MODEL STUDIES LINKING CARBON-MONOXIDE AND-OR NICOTINE TO ARTERIOSCLEROSIS AND CARDIOVASCULAR-DISEASE

The cardiovascular effects of animal exposure to carbon monoxide and/or nicotine are surveyed. The myocardial effects are produced by carbon monoxide as well as nicotine and lead to decreased myocardial oxygen tensions with compensatory increases in coronary blood flow. There is an increased tendency to arrhythmia. Carbon monoxide exposure leads to degenerative changes and partial necrosis of myofibrils, similar to the changes observed after hypoxia. After nicotine exposure, moderate fibrosis and calcification may be seen in arterial media, although no injuring effects on intima have been observed. The effects of carbon monoxide exposure on arterial intima have been reevaluated, and previous findings of arterial intimal changes have not been confirmed. It is concluded that tobacco smokers' enhanced risk of heart infarct is caused by the myocardial effects of nicotine and carbon monoxide. The structural changes in the arterial media probably are caused primarily by nicotine, and secondarily by carbon monoxide. The compounds responsible for the enhanced intimal changes in the smokers are not identified with certainty, but may be related to carbon monoxide induced changes in cholesterol metabolism. © 1979.