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活性氧介导吸烟者体内颈内动脉和内乳动脉功能差异。

Reactive oxygen species mediate functional differences in human radial and internal thoracic arteries from smokers.

机构信息

Heart Surgery Center Basel-Bern, University Hospital, Bern, Switzerland.

出版信息

J Vasc Surg. 2010 Feb;51(2):438-44. doi: 10.1016/j.jvs.2009.09.040. Epub 2009 Dec 24.

DOI:10.1016/j.jvs.2009.09.040
PMID:20036100
Abstract

OBJECTIVE

Smoking not only increases the risk that coronary heart disease will develop but also morbidity and mortality in patients with known coronary atherosclerosis and after coronary artery bypass grafting. Excessive generation of reactive oxygen species (ROS) has been implicated as the final common pathway for the development of endothelial dysfunction in various cardiovascular risk factors. This study assessed the influence of smoking on two different human arteries routinely used as coronary artery bypass graft conduits.

METHODS

Isometric tension was recorded on discarded segments of human left internal thoracic artery (ITA) and the radial artery (RA) from smokers and nonsmokers.

RESULTS

The contractile response to endothelin-1 was significantly stronger in arteries from smokers than in those from nonsmokers. By contrast, endothelium-dependent relaxant responses to acetylcholine were attenuated in RA rings but enhanced in ITA rings from smokers. In additional experiments, 5-(&6)-chloromethyl-2'-7'-dichlorodihydro-fluorescein diacetate (DCDHF) was used to photochemically detect ROS by confocal imaging of intact ITA and RA. Enhanced production of ROS was induced by exposure of tissues to 28 degrees C. While during exposure to 28 degrees C, basal fluorescence emission was unchanged in ITA rings, it increased significantly in RA rings, indicating enhanced formation of ROS in this peripheral artery.

CONCLUSIONS

Data suggest that smoking induces endothelial dysfunction by increasing vascular ROS production. Different levels of endogenous antioxidant enzyme activities and the degree of atherosclerotic changes might modulate physiologic and pharmacologic vasoreactivity and be responsible for decreased graft patency of RA compared with ITA conduits, especially in active smokers.

摘要

目的

吸烟不仅会增加冠心病的发病风险,还会增加已知冠状动脉粥样硬化和冠状动脉旁路移植术后患者的发病率和死亡率。过量产生的活性氧(ROS)被认为是各种心血管危险因素导致内皮功能障碍的最终共同途径。本研究评估了吸烟对两种常用作冠状动脉旁路移植术移植物的不同人类动脉的影响。

方法

记录来自吸烟者和不吸烟者的人体左内乳动脉(ITA)和桡动脉(RA)废弃段的等长张力。

结果

与不吸烟者相比,吸烟者动脉对内皮素-1的收缩反应明显更强。相比之下,RA 环内皮依赖性舒张反应减弱,但吸烟者的 ITA 环增强。在额外的实验中,使用 5-(6)-氯甲基-2'-7'-二氯二氢荧光素二乙酸酯(DCDHF)通过对完整的 ITA 和 RA 的共聚焦成像来光化学检测 ROS。组织暴露于 28°C 会诱导 ROS 的产生。虽然在暴露于 28°C 时,ITA 环的基础荧光发射没有变化,但 RA 环的荧光发射显著增加,表明这种外周动脉中 ROS 的形成增加。

结论

数据表明,吸烟通过增加血管 ROS 的产生诱导内皮功能障碍。不同水平的内源性抗氧化酶活性和动脉粥样硬化程度可能调节生理和药理血管反应,并导致与 ITA 移植物相比,RA 的移植物通畅率降低,尤其是在活跃吸烟者中。

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