title: Exposure to environmental tobacco smoke increases myocardial infarct size in rats.
abstract: BACKGROUND
  Exposure to environmental tobacco smoke (ETS) has been epidemiologically linked to death from ischemic heart disease in nonsmokers. 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/reperfusion model.
  
  
  RESULTS
  Sprague-Dawley rats exposed to ETS (four Marlboro cigarettes per 15 minutes, 6 hours per day, 5 days per week) for 3 days (n = 24), 3 weeks (n = 21), or 6 weeks (n = 12) and control rats (n = 24, n = 21, and n = 12, respectively) were subjected to 35 minutes of left coronary artery occlusion and 2 hours of reperfusion. Infarct size and risk area were determined by triphenyltetrazolium chloride and phthalocyanine blue staining, respectively. Air nicotine, carbon monoxide, and total particulates were measured during ETS exposure. Serum lipids, plasma carbon monoxide hemoglobin (COHb), nicotine, and cotinine concentrations were measured in additional groups (6 to 13 rats each) exposed to 3 days, 3 weeks, or 6 weeks of ETS and controls. Average air nicotine, carbon monoxide, and total particulate concentrations were 1103 micrograms/m3, 92 ppm, and 60 mg/m3 for the ETS-exposed rats. Infarct size (infarct mass/risk area x 100%) increased significantly in the ETS groups compared with the control groups in a dose-dependent manner (P = .023), with longer exposure associated with larger infarct size. Infarct size nearly doubled with 6 weeks of ETS exposure (61 +/- 5% versus 34 +/- 3% for control, mean +/- SEM). Plasma COHb, nicotine, and cotinine levels increased significantly in the ETS groups in a dose-dependent manner (all P < .001).
  
  
  CONCLUSIONS
  Exposure to passive smoking increases myocardial infarct size in a rat model of ischemia and reperfusion. This increase of infarct size exhibited a dose-response relation. These results are consistent with epidemiological studies demonstrating that ETS increases the risk of heart death.
authors.affiliation: Department of Medicine, University of California, San Francisco 94143-0124.
authors.forename: B Q
authors.initials: BQ
authors.lastname: Zhu
authors.forename: Y P
authors.initials: YP
authors.lastname: Sun
authors.forename: R E
authors.initials: RE
authors.lastname: Sievers
authors.forename: S A
authors.initials: SA
authors.lastname: Glantz
authors.forename: W W
authors.initials: WW
authors.lastname: Parmley
authors.forename: C L
authors.initials: CL
authors.lastname: Wolfe
mesh_terms: D000818:Animals; D001760:Bleeding Time; D002263:Carboxyhemoglobin / Q000032:analysis; D003367:Cotinine / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology / Q000473:pathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology*; D009538:Nicotine / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D013997:Time Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D008055:Lipids; D014028:Tobacco Smoke Pollution; D009538:Nicotine; D002263:Carboxyhemoglobin; D003367:Cotinine