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 art
ery wall, we developed a model to measure the rate of LDL accumulation
in individually perfused rat carotid arteries after the artery had be
en perfused with plasma taken from mts exposed to ETS (ETS-plasma). Me
thods and Results Rats were exposed to ETS in a chamber in which stead
y-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 fluores-
atherosclerosis cently labeled LDL, and rate of LDL accumulation (mV/m
in) and lumen volume (mV) (volume of fluorescently labeled LDL solutio
n) were determined. Perfusion with ETS-plasma increased the rate of LD
L. accumulation (mean+/-SEM, 6.9+/-1.8 mV/min) compared with control (
1.6+/-0.40 mV/min, P less than or equal to.02). LDL accumulation was p
rimarily dependent on LDL interaction with ETS-plasma rather than the
interaction of ETS-plasma with the artery wall. Also, ETS-plasma signi
ficantly increased lumen volume (43.3+/-5.1 mV) compared with control
(35.1+/-4.4 mV, P less than or equal to.005). Conclusions Exposure to
ETS acutely increased LDL accumulation in perfused arteries. Repeated
exposure to ETS may represent important early events in atherogenesis.