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