Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1994;89:1282-1290

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhu, B. Q.
Right arrow Articles by Wolfe, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhu, B. Q.
Right arrow Articles by Wolfe, C. L.

Circulation, Vol 89, 1282-1290, Copyright © 1994 by American Heart Association


ARTICLES

Exposure to environmental tobacco smoke increases myocardial infarct size in rats

BQ Zhu, YP Sun, RE Sievers, SA Glantz, WW Parmley and CL Wolfe
Department of Medicine, University of California, San Francisco 94143- 0124.

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. METHODS AND 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.


This article has been cited by other articles:


Home page
Proc. Natl. Acad. Sci. USAHome page
M. Wang, J. Tan, Y. Wang, K. K. Meldrum, C. A. Dinarello, and D. R. Meldrum
IL-18 binding protein-expressing mesenchymal stem cells improve myocardial protection after ischemia or infarction
PNAS, October 13, 2009; 106(41): 17499 - 17504.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
J P Pell, S Haw, S Cobbe, D E Newby, A C H Pell, C Fischbacher, S Pringle, D Murdoch, F Dunn, K Oldroyd, et al.
Secondhand smoke exposure and survival following acute coronary syndrome: prospective cohort study of 1261 consecutive admissions among never-smokers
Heart, September 1, 2009; 95(17): 1415 - 1418.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
K. Meurrens, S. Ruf, G. Ross, R. Schleef, K. von Holt, and K.-D. Schluter
Smoking accelerates the progression of hypertension-induced myocardial hypertrophy to heart failure in spontaneously hypertensive rats
Cardiovasc Res, November 1, 2007; 76(2): 311 - 322.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
D. Xiao, X. Huang, S. Yang, and L. Zhang
Direct Effects of Nicotine on Contractility of the Uterine Artery in Pregnancy
J. Pharmacol. Exp. Ther., July 1, 2007; 322(1): 180 - 185.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
T. Raupach, K. Schafer, S. Konstantinides, and S. Andreas
Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm
Eur. Heart J., February 2, 2006; 27(4): 386 - 392.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
A. Mirza, V. Eder, G. Y Rochefort, J.-M. Hyvelin, M. C. Machet, L. Fauchier, and P. Bonnet
CO Inhalation at Dose Corresponding to Tobacco Smoke Worsens Cardiac Remodeling after Experimental Myocardial Infarction in Rats
Toxicol. Sci., June 1, 2005; 85(2): 976 - 982.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. Barnoya and S. A. Glantz
Cardiovascular Effects of Secondhand Smoke: Nearly as Large as Smoking
Circulation, May 24, 2005; 111(20): 2684 - 2698.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
R. D. Brook, B. Franklin, W. Cascio, Y. Hong, G. Howard, M. Lipsett, R. Luepker, M. Mittleman, J. Samet, S. C. Smith Jr, et al.
Air Pollution and Cardiovascular Disease: A Statement for Healthcare Professionals From the Expert Panel on Population and Prevention Science of the American Heart Association
Circulation, June 1, 2004; 109(21): 2655 - 2671.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
A. Bhatnagar
Cardiovascular pathophysiology of environmental pollutants
Am J Physiol Heart Circ Physiol, February 1, 2004; 286(2): H479 - H485.
[Full Text] [PDF]


Home page
Exp. Biol. Med.Home page
J. Zhang, Y. Liu, J. Shi, D. F. Larson, and R. R. Watson
Side-Stream Cigarette Smoke Induces Dose-Response in Systemic Inflammatory Cytokine Production and Oxidative Stress
Experimental Biology and Medicine, October 1, 2002; 227(9): 823 - 829.
[Abstract] [Full Text] [PDF]


Home page
Journal of Renin-Angiotensin-Aldosterone SystemHome page
B.-q. Zhu, R. E Sievers, A. E. Browne, R. T Hillman, K. Chair, R. J Lee, K. Chatterjee, S. A Glantz, and W. W Parmley
The renin-angiotensin system does not contribute to the endothelial dysfunction and increased infarct size in rats exposed to second hand smoke
Journal of Renin-Angiotensin-Aldosterone System, March 1, 2002; 3(1): 54 - 60.
[Abstract] [PDF]


Home page
J Am Coll CardiolHome page
S. J. Hutchison, S. A. Glantz, B.-Q. Zhu, Y.-P. Sun, T. M. Chou, K. Chatterjee, P. C. Deedwania, W. W. Parmley, and K. Sudhir
In-utero and neonatal exposure to secondhand smoke causes vascular dysfunction in newborn rats
J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1463 - 1467.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
K. Steenland, M. Thun, C. Lally, and C. Heath
Environmental Tobacco Smoke and Coronary Heart Disease in the American Cancer Society CPS-II Cohort
Circulation, August 15, 1996; 94(4): 622 - 628.
[Abstract] [Full Text]


Home page
JAMAHome page
S. A. Glantz and W. W. Parmley
Passive Smoking and Heart Disease: Mechanisms and Risk
JAMA, April 5, 1995; 273(13): 1047 - 1053.
[Abstract] [PDF]