Nicotine does not influence arterial lipid deposits in rabbits exposed to second-hand smoke

Article

关键词: SMOOTH-MUSCLE CELLS;    PASSIVE SMOKING;    ENDOTHELIAL-CELLS;    CIGARETTE-SMOKING;    CARDIOVASCULAR-DISEASE;    GROWTH-FACTOR;    L-ARGININE;    LIPOPROTEIN;    PROLIFERATION;    METABOLISM;   

DOI  :  10.1161/hc3301.092788

来源: SCIE

【 摘 要 】

Background-Second-hand smoke (SHS) accelerates atherogenesis and impairs vascular function. The role of nicotine in this process has not been defined. Methods and Results-To examine the potential effects of nicotine on atherogenesis and vascular function, 48 rabbits receiving a 0.5% cholesterol diet were randomized to control (cholesterol diet only), SHS from nicotine- standard research cigarettes (SHS-ST), and SHS from nicotine-free research cigarettes (SHS-NF). The SHS rabbits were exposed to 48 nicotine-standard (12 animals) or nicotine-free (12 animals) cigarettes/d, 5 d/wk for 10 weeks. Air carbon monoxide and particulates and plasma carboxyhemoglobin were significantly higher in the 2 SHS groups than the control group (P <0.001). The SHS-ST group had significant increases in plasma nicotine and cotinine compared with the other groups (P <0.001). There was no difference in serum lipids. Lipid lesions were increased in both SHS groups (54 +/-5% [SEM] aorta and 66 +/-4% pulmonary artery, 53 +/-7% and 69 +/-4%, and 39 +/-4% and 43 +/-3% in the SHS-ST, SHS-NF, and control groups, respectively; P=0.049 aorta and P <0.001 pulmonary artery). Conclusions-SHS exposure increased arterial lipid lesions, but nicotine did not contribute significantly to this effect. This effect is presumably due to other combustion products in the smoke.

【 授权许可】

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