. Considered a major public health problem, which seriously affects the quality of life of patients and their partners, ED becomes increasingly prevalent with age and chronic smoking is a major risk factor in the development of ED.
To review available evidence concerning the effects of cigarette smoking on vascular changes associated with decreased nitric oxide (NO) bioavailability and increased reactive oxygen species (ROS) generation.
We examined epidemiological and clinical data linking cigarette smoking and ED, and the effects of smoking on vascular NO bioavailability and ROS generation.
There are strong parallels between smoking and ED and considerable evidence supporting the concept that smoking-related ED is associated with reduced bioavailability of NO because of increased ROS.
Cigarette smoking-induced ED in human and animal models is associated with impaired arterial flow to the penis or acute vasospasm of the penile arteries. Long-term smoking produces detrimental effects on the vascular endothelium and peripheral nerves and also causes ultrastructural damage to the corporal tissue, all considered to play a role in chronic smoking-induced ED. Clinical and basic science studies provide strong indirect evidence that smoking may affect penile erection by the impairment of endothelium-dependent smooth muscle relaxation or more specifically by affecting NO production via increased ROS generation. Whether nicotine or other products of cigarette smoke mediate all effects related to vascular damage is still unknown.
Smoking prevention represents an important approach for reducing the risk of ED. The characterization of the components of cigarette smoke leading to ED and the mechanisms by which these components alter signaling pathways activated in erectile responses are necessary for a complete comprehension of cigarette smoking-associated ED.
美国有三千万男性患有勃起功能障碍（ED），预计到2025年这一数字将翻倍。ED被视为一个重大的公共卫生问题，严重影响患者及其伴侣的生活质量，且随着年龄增长愈发普遍，长期吸烟是ED发生的主要危险因素。
综述关于吸烟对与一氧化氮（NO）生物利用度降低和活性氧（ROS）生成增加相关的血管变化影响的现有证据。
我们研究了将吸烟与ED联系起来的流行病学和临床数据，以及吸烟对血管NO生物利用度和ROS生成的影响。
吸烟与ED之间存在密切关联，有大量证据支持这样的概念，即与吸烟相关的ED与由于ROS增加导致的NO生物利用度降低有关。
在人类和动物模型中，吸烟引起的ED与阴茎动脉血流受损或阴茎动脉急性血管痉挛有关。长期吸烟对血管内皮和周围神经产生有害影响，还会导致海绵体组织的超微结构损伤，所有这些都被认为在慢性吸烟引起的ED中起作用。临床和基础科学研究提供了有力的间接证据，表明吸烟可能通过损害内皮依赖性平滑肌舒张，或更具体地说，通过增加ROS生成影响NO产生，从而影响阴茎勃起。香烟烟雾中的尼古丁或其他成分是否介导了所有与血管损伤相关的影响尚不清楚。
预防吸烟是降低ED风险的重要途径。要全面理解与吸烟相关的ED，需要明确导致ED的香烟烟雾成分及其改变勃起反应中激活的信号通路的机制。
