Gvozdjáková A, Bada V, Sány L, Kucharská J, Krutý F, Bozek P, Trstanský L, Gvozdják J
Cardiovasc Res. 1984 Apr;18(4):229-32. doi: 10.1093/cvr/18.4.229.
The effect of inhalation of cigarette smoke (passive smoking) on the oxidative and phosphorylating processes of rabbit myocardial mitochondria was studied in three experimental models after a single smoke lasting 30 min, after 2 weeks smoking twice daily and after 8 weeks smoking twice daily. A significant decrease in respiration as well as in the phosphorylation rate of mitochondria was found; whereas the respiratory control index and coefficient of oxidative phosphorylation did not change. Both factors of cigarette smoke (carbon monoxide and nicotine) participate in the metabolic injury of mitochondria. Long term cigarette smoking causes considerable metabolic and morphological alterations to the heart muscle which can be characterised as smoke cardiomyopathy.
在三个实验模型中，研究了吸入香烟烟雾（被动吸烟）对兔心肌线粒体氧化和磷酸化过程的影响，这三个模型分别是单次持续30分钟吸烟后、每日吸烟两次持续2周后以及每日吸烟两次持续8周后。结果发现线粒体的呼吸以及磷酸化速率显著降低；而呼吸控制指数和氧化磷酸化系数没有变化。香烟烟雾的两个成分（一氧化碳和尼古丁）均参与了线粒体的代谢损伤。长期吸烟会导致心肌出现相当大的代谢和形态学改变，这种改变可被描述为烟雾性心肌病。
