Effects of chronic smoking on platelet function

Rival, J; Riddle, Jeanne M.; Stein, Paul D.

doi:10.1016/0049-3848(87)90258-1

Cited by 80 publications

(32 citation statements)

References 26 publications

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“…The responsiveness of leukocytes and platelets to a variety of agonists might be increased by smoking or by nicotine/cotinine. Thus, smoking-or nicotine-activated leukocytes (Nowak et al 1990;Bridges et al 1993) and platelets (Rival et al 1987;Blache et al 1992;Nowak et al 1996) may be the origin of increased eicosanoid synthesis. Nicotine stimulates the release of catecholamines from the adrenal gland (Benowitz 1991) and the release of serotonin from gastrointestinal enterochromaffin cells (Racké and Schwörer 1992), which are thought to be the main source of platelet serotonin (Verbeuren 1989).…”

Section: Discussionmentioning

confidence: 95%

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Saareks

Ylitalo

Alanko

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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This study investigated the effects of smoking cessation with and without nicotine substitution on the excretion of major urinary metabolites of thromboxane A2 and prostacyclin, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha, respectively, as well as on the excretion of leukotriene E4 in man. Urine samples were obtained from 20 healthy non-smoking controls and from 60 healthy smoking volunteers before, and 3, 7 and 14 days after smoking cessation. Fifteen smokers quit smoking without nicotine substitution, 15 used nicotine chewing gum and 30 used nicotine patches as a substitution therapy. Urinary thiocyanate as well as cotinine and trans-3'-hydroxycotinine excretions were used as compliance and nicotine substitution indicators. 11-Dehydrothromboxane B2, 2,3-dinor-6-ketoprostaglandin F1alpha and leukotriene E4 excretion was about two, three and five times higher in smokers than in controls, respectively. Three days after smoking cessation without nicotine substitution, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha levels were lowered to 75% (P<0.01) and 80% (P<0.05) of the initial values, and after 14 days to 50% (P<0.01) and 60% (P<0.05), respectively. In 3 days leukotriene E4 excretion was dropped to 70% of the initial value (P<0.05), but no further decrease was observed during the study. In individuals using nicotine chewing gum or nicotine patches no significant changes were observed in the analytes during the 2-week follow-up. The increased systemic eicosanoid synthesis observed in smokers may be involved in the harmful cardiovascular effects of smoking. The fact that eicosanoid production remains at pre-cessation level in volunteers who quit smoking but use nicotine substitution may be involved in the risk of cardiovascular complications reported during nicotine replacement therapy.

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Section: Discussionmentioning

confidence: 95%

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Saareks

Ylitalo

Alanko

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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“…This creates hypoxemia (abnormally low amount of oxygen transported by the blood) in both passive and active smokers and leads to an increased number of circulating red blood cell 56 that also are a major components of the blood clot formation. Finally, cigarette smoke induces platelet dysfunction as platelets from smokers aggregate spontaneously and in greater proportion following oxidative stress 88 , suggesting that they are hyper activated even at basal…”

Section: Effect Of Cigarette Smoking On Thrombosismentioning

confidence: 99%

SASH1, a new potential link between smoking and atherosclerosis

et al. 2015

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“…10,11 Multiple studies have shown that CSE affects platelet function. [12][13][14] Platelets isolated from smokers exhibit increased aggregation as compared to nonsmokers. 13 On the other hand, data on CSE and fibrinogen are limited.…”

Section: Cse Increases the Risk For Arterial Thrombosis And In The Comentioning

confidence: 99%

Effects of Cigarette Smoke Exposure on Clot Dynamics and Fibrin Structure

Barua

Srikanth

et al. 2010

ATVB

114

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Objectives-The purpose of this study was to examine the effect of cigarette smoke exposure (CSE) on clot dynamics and fibrin architecture and to isolate the relative contribution of platelets and fibrinogen to clot dynamics. Methods and Results-From young healthy males smokers (nϭ34) and nonsmokers (nϭ34) a baseline blood was drawn, and smokers had another blood draw after smoking 2 regular cigarettes. Using thromboelastography (TEG) the degree of platelet-fibrin interaction was measured. In additional experiments, abciximab (20 g/mL) was added to the smokers samples (nϭ27) to reduce the effects of platelet function from the TEG parameters. The maximum clot strength (G) obtained with abciximab measured mainly the contribution of fibrinogen to clot strength (GF). By subtracting GF from G, the contribution of platelets to clot strength (GP) was presumed. A significant difference was found for all TEG parameters between nonsmokers versus postsmoking and pre-versus postsmoking samples. Postsmoking both GF and GP were significantly higher as compared to presmoking. On electron microscopy and turbidity analysis, postsmoking fibrin clots were significantly different compared to presmoking and nonsmoking samples. Conclusions-Acute CSE changes clot dynamics and alters fibrin architecture. Both functional changes in fibrinogen and platelets appear to contribute to heightened thrombogenicity after acute CSE.

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Effects of chronic smoking on platelet function

Cited by 80 publications

References 26 publications

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

SASH1, a new potential link between smoking and atherosclerosis

Effects of Cigarette Smoke Exposure on Clot Dynamics and Fibrin Structure

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