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.

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The effect of ethanol on the metabolism of the heart muscle was studied in two series of experiments in the rat. In an acute model, a single injection of 250 mg ethanol/l00 g body weight was given intraperitoneally. Blood glucose, lactate, NEFA, and myocardial glycogen content were analyzed at 15, 30, and 60 min. All these parameters increased when measured 15 and 30 min after the ethanol injection, but they all returned to normal levels at 60 min. A model of chronic alcohol intake was investigated for 10 weeks. The same dose of ethanol was injected daily to the experimental animals whereas the control rats received an isocaloric dose of glucose. Chronic administration of ethanol caused changes not only in the glycolytic cycle of the myocardium (diminished glycolytic activity), but also in the oxidative phosphorylation of myocardial mitochondria (decrease of homogenate and mitochondria respiration as well as of respiratory control ratio of isolated mitchondria).

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