摘要

AIMS:Electronic (e)-cigarettes have been marketed as a 'healthy' alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms.
METHODS AND RESULTS:Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental effects on endothelial function, markers of oxidative stress, inflammation, and lipid peroxidation than vapour containing nicotine. These effects of e-cigarette vapour were largely absent in mice lacking phagocytic NADPH oxidase (NOX-2) or upon treatment with the endothelin receptor blocker macitentan or the FOXO3 activator bepridil. We also established that the e-cigarette product acrolein, a reactive aldehyde, recapitulated many of the NOX-2-dependent effects of e-cigarette vapour using in vitro blood vessel incubation.
CONCLUSIONS:E-cigarette vapour exposure increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. Our study identifies the toxic aldehyde acrolein as a key mediator of the observed adverse vascular consequences. Thus, e-cigarettes have the potential to induce marked adverse cardiovascular, pulmonary, and cerebrovascular consequences. Since e-cigarette use is increasing, particularly amongst youth, our data suggest that aggressive steps are warranted to limit their health risks.

译文

目的: 电子香烟已经作为传统可燃香烟的 “健康” 替代品和有效的戒烟方法在市场上销售。然而，支持这些说法的数据很少。事实上，电子烟与血管系统和肺部的内皮功能障碍和氧化应激有关。这些副作用的潜在机制仍不清楚。在这里，我们研究了电子烟蒸汽对吸烟者和实验动物血管功能的影响，以确定潜在的机制。
方法和结果: 急性电子烟吸烟对慢性吸烟者的内皮功能产生了明显的损害，这是由流量介导的扩张决定的。在小鼠中，没有尼古丁的电子烟蒸汽比含有尼古丁的蒸汽对内皮功能、氧化应激、炎症和脂质过氧化的标记有更有害的影响。电子烟蒸汽的这些影响在缺乏吞噬细胞 NADPH 氧化酶 (NOX-2) 的小鼠中很大程度上不存在，或者在使用内皮素受体阻滞剂 macitentan 或 FOXO3 激活剂 bepridil 治疗时。我们还确定了电子烟产品丙烯醛，一种反应性醛，利用体外血管孵育概括了电子烟蒸汽的许多 NOX-2-dependent 效果。
结论: 电子烟蒸汽暴露通过 NOX-2-dependent 机制增加血管、大脑和肺的氧化应激。我们的研究确定毒性醛丙烯醛是观察到的不良血管后果的关键介质。因此，电子烟有可能诱发明显的心血管、肺和脑血管不良后果。由于电子烟的使用正在增加，特别是在年轻人中，我们的数据表明，必须采取积极措施来限制他们的健康风险。