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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2012 Oct 4;32(12):2901–2909. doi: 10.1161/ATVBAHA.112.300208

Figure 3. Effect of Tobacco Smoke Exposure on the Development of Aneurysms.

Figure 3

After EP, smoke exposure resulted in significantly increased AAA diameter in both MMP-9 and MMP-12 deficient mice (A). Representative sections of mouse aorta were stained with Verhoff-von Giesen (B); in smoke-free MMP-9 deficient animals, aortic elastin fibers were relatively intact with minimal inflammation, whereas, in smoke-exposed animals there was considerable elastin degradation. As with MMP elastases, the absence of either Cat-S or Neutrophil Elastase (C) did not inhibit the increased %ΔAD induced by smoke exposure. Aortic dilatation was evaluated in mice exposed to 2, 4 or 6 weeks of TS (and smoke-free controls) that underwent EP and were maintained in smoke-free conditions until harvest (D). Four weeks of TS was sufficient to enhance AAA after EP. Animals exposed to 6 weeks of TS (or 6 weeks of smoke-free conditions) were then maintained in smoke-free conditions for 0, 2, 4 or 6 weeks before EP and were harvested at day 14 (E). Remote smoke-exposure resulted in larger aneurysms in all groups. The cotinine (F) in the urine of the animals declined rapidly after smoke cessation, and was indistinguishable from smoke-free mice by 6 weeks following perfusion.