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1 Biomedical Engineering, University of California, Irvine, Irvine, California, United States
2 Department of Community and Environmental Medicine, University of California, Irvine, Irvine, California, United States
3 Community & Environmental Medicine, University of California, Irvine, Irvine, California, United States
* To whom correspondence should be addressed. E-mail: gkassab{at}iupui.edu.
Cigarette smoking (CS) is a major risk factor for vascular disease. The aim of this study was to quantitatively assess the influence of CS on mouse arteries. We studied the effect of short-term (6 weeks) and long-term (16 weeks) CS exposure on structural and mechanical properties of coronary arteries in comparison to control mice. We also examined the reversibility of the deleterious effects of CS on structural (e.g., wall thickness, WT), mechanical (e.g., stiffness) and biochemical (e.g., NO byproducts) properties with the cessation of CS. The left and right coronary arteries were cannulated in situ and mechanically distended. The stress, strain, elastic modulus and WT of coronary arteries were determined. Western blot was used to analyze endothelial NO synthase (eNOS) in the femoral and carotid arteries of the same mice and NO byproducts were determined by measuring the levels of nitrite. Our results show that the mean arterial pressure was increased by CS. Furthermore, CS significantly increased the elastic modulus, decreased stress and strain, increased the WT and wall thickness-to-radius ratio when compared to control. The reduction of eNOS protein expression was found only after long-term CS exposure. Moreover, the NO metabolite was markedly decreased in CS mice after short-term and long-term exposure of CS. These findings suggest that 16 weeks of CS exposure can cause an irreversible deterioration of structural and elastic properties of mouse coronary arteries. The decrease in endothelium-derived NO in CS mice was seen to significantly correlate with the remodeling of arterial wall.
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