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Elevated elastase activity in patients with chronic obstructive pulmonary disease (COPD) is attributable to the direct effect of nicotine. COPD is also known to be an independent predictor of abdominal aortic aneurysm (AAA) growth and rupture. The purpose of this study is to determine the effect of nicotine on elastase activity release from neutrophils of AAA patients. Human neutrophils were extracted from the blood of subjects in the following six groups, n = 10 in each group: smoking AAA (SAAA), nonsmoking AAA (NSAAA), smoking aortic occlusive disease (SAOD), nonsmoking aortic occlusive disease (NSAOD), smoking controls (SC), and nonsmoking controls (NSC). After incubation with varying nicotine concentrations (0-1000 microg/ml), the released elastase activity was determined. There is generally an elevation in elastase activity release by neutrophils of smokers compared to nonsmokers. Nicotine exposure stimulated increased elastase activity release in AOD and AAA, and the increase was especially pronounced in the SAAA and SAOD groups. The elevation was greatest in the SAAA group while the release was lowest in the NSAOD group. There is a direct correlation between elastase activity release and nicotine concentration. The data suggest that COPD and AAA development, which may occur by similar initial mechanisms may also be aggravated by nicotine-induced neutrophil elastase activity release. In addition, the results indicate that nicotine is playing an active role in the development of vascular disease by inducing neutrophils to release elastase activity.
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