Acute effects of passive smoking on peripheral vascular function.
Environmental tobacco smoke (ETS) acutely affects peripheral and coronary vascular tone. Whether ETS exerts specific deleterious effects on aortic wave reflection through nicotine exposure, whether they persist after ETS cessation, and whether the smoke environment impairs microvascular function and increases asymmetrical dimethyl-arginine levels are not known. We tested these hypotheses in a randomized, crossover study design in 11 healthy male nonsmokers. The effects of 1 hour of exposure to ETS, as compared with a nontobacco smoke and normal air, on augmentation index corrected for heart rate and skin microvascular hyperemia to local heating were examined. Augmentation index increased both during (P=0.01) and after (P<0.01) the ETS session but remained unchanged in the nontobacco smoke session when compared with normal air. Nicotine levels after the exposure were related to the peak rise in augmentation index (r=0.84; P<0.01), denoting a predominant role of nicotine in ETS vascular effects. This was confirmed in a second set of experiments (n=14), where the sublingual administration of nicotine was associated with an acute impairment in wave reflection as compared with placebo (P=0.001). Both ETS and nontobacco smokes increased plasma asymmetrical dimethyl-arginine levels (P<0.001), but only ETS reduced the late rise in skin blood flow in response to heating (P=0.03). In conclusion, passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. However, both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels.
Argacha
Jean-François
JF
Department of Cardiology, Erasme Hospital, 808 Lennik St, 1070 Brussels, Belgium. jfxa@skynet.be
Adamopoulos
Dionysios
D
Gujic
Marko
M
Fontaine
David
D
Amyai
Nadia
N
Berkenboom
Guy
G
van de Borne
Philippe
P
D000208:Acute Disease; D000286:Administration, Sublingual; D000328:Adult; D001011:Aorta / Q000502:physiology; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002263:Carboxyhemoglobin / Q000378:metabolism; D018592:Cross-Over Studies; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D004781:Environmental Exposure / Q000009:adverse effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D009538:Nicotine / Q000008:administration & dosage / Q000097:blood; D018722:Nicotinic Agonists / Q000008:administration & dosage / Q000097:blood; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012867:Skin / Q000098:blood supply; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D018722:Nicotinic Agonists; D014028:Tobacco Smoke Pollution; D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D009538:Nicotine; D002263:Carboxyhemoglobin; D001120:Arginine; D019001:Nitric Oxide Synthase