Acute effects of cigarette smoking on platelet-dependent thrombin generation

Hioki, Hiroyuki; Aoki, Nobuo; Kawano, Koichi; Hòmori, Masashi; Hasumura, Yukihisa; Yasumura, T.; Maki, Akira; Yoshino, Hideaki; Yanagisawa, Atsuo; Ishikawa, Kinya

doi:10.1053/euhj.1999.1938

Cited by 112 publications

(69 citation statements)

References 27 publications

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“…It is noteworthy that exposure to some of these toxicants, albeit from traditional tobacco smoking and other sources, was found to be associated with an enhanced platelet activation phenotype 6. Furthermore, while the effects of nicotine on platelet activation/aggregation are still controversial,16, 105, 106, 107, 108 particulate matter109, 110 and acrolein93 were indeed found to enhance platelet function.…”

Section: Discussionmentioning

confidence: 99%

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

100

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BackgroundCardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e‐cigarettes are “safer/less harmful” than conventional cigarettes, their usage—among a variety of ages—has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e‐cigarettes on the cardiovascular system, which is also the subject of significant debate.Methods and ResultsWe employed a passive e‐VapeTM vapor inhalation system and developed an in vivo whole‐body e‐cigarette mouse exposure protocol that mimics real‐life human exposure scenarios/conditions and investigated the effects of e‐cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e‐cigarette–exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air–exposed platelets. E‐cigarette–exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e‐cigarette–exposed mice exhibited a shortened thrombosis occlusion and bleeding times.ConclusionsTaken together, our data demonstrate for the first time that e‐cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e‐cigarette exposure should not be underestimated and warrant further investigation.

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Section: Discussionmentioning

confidence: 99%

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

100

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“…3 Platelet-dependent thrombin generation is elevated in smokers even after they abstain from smoking for several hours. 4 It has been suggested that a higher number of active platelets in chronic smokers leads to increased thrombin generation and increased thrombotic risk. 5 Many studies, mainly of platelet aggregation in response to exogenous agonists like ADP and serotonin, show increased response after exposure to cigarette smoke.…”

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confidence: 99%

Differences Between Mainstream and Sidestream Cigarette Smoke Extracts and Nicotine in the Activation of Platelets Under Static and Flow Conditions

2004

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Background-Cigarette smoke is a primary risk factor for cardiovascular diseases. Enhanced function of the hemostatic system, in which platelets play a major role, is a significant underlying mechanism in cardiovascular disease and its progression. Epidemiological studies, complemented by physiological and biochemical data, show that cigarette smoke adversely affects platelet function, both in smokers and in nonsmokers exposed to sidestream smoke. Methods and Results-The thrombogenic potential of platelets subjected to mainstream smoke extracts, sidestream extracts, and nicotine was measured in vitro under static and dynamic flow conditions. Platelet activation state was measured with a modified prothrombinase-based method. Mainstream and sidestream smoke extracts caused increased platelet activation. Although low-tar mainstream extracts activated platelets less than high-tar extracts, the sidestream extracts were almost equally potent. Modification of the filters of low-tar cigarettes, by blocking the air-bypass holes, raised activation rates by mainstream extracts to the level of high-tar extracts. Nicotine (50 nmol/L and 5 mol/L) inhibited platelet activation under both flow and static conditions. Conclusions-Cigarette smoke extracts directly cause platelet activation but also markedly increase the susceptibility of platelets to activation by shear stress. In contrast, nicotine, although also a constituent of cigarette smoke, significantly reduces platelet susceptibility to shear stress.

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“…22,23 Trombosit bağımlı trombin düzeyi sigara içimi sonrası belirgin düzeyde artmaktadır. 24 Ayrıca sigara içiminin kan viskozitesinde doz bağımlı artışa neden olduğunu gösteren bir çalışma vardır. 7 Sigaranın tromboembolik olaylara ve vasküler dolaşım bozukluğuna neden olduğu öteden beri bilinen bir gerçektir.…”

Section: Discussionunclassified

The Effects of Smoking on Plasma Viscosity and Related Biochemical Parameters

Yılmaz¹,

Atıcı²,

Kayhan³

et al. 2012

Solunum

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ÖZETAmaç: Bu çalışmanın amacı tromboemboli ve vasküler dolaşım bozukluğu için bir risk faktörü olduğu bilinen sigara kullanımının, mikrosirkülasyonu düzenleyen plazma viskozitesi ve diğer hemoreolojik faktörler üzerindeki etkilerini araştırmaktır.Gereç ve Yöntem: Tanımlayıcı tipte yapılan çalışmaya Haziran 2010-Haziran 2011 tarihleri arasında polikliniğimize başvuranlar arasından sağlıklı olduğu belirlenen ve çalışmaya katılmayı kabul eden ardışık 60 kişi alındı. Çalışma grubu sigara kullanma özellik-lerine göre sigara içen, sigarayı bırakmış olan ve sigara içmeyen olarak üçe ayrıldı. Çalışmaya alınanların fizik muayeneleri, akciğer grafileri ve solunum fonksiyon testleriyle birlikte hemogram, sedimantasyon hızı, kolesterol, trigliserid, protein ve plazma viskozite düzeyleri ölçüldü. Plazma viskozite ölçümü için Brookfield LVDV II viskometre cihazı kullanıldı.Bulgular: Çalışma gruplarının ortalama plazma viskozite düzeyle-ri, sigara içen grupta 1,29±0,26 cP, sigarayı bırakmış olan grupta 1,33±0,25 cP, hiç sigara içmeyen grupta 1,31±0,24 cP ve tümünde 1,31±0,25 cP olarak bulundu. Gruplar arasında bu değerler açısın-dan anlamlı bir fark yoktu. Sigara kullanma düzeyi (paket/yıl) ile total protein ve albümin düzeyleri arasında pozitif; total kolesterol, trigliserid ve yüksek dansiteli lipoprotein düzeyleri arasında negatif bir ilişki saptandı (p<0,05). Fibrinojen düzeyi bu çalışmada plazma viskozitesini etkileyen tek faktör olarak belirlendi. Fibrinojen düzeyi ile yaş, kilo ve vücut kitle indeksi değişkenleri arasında pozitif korelasyon saptandı (p<0,05).Sonuç: Sağlıklı kişilerde sigara kullanımı ile plazma viskozitesi arasında anlamlı bir ilişki bulunmamıştır. Ancak sigara kullanımı, diğer bazı hemoreolojik faktörleri etkileyebilir.Anahtar Kelimeler: Plazma viskozitesi, fibrinojen, sigara ABSTRACTObjective: The aim of the study was to investigate the effects of smoking, which is known as a risk factor for thromboembolism and circulatory disorders, on plasma viscosity and the other hemorheologic factors determining the microcirculation in healthy individuals. Materials and Methods:After their acceptance sixty apparently healthy individuals attending our outpatient clinic between June 2010 and June 2011 were enrolled in this descriptive type of investigation. The study groups were classified as smokers, non-smokers, and ex-smokers according to smoking habits. After taking medical history of the volunteers; physical examination, chest radiography, pulmonary function tests were carried out. After 8 hours of fasting, blood samples were taken to determine the hemogram, sedimentation rate, cholesterol, triglyceride, protein and plasma viscosity levels. Plasma viscosity leves were measured by Brookfield LVDV II viscometer.Results: Plasma viscosity values were found in the smokers, ex-smokers, and the non-smokers to be 1.29±0.26 cP, 1.33±0.25 cP, 1.31±0.24 cP respectively. The average value in all participants being 1.31±0.25 cP. Although these levels did not differ between the groups, the intensity of smoking (estimated in...

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Acute effects of cigarette smoking on platelet-dependent thrombin generation

Cited by 112 publications

References 27 publications

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Differences Between Mainstream and Sidestream Cigarette Smoke Extracts and Nicotine in the Activation of Platelets Under Static and Flow Conditions

The Effects of Smoking on Plasma Viscosity and Related Biochemical Parameters

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