Smoke cardiomyopathy: disturbance of oxidative processes in myocardial mitochondria.
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.
D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D011773:Pyruvates / Q000378:metabolism; D011817:Rabbits; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D011773:Pyruvates; D014028:Tobacco Smoke Pollution