Only two-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers

Morita, Hirohiko; Ikeda, Hisao; Haramaki, Nobuya; Eguchi, Hironobu; Imaizumi, Tsutomu

doi:10.1016/j.jacc.2004.10.061

Cited by 95 publications

(69 citation statements)

References 31 publications

(28 reference statements)

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“…However, since the parameters of the VEP (neuronal activation) were not different in the 3 groups (smokers, nonsmokers, former smokers), the neuronal mechanism was probably not responsible for the impaired visually evoked flow response in the former smokers. The acute effects of smoking, like increased platelet aggregability, increased carboxyhemoglobin level of the blood, or inactivation of NO by reactive oxygen species of cigarette smoke, might worsen the cerebrovascular response, but only temporarily [14,15,16]. In our study, the impact of acute effects of smoking is unlikely after more than half a year of smoking cessation.…”

Section: Discussionmentioning

confidence: 74%

Effect of Smoking Cessation on Visually Evoked Cerebral Blood Flow Response in Healthy Volunteers

et al. 2009

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Background/Aims: In our previous study, impaired visually evoked flow velocity response was demonstrated in young chronic smokers. Our aim was to study whether impaired cerebrovascular reactivity is reversible 6–18 months after smoking cessation. Methods: Flow velocity changes, evoked by visual stimulus, were recorded in the posterior cerebral arteries in 15 smokers, 15 former smokers and 15 nonsmokers. The stimulation protocol consisted of 10 cycles with a resting phase of 20 s (baseline) and a stimulating phase of 40 s for each cycle. Relative changes of flow velocity were expressed in relation to baseline. Breath holding index, visual evoked potential and intima-media thickness were also examined. Results: Repeated measures ANOVA revealed marked difference in the flow velocity time courses between the 3 groups (p < 0.01). The flow response was significantly worse in former smokers than in nonsmokers (p < 0.002), however, no significant difference was found between former and current smokers (p = 0.0556). Conclusion: This is the first transcranial Doppler study demonstrating long-term impairment of visually evoked cerebrovascular response after smoking cessation. These findings indicate that the impairment of neurovascular coupling caused by smoking is due to structural changes of the vessels, rather than acute effect of smoking.

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Section: Discussionmentioning

confidence: 74%

Effect of Smoking Cessation on Visually Evoked Cerebral Blood Flow Response in Healthy Volunteers

et al. 2009

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“…20 Smoking-induced platelet activation may involve increased oxidative stress and is improved within 2 weeks of quitting. 21,22 Cigarette smoking is associated with a more atherogenic lipid profile, including decreased levels of high-density lipoprotein-cholesterol and higher levels of LDL-cholesterol levels. 23 Nicotine, by releasing catecholamines, induces lipolysis and releases plasma free fatty acids with a subsequent rise in triglycerides and very-LDL levels.…”

mentioning

confidence: 99%

Smoking and Aortic Diseases

Kakafika

Mikhailidis

2007

Circ J

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Cigarette smoking is a major cause of cardiovascular disease (CVD) and is responsible for approximately 11% of the annual total CVD deaths in the United States. 1 Smoking acts synergistically with other vascular risk factors (eg, hypertension, dyslipidaemia and diabetes) to increase vascular morbidity and mortality. 2 However, smoking has a variable magnitude of increased risk for different vascular diseases: the risk is highest for peripheral arterial disease and aortic aneurysm, and is lowest for coronary artery and cerebrovascular diseases. 2 These effects are thought to reverse after smoking cessation. The constituents of cigarette smoke with the major contribution to pathogenesis of vascular disease are nicotine, carbon monoxide, oxidant gases and polycyclic aromatic hydrocarbons. 2 Nonsmokers who are exposed to "secondhand" smoke experience on average a 30% excess risk of ischemic heart disease and nonfatal myocardial infarction. 3 Secondhand smoke exposure has been shown to activate platelets and to produce endothelial dysfunction, in both experimental animals and humans. 3 The mechanisms by which smoking causes acute cardiovascular events include endothelial dysfunction, thrombosis and inflammation.Endothelial dysfunction is an initiating event in atherogenesis, as well as a major factor in causing acute cardiovascular events. Cigarette smoking impairs flow-mediated endothelium-dependent peripheral arterial vasodilatation, an effect that is, at least partly, reversible after smoking Circulation Journal Vol.71, August 2007 cessation. 4 Smokers without atherosclerosis have coronary vasoconstrictor responses to acetylcholine that, in the presence of normal endothelium, produce vasodilatation. 5 Indeed, the oxidant chemicals of smoke degrade nitric oxide (NO) and reduce NO release, with subsequent impairment of vascular dilation and platelet function. 2 Smokers have lower than normal levels of antioxidant vitamins, reflecting their consumption in response to ongoing oxidant stress. 6 In addition, nicotine itself alters the structural and functional characteristics of vascular smooth muscle cells (VSMC) and endothelial cells. 7,8 Experimental data show that human aortic endothelial cells undergo apoptotic changes when they are exposed to cigarette smoke extracts. 9 This process may be prevented by pre-activation of NO synthase by Larginine. 9,10 Furthermore, smoking causes an increase in vascular superoxide production, which results in decreased NO bioactivity and concomitantly increases production of vasoconstrictor eicosanoids. 11 Cigarette smoke extracts, but not nicotine, also inhibit prostacyclin (PGI2: a vasodilator and inhibitor of platelet aggregation) synthesis in human, rabbit and rat vascular tissue. 12 Smoking-mediated endothelial dysfunction also results in reduced secretion of tissue plasminogen activator (tPA) 13 and increased secretion of plasminogen activator inhibitor (PAI)-1, 1 which results in impaired fibrinolysis. This acts in concert with the increased levels of tissue factor and fibrin...

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“…Активные формы кислорода -свободные радикалы -находящиеся во вдыхаемом дыму являются причиной окисления ЛПНП в плазме крови; окисленные ЛПНП, стимулируют процессы воспаления за счет прили-пания моноцитов к стенке сосудов, что является пусковым механизмом воспалительных изменений в интиме артерий, который приводит к прогрессированию атеросклероза [232,[239][240][241][242] . В экспериментальных работах, показано, что эти эффекты полностью или частично обратимы в течение очень короткого времени [243,244] . Обратимый ответ пре-кращение курения на риск ССЗ объясняется двойным дей-ствием курения -острым и действием на гемостаз и ста-бильность атеросклеротической бляшки и более длитель-ным действием на процессы формирования бляшки .…”

Section: механизм увеличивающий риск от куренияunclassified

A Ten Year Overview of Surgical and Interventional Arrhythmology in Russia. Service Peculiar Features in the Far East

Богачевская¹,

Bogachevskiy²

2017

Soc.Asp.Pop.Hlth

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Only two-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers

Cited by 95 publications

References 31 publications

Effect of Smoking Cessation on Visually Evoked Cerebral Blood Flow Response in Healthy Volunteers

Effect of Smoking Cessation on Visually Evoked Cerebral Blood Flow Response in Healthy Volunteers

Smoking and Aortic Diseases

A Ten Year Overview of Surgical and Interventional Arrhythmology in Russia. Service Peculiar Features in the Far East

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