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Laboratory and Animal Investigations |

Secondhand Tobacco Smoke Impairs Rabbit Pulmonary Artery Endothelium-Dependent Relaxation*

Stuart J. Hutchison, MD; Richard E. Sievers, BS; Bo-Qing Zhu, MD; Yi-Ping Sun, MD; Duncan J. Stewart, MD; William W. Parmley, MD; Kanu Chatterjee, MB, FCCP
Author and Funding Information

*From the Division of Cardiology (Mr. Sievers, and Drs. Zhu, Sun, Parmley, and Chatterjee), University of California, San Francisco, San Francisco, CA; and the Division of Cardiology (Drs. Hutchison and Stewart), St. Michael’s Hospital, Toronto, Ontario, Canada.

Correspondence to: Kanu Chatterjee, MB, FCCP, Chatterjee Center For Cardiac Research, University of California, San Francisco, Moffit Hospital Room 1176, San Francisco, CA 94143-0124



Chest. 2001;120(6):2004-2012. doi:10.1378/chest.120.6.2004
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Objectives: To determine whether secondhand smoke (SHS) induces pulmonary artery endothelial dysfunction, and whether dietary l-arginine supplementation is preventive.

Background: SHS causes coronary and peripheral arterial endothelial dysfunction.

Methods: The effects of l-arginine supplementation (2.25% solution) and SHS (10 weeks) on pulmonary vascular reactivity were examined in 32 rabbits fed a normal diet. Endothelium-dependent relaxation of precontracted pulmonary artery segments was studied using acetylcholine and calcium ionophore. Endothelium-independent relaxation was studied using nitroglycerin. Endothelial and serum l-arginine levels were measured by chromatography. In eight SHS-exposed and in eight control rats, pulmonary artery nitric oxide synthase (NOS) activity and arginase activity were studied using the titrated arginine to citrulline conversion assay.

Results: SHS reduced maximal acetylcholine-induced (p = 0.04) and calcium ionophore-induced (p = 0.02) relaxation. l-Arginine increased maximal acetylcholine-induced (p = 0.047) vasodilation. SHS and l-arginine did not influence nitroglycerin-induced relaxation. SHS reduced endothelial l-arginine (p = 0.04) but not serum l-arginine. l-Arginine supplementation increased endothelial (p = 0.007) and serum l-arginine (p < 0.0005). Endothelium-dependent relaxation induced by acetylcholine and calcium ionophore varied directly with endothelial (r = 0.67, r = 0.67) and serum l-arginine (r = 0.43, r = 0.45), respectively. SHS reduced constitutive NOS activity (p = 0.03).

Conclusions: SHS reduces pulmonary artery endothelium-dependent relaxation by decreasing NOS activity and possibly by decreasing endothelial arginine content. l-Arginine supplementation increases serum and endothelial l-arginine stores and prevents SHS-induced endothelial dysfunction. l-Arginine may offset the deleterious effect of SHS on pulmonary arteries by substrate loading of the nitric oxide pathway.

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