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Tobacco studies (3)

 

TWO STUDIES, ONE SHOWS THAT TOBACCO INCREASES THE PRODUCTION OF LDL (THE BAD LIPOPROTEIN), THE OTHER THAT IT PROMOTES BLOOD CLOTTING.--jk 

 

Effect of Environmental Tobacco Smoke on LDL Accumulation in the Artery Wall

Circulation. 1996;94:2248-2253.)
© 1996 American Heart Association, Inc

 

K.A. Roberts, PhD; A.A. Rezai, BS; K.E. Pinkerton, PhD; J.C. Rutledge, MD

the Departments of Internal Medicine and Veterinary Anatomy, Physiology, and Cell Biology, University of California, Davis.

Correspondence to John C. Rutledge, MD, Division of Cardiovascular Medicine, T.B. 172, Bioletti Way, University of California, Davis, CA 95616.

Background Previous research has shown that exposure to environmental tobacco smoke (ETS) increases the risk of atherosclerosis. To test the hypothesis that exposure to ETS increases LDL accumulation in the artery wall, we developed a model to measure the rate of LDL accumulation in individually perfused rat carotid arteries after the artery had been perfused with plasma taken from rats exposed to ETS (ETS-plasma).

Methods and Results Rats were exposed to ETS in a chamber in which steady-state sidestream smoke was continuously circulating. After exposure, blood from the animals was collected. Carotid arteries from unexposed rats were perfused first with normal plasma containing fluorescently labeled LDL. Then, the same arteries (10 arteries from five rats) were perfused with ETS-plasma plus fluorescently labeled LDL. Photometric measurements were made during perfusion of the arteries with fluorescently labeled LDL, and rate of LDL accumulation (mV/min) and lumen volume (mV) (volume of fluorescently labeled LDL solution) were determined. Perfusion with ETS-plasma increased the rate of LDL accumulation (mean±SEM, 6.9±1.8 mV/min) compared with control (1.6±0.40 mV/min, P .02). LDL accumulation was primarily dependent on LDL interaction with ETS-plasma rather than the interaction of ETS-plasma with the artery wall. Also, ETS-plasma significantly increased lumen volume (43.3±5.1 mV) compared with control (35.1±4.4 mV, P .005).

Conclusions Exposure to ETS acutely increased LDL accumulation in perfused arteries. Repeated exposure to ETS may represent important early events in atherogenesis.


Key Words: smoking • lipoproteins • arteries • atherosclerosis


 

 

AMERICAN HEART ASSOCIATION AT

http://www.circ.ahajournals.org/cgi/content/abstract/99/11/1411

 

Endothelial Dysfunction, Impaired Endogenous Fibrinolysis, and Cigarette Smoking

 

 

A Mechanism for Arterial Thrombosis and Myocardial Infarction

David E. Newby, BA, BSc, BM, MRCP; Robert A. Wright, MB, ChB, MRCP; Catherine Labinjoh, BSc, MB, ChB, MRCP; Christopher A. Ludlam, PhD, FRCP, FRCPath; Keith A. A. Fox, BSc, MB, ChB, FRCP, FESC; Nicholas A. Boon, MD, FRCP; David J. Webb, MD, FRCP, FRCPE, FFPM

From the Clinical Pharmacology Unit and Research Centre, University of Edinburgh, Western General Hospital (D.E.N., C.L., D.J.W.), and the Departments of Cardiology (D.E.N., R.A.W., C.L., K.A.A.F., N.A.B.) and Haematology (C.A.L.), University of Edinburgh, Royal Infirmary, Edinburgh, Scotland, UK. Dr Wright is now at the Department of Cardiology, The Ayr Hospital, Ayr, Scotland, UK.

Correspondence to Dr D.E. Newby, Clinical Pharmacology Unit and Research Centre, University of Edinburgh, Western General Hospital, Crewe Rd, Edinburgh EH4 2XU, Scotland, UK. E-mail d.e.newby@ed.ac.uk

Background—Effective endogenous fibrinolysis requires rapid release of tissue plasminogen activator (tPA) from the vascular endothelium. Smoking is a known risk factor for arterial thrombosis and myocardial infarction, and it causes endothelial dysfunction. We therefore examined the effects of cigarette smoking on substance P–induced tPA release in vivo in humans.

Methods and Results—Blood flow and plasma fibrinolytic factors were measured in both forearms of 12 smokers and 12 age- and sex-matched nonsmokers who received unilateral brachial artery infusions of substance P (2 to 8 pmol/min). In both smokers and nonsmokers, substance P caused dose-dependent increases in blood flow and local release of plasma tPA antigen and activity (P<0.001 for all) but had no effect on the local release of plasminogen activator inhibitor type 1. Compared with nonsmokers, increases in forearm blood flow (P=0.03) and release of tPA antigen (P=0.04) and activity (P<0.001) caused by substance P were reduced in smokers. The area under the curve for release of tPA antigen and activity decreased by 51% and 53%, respectively.

Conclusions—Cigarette smoking causes marked inhibition of substance P–induced tPA release in vivo in humans. This provides an important mechanism whereby endothelial dysfunction may increase the risk of atherothrombosis through a reduction in the acute fibrinolytic capacity.

 

Carotid arteriosclerosis in identical twins discordant for cigarette smoking

 

Circulation, Vol 80, 10-16, Copyright © 1989 by American Heart Association

 

Plaque found to bed 3.2 times greater in smoking twins--jk

A Haapanen, M Koskenvuo, J Kaprio, YA Kesaniemi and K Heikkila
Department of Public Health, University of Turku, Finland.

From a nationwide twin panel, identical twin pairs with highest discordance in cigarette smoking were selected for a study of arteriosclerosis (49 pairs with a mean age of 52 years). Smoking history was obtained in 1975, 1981, and 1986. The mean life-long smoking dose of the smoking cotwins was 20 package-years. The smoking and nonsmoking cotwins had similar systolic and diastolic blood pressures, total plasma cholesterol level, body mass index, and some psychosocial factors; the only difference was found in use of alcohol, which was greater among smoking cotwins. Duplex sonography of carotid arteries was performed. Carotid artery stenoses (narrowing of area of the lumen with 15-60%) were found in nine pairs: in nine smoking twins and in two of their nonsmoking cotwins (p = 0.036). The total area of carotid plaques was 3.2 times larger in smoking cotwins (p less than 0.001). The thickness of the inner layer of carotid arteries was more marked in smoking cotwins (p less than 0.001). The size of plaques and the degree of inner layer thickening correlated with the dose of smoking (NS). The association of smoking with carotid arteriosclerosis was highly significant even after the adjustment for age, total plasma cholesterol level, diastolic blood pressure, and body mass index in multiple logistic regression analyses.

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SMOKING SHORTENS LIFE AN AVERAGE OF 7 MINUTES PER CIGARETTE
 

FOR AN ARTICLE EXPLAINING WITH EXCEPTIONAL CLARITY CANCER; FOR ARTICLE ON LUNG CANCER, AND 2 DOZEN RELATED ARTICLES

 

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