Changes in cardiac function of rats

dioxide were examined by electrocardiographic records. Bradycardia and arrhythmias were observed following exposure to 20 ppm for 3 hours (76). These alterations were attributed to changes in parasympathetic nervous activity following exposure. The levels used were high relative to those obtained from unaged tobacco smoke. In addition, it has been suggested that enzyme-inhibiting effects associated with cigarette smoking are due to nicotine N-oxide and nitrogen dioxide. Because thiols are readily oxidized to disulfides by either nitric oxide or nitrogen dioxide, they are potent inhibitors of thioldependent enzymes (126). In the presence of cigarette smoke, scavenger cells such as macrophages may not be readily activated. In the respiratory system, the major histological sites of damage by nitrogen dioxide are the terminal and respiratory bronchioles and the proximal portions of the alveolar ducts. Nitrogen oxides are also suspected of contributing to the development of pulmonary emphysema (43) and the acceleration of platelet aggregation (191).