Abstract

Background: To assess the vasodilatory response to acetylcholine (Ach, endothelium-dependent vasodilator) and Na nitroprusside (SNP, endothelium-independent vasodilator) in the skin microcirculation of habitual cigarette smokers.

Methods: Male healthy habitual smokers taking no medication acting on the cardiovascular system were included. They were divided in younger (Group 1, n = 10, age: 18 to 35 years; mean = 7 pack-years) and older (Group 2, n = 10, age: 40 to 60 years; mean =30 pack-years). Younger (Group 3, n = 10) and older controls (Group 4, n = 10) consisted of age-matched non-smokers. On the day of the experiment the subjects of Groups 1 and 2 were asked to smoke at least 15 cigarettes starting in the morning. At 4 p.m. they had to smoke within 5 min a filter cigarette containing 1 mg nicotine. Subjects of Groups 3 and 4 had a sham-smoking session at 4 p.m. Ach, 1%, and SNP, 0.1%, were administered transcutaneously for 7 min on the volar face of the right forearm using iontophoresis. This was done 15 min and 40 min after the end of the smoking session for Ach and SNP, respectively. The skin blood flow responses were evaluated using a laser-Doppler flowmeter allowing to scan the surface of Ach and SNP application (circular area, 1 cm diameter).

Results: The following Table shows the peak changes induced by Ach and SNP (perfusion units, means±SD):

YoungerOlder
AchSNPAchSNP
Non-smokers505±65425±99473±91392±71
Smokers466±102416±59302±50**301±104*
YoungerOlder
AchSNPAchSNP
Non-smokers505±65425±99473±91392±71
Smokers466±102416±59302±50**301±104*
*

p<0.05;

**

p<0.01, Smokers versus Non-smokers

YoungerOlder
AchSNPAchSNP
Non-smokers505±65425±99473±91392±71
Smokers466±102416±59302±50**301±104*
YoungerOlder
AchSNPAchSNP
Non-smokers505±65425±99473±91392±71
Smokers466±102416±59302±50**301±104*
*

p<0.05;

**

p<0.01, Smokers versus Non-smokers

Conclusion: These data show that the vasodilatory response of the skin microvasculature is impaired in subjects having smoked cigarettes for many years. This abnormality involves both the Ach and the SNP responses, which implies a diminished relaxant capacity of vascular smooth muscle cells, even if an underlying endothelial dysfunction cannot be ruled out.

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