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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01046.2001
Submitted on November 30, 2001
Accepted on April 16, 2002
1 Internal Medicine, University of California, Davis, Davis, CA, USA
2 Cell Biology and Neuroscience, University of California, Riverside, Riverside, CA, USA
3 Institute of Toxicology and Environmental Health, University of California, Davis, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: aemullick{at}ucdavis.edu.
We hypothesized that reactive carbonyls generated from smoke exposure cause increased arterial LDL accumulation and endothelial layer permeability. Additionally, we hypothesized that estrogen supplementation was protective against chronic environmental tobacco smoke (ETS) exposure to the artery wall. Quantitative fluorescence microscopy was used to determine artery injury following exposure. For our chronic studies, ovariectomized rats treated with subcutaneous placebo or 17-ß estradiol pellets were exposed to ETS or filtered air for 6 weeks. ETS exposure increased carotid artery LDL accumulation over 4-fold compared to filtered air exposure, an effect largely mediated by increased permeability. No protective effect of estradiol was observed. Acute ETS exposure of a buffer solution containing LDL resulted in over a 6-fold increase in the highly reactive carbonyl glyoxal. Perfusion of this solution through carotid arteries resulted in a 105% increase in permeability. Moreover, perfusion of glyoxal alone caused a 50% increase in carotid artery permeability. This endothelial damage and changes in lipid accumulation may serve as an initiating event in atheroma formation in individuals exposed to ETS.
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