Effects of Long-Term Cigarette Smoking on Endothelium-Dependent Responses in Humans
Section snippets
METHODS
The study group was composed of 35 healthy long-term smokers (20 men and 15 women) and 16 healthy age-matched nonsmokers (8 men and 8 women). For smokers to be included in the study, they must have smoked >10 cigarettes/day for >1 year. All subjects were evaluated by medical history, physical examination, electrocardiography, and routine blood tests and urinalyses to exclude conditions that could affect the results of the study. Specifically, subjects were excluded if they had a history of
RESULTS
The clinical characteristics of smokers and nonsmokers are listed in Table 1. There were no significant differences between the 2 groups with regard to the age, heart rate, blood pressure, or serum lipid profile. Carboxyhemoglobin levels were significantly higher in smokers than nonsmokers: 5.1 ± 2.1% versus 0.8 ± 0.4%, respectively (p <0.001). The basal forearm blood flow values in smokers and nonsmokers were not significantly different: 3.6 ± 1.2 and 3.2 ± 1.0 ml·min−1 · 100 ml−1,
DISCUSSION
A reduced responsiveness of the vasculature to the stimulated release, or basal production of, endothelium-derived nitric oxide is regarded as a marker of an early functional change in the endothelium that can occur before morphologic changes are apparent.13, 14In this study, long-term smokers without clinical evidence of vascular disease demonstrated an abnormality in endothelial function manifested by a reduction in basal, but not stimulated, nitric oxide-mediated vasodilation when compared
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Decreased expression of neuronal nitric oxide synthase contributes to the endothelial dysfunction associated with cigarette smoking in human
2020, Nitric Oxide - Biology and ChemistryCitation Excerpt :Few studies have investigated the contribution of nitric oxide synthases (NOS) and the role of this enzyme remains yet poorly understood and controversial. Intrabrachial infusion of NG-monomethyl-l-arginine, (LNMMA), a non-selective inhibitor of NOS, decreased vasodilatation in the forearm blood flow in a more pronounced way in long-term smokers than in nonsmokers [16]. Similarly, microdialysis infusion with NG-nitro-l-arginine methyl ester, (l-NAME), another non-selective NOS inhibitor, attenuated the ACh-induced cutaneous vasodilation in nonsmokers but not in smokers [17].
Smoking and the Endothelium
2018, Endothelium and Cardiovascular Diseases: Vascular Biology and Clinical SyndromesEffect of smoking on endothelium-independent vasodilatation
2015, AtherosclerosisCitation Excerpt :The novel finding of this study is that, by using low NTG doses, it is possible to demonstrate that smoking is associated with an early impairment of endothelium-independent arterial dilatation in young healthy subjects without any other CVRFs. While an impairment of endothelium-dependent vasodilatation has consistently been found in smokers, controversial results were reported about endothelium-independent vasodilatation [1–8]. Celermajer et al. [1] found a lower NMD in smokers, as compared with controls, but the same group failed to demonstrate a significant independent relation between smoking and NMD in another study [12].
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2010, European Journal of PharmacologyCitation Excerpt :Flow-mediated dilatation of the brachial artery induced by forearm occlusion was reduced in smoking subjects and an increase in the femoral artery diameter in response to exercise was less in smokers than in nonsmoking subjects, suggesting that endothelial dysfunction represents the underlying mechanism (Gaenzer et al., 2001). McVeigh et al. (1996) provided evidence suggesting that long-term cigarette smokers exhibited an impairment in basal, but not stimulated, NO-mediated vasodilatation that was evaluated by measurement of forearm blood flow decrease in response to L-NMMA and its increase following infusions of methacholine and sodium nitroprusside. However, Holay et al. (2004) noted that brachial artery flow-mediated vasodilatation was lower in passive and active smokers than in nonsmokers, whereas GTN-induced dilatation was similar in all 3 groups.
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