EXPOSURE TO ENVIRONMENTAL TOBACCO-SMOKE INCREASES MYOCARDIAL INFARCT SIZE IN RATS

Background Exposure to environmental tobacco smoke (ETS) has been epid emiologically linked to death from ischemic heart disease in nonsmoker s. In this study, we evaluated the influence of 3 days, 3 weeks, and 6 weeks of ETS exposure on myocardial infarct size in a rat ischemia/re perfusion model. Methods and Results Sprague-Dawley rats exposed to ET S (four Marlboro cigarettes per 15 minutes, 6 hours per day, 5 days pe r week) for 3 days (n=24), 3 weeks (n=21), or 6 weeks (n=12) and contr ol rats (n=24, n=21, and n=12, respectively) were subjected to 35 minu tes of left coronary artery occlusion and 2 hours of reperfusion. Infa rct size and risk area were determined by triphenyltetrazolium chlorid e and phthalocyanine blue staining, respectively. Air nicotine, carbon monoxide, and total particulates were measured during ETS exposure. S erum lipids, plasma carbon monoxide hemoglobin (COHb), nicotine, and c otinine concentrations were measured in additional groups (6 to 13 rat s each) exposed to 3 days, 3 weeks, or 6 weeks of ETS and controls. Av erage air nicotine, carbon monoxide, and total particulate concentrati ons were 1103 mu g/m(3), 92 ppm, and 60 mg/m(3) for the ETS-exposed ra ts. Infarct size (infarct mass/risk area x 100%) increased significant ly in the ETS groups compared with the control groups in a dose-depend ent manner (P=.023), with longer exposure associated with larger infar ct size. Infarct size nearly doubled with 6 weeks of ETS exposure (61/-5% versus 34+/-3% for control, mean+/-SEM). Plasma COHb, nicotine, a nd cotinine levels increased significantly in the ETS groups in a dose -dependent manner (all P<.001). Conclusions Exposure to passive smokin g increases myocardial infarct size in a rat model of ischemia and rep erfusion. This increase of infarct size exhibited a dose-response rela tion. These results are consistent with epidemiological studies demons trating that ETS increases the risk of heart death.