Platelet Spontaneous Aggregation in Platelet-Rich Plasma Is Increased in Habitual Smokers
Cigarette smoking is a well-known risk factor for atherosclerotic disorders. Several authors have suggested that platelet aggregability is important in smoking-induced vascular injury. When platelet-rich plasma is stirred at 37°C in the absence of chemical stimulants, small aggregates of platelets m...
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Veröffentlicht in: | Thrombosis research 1999-03, Vol.93 (6), p.271-278 |
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description | Cigarette smoking is a well-known risk factor for atherosclerotic disorders. Several authors have suggested that platelet aggregability is important in smoking-induced vascular injury. When platelet-rich plasma is stirred at 37°C in the absence of chemical stimulants, small aggregates of platelets may be formed, but it was difficult to detect small aggregates by conventional aggregometer using optical density. Recent technological advances have made it possible to detect small aggregates by using a newly developed assay system that employs laser light scattering. In the present study, we attempted to measure platelet aggregation by this method, using laser light scattering in 54 nonsmoking healthy males and 51 healthy male habitual smokers who were age matched. In smokers, blood was obtained after 10 hours of smoking abstinence. No significant difference in platelet aggregation was induced by 1 μM or 5 μM of ADP between smokers and nonsmokers. In smokers, plasma fibrinogen levels and the number of small aggregates formed in the absence of chemical stimulants was significantly higher than in nonsmokers. Small aggregates formed in the absence of stimulants correlated positively with the concentrations of von Willebrand factor (vWF) antigen (
r=0.2654
,
p |
doi_str_mv | 10.1016/S0049-3848(98)00184-4 |
format | Article |
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r=0.2654
,
p<0.01) and of fibrinogen (
r=0.2834
,
p<0.01). The formation of these small aggregates was inhibited by monoclonal antibody against GPIIb/IIIa blocking fibrinogen binding to GPIIb/IIIa but not inhibited at all by monoclonal antibody against GPIb blocking vWF binding to GPIb. From these results, enhanced platelet aggregability in smokers was confirmed, and it was suggested that GPIIb/IIIa is concerned in platelet spontaneous aggregation, although vWF may not directly influence on the platelet spontaneous aggregation. Since the mechanism of spontaneous aggregation and the effect of increased spontaneous aggregability on the progression of atherosclerosis remains unclear, further study was considered necessary.</description><identifier>ISSN: 0049-3848</identifier><identifier>EISSN: 1879-2472</identifier><identifier>DOI: 10.1016/S0049-3848(98)00184-4</identifier><identifier>PMID: 10093968</identifier><identifier>CODEN: THBRAA</identifier><language>eng</language><publisher>New York, NY: Elsevier Ltd</publisher><subject>Adult ; Biological and medical sciences ; Fibrinogen ; Habitual smoker ; Humans ; Male ; Medical sciences ; Middle Aged ; Platelet Aggregation ; Platelet spontaneous aggregation ; Risk Factors ; Smoking - adverse effects ; Thrombosis - etiology ; Time Factors ; Tobacco, tobacco smoking ; Toxicology ; von Willbrand factor</subject><ispartof>Thrombosis research, 1999-03, Vol.93 (6), p.271-278</ispartof><rights>1999 Elsevier Science Ltd</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-3d4b30cf930b4f0bd6b28d3ce3e77048dd23ca756a1071a981be0dade8b567913</citedby><cites>FETCH-LOGICAL-c456t-3d4b30cf930b4f0bd6b28d3ce3e77048dd23ca756a1071a981be0dade8b567913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0049-3848(98)00184-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1763917$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10093968$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fusegawa, Yuichi</creatorcontrib><creatorcontrib>Goto, Shinya</creatorcontrib><creatorcontrib>Handa, Shunnosuke</creatorcontrib><creatorcontrib>Kawada, Tsutomu</creatorcontrib><creatorcontrib>Ando, Yasuhiko</creatorcontrib><title>Platelet Spontaneous Aggregation in Platelet-Rich Plasma Is Increased in Habitual Smokers</title><title>Thrombosis research</title><addtitle>Thromb Res</addtitle><description>Cigarette smoking is a well-known risk factor for atherosclerotic disorders. Several authors have suggested that platelet aggregability is important in smoking-induced vascular injury. When platelet-rich plasma is stirred at 37°C in the absence of chemical stimulants, small aggregates of platelets may be formed, but it was difficult to detect small aggregates by conventional aggregometer using optical density. Recent technological advances have made it possible to detect small aggregates by using a newly developed assay system that employs laser light scattering. In the present study, we attempted to measure platelet aggregation by this method, using laser light scattering in 54 nonsmoking healthy males and 51 healthy male habitual smokers who were age matched. In smokers, blood was obtained after 10 hours of smoking abstinence. No significant difference in platelet aggregation was induced by 1 μM or 5 μM of ADP between smokers and nonsmokers. In smokers, plasma fibrinogen levels and the number of small aggregates formed in the absence of chemical stimulants was significantly higher than in nonsmokers. Small aggregates formed in the absence of stimulants correlated positively with the concentrations of von Willebrand factor (vWF) antigen (
r=0.2654
,
p<0.01) and of fibrinogen (
r=0.2834
,
p<0.01). The formation of these small aggregates was inhibited by monoclonal antibody against GPIIb/IIIa blocking fibrinogen binding to GPIIb/IIIa but not inhibited at all by monoclonal antibody against GPIb blocking vWF binding to GPIb. From these results, enhanced platelet aggregability in smokers was confirmed, and it was suggested that GPIIb/IIIa is concerned in platelet spontaneous aggregation, although vWF may not directly influence on the platelet spontaneous aggregation. Since the mechanism of spontaneous aggregation and the effect of increased spontaneous aggregability on the progression of atherosclerosis remains unclear, further study was considered necessary.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Fibrinogen</subject><subject>Habitual smoker</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Platelet Aggregation</subject><subject>Platelet spontaneous aggregation</subject><subject>Risk Factors</subject><subject>Smoking - adverse effects</subject><subject>Thrombosis - etiology</subject><subject>Time Factors</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><subject>von Willbrand factor</subject><issn>0049-3848</issn><issn>1879-2472</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0ElLxDAYgOEgio7LT1B6ENFDNWnSLCcRcRkQFEcPnkKafB2jXcakI_jv7dhxuXkKgefL8iK0S_AxwYSfTDBmKqWSyUMljzAmkqVsBY2IFCrNmMhW0eiHbKDNGF96JIjK19EGwVhRxeUIPd1VpoMKumQya5vONNDOY3I2nQaYms63TeKb5Nuk994-L3axNsk4JuPGBjAR3AJdm8J3c1Mlk7p9hRC30Vppqgg7y3ULPV5ePJxfpze3V-Pzs5vUspx3KXWsoNiWiuKClbhwvMikoxYoCIGZdC6j1oicG4IFMUqSArAzDmSRc6EI3UIHw7mz0L7NIXa69tFCVQ1_0VzxPGNU9jAfoA1tjAFKPQu-NuFDE6wXTfVXU70IppXUX0016-f2lhfMixrcn6khYg_2l8BEa6oymMb6-OsEp4qInp0ODPoa7x6CjtZDY8H5ALbTrvX_vOQTykuTXw</recordid><startdate>19990315</startdate><enddate>19990315</enddate><creator>Fusegawa, Yuichi</creator><creator>Goto, Shinya</creator><creator>Handa, Shunnosuke</creator><creator>Kawada, Tsutomu</creator><creator>Ando, Yasuhiko</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19990315</creationdate><title>Platelet Spontaneous Aggregation in Platelet-Rich Plasma Is Increased in Habitual Smokers</title><author>Fusegawa, Yuichi ; Goto, Shinya ; Handa, Shunnosuke ; Kawada, Tsutomu ; Ando, Yasuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-3d4b30cf930b4f0bd6b28d3ce3e77048dd23ca756a1071a981be0dade8b567913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Fibrinogen</topic><topic>Habitual smoker</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Platelet Aggregation</topic><topic>Platelet spontaneous aggregation</topic><topic>Risk Factors</topic><topic>Smoking - adverse effects</topic><topic>Thrombosis - etiology</topic><topic>Time Factors</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><topic>von Willbrand factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fusegawa, Yuichi</creatorcontrib><creatorcontrib>Goto, Shinya</creatorcontrib><creatorcontrib>Handa, Shunnosuke</creatorcontrib><creatorcontrib>Kawada, Tsutomu</creatorcontrib><creatorcontrib>Ando, Yasuhiko</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Thrombosis research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fusegawa, Yuichi</au><au>Goto, Shinya</au><au>Handa, Shunnosuke</au><au>Kawada, Tsutomu</au><au>Ando, Yasuhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet Spontaneous Aggregation in Platelet-Rich Plasma Is Increased in Habitual Smokers</atitle><jtitle>Thrombosis research</jtitle><addtitle>Thromb Res</addtitle><date>1999-03-15</date><risdate>1999</risdate><volume>93</volume><issue>6</issue><spage>271</spage><epage>278</epage><pages>271-278</pages><issn>0049-3848</issn><eissn>1879-2472</eissn><coden>THBRAA</coden><abstract>Cigarette smoking is a well-known risk factor for atherosclerotic disorders. Several authors have suggested that platelet aggregability is important in smoking-induced vascular injury. When platelet-rich plasma is stirred at 37°C in the absence of chemical stimulants, small aggregates of platelets may be formed, but it was difficult to detect small aggregates by conventional aggregometer using optical density. Recent technological advances have made it possible to detect small aggregates by using a newly developed assay system that employs laser light scattering. In the present study, we attempted to measure platelet aggregation by this method, using laser light scattering in 54 nonsmoking healthy males and 51 healthy male habitual smokers who were age matched. In smokers, blood was obtained after 10 hours of smoking abstinence. No significant difference in platelet aggregation was induced by 1 μM or 5 μM of ADP between smokers and nonsmokers. In smokers, plasma fibrinogen levels and the number of small aggregates formed in the absence of chemical stimulants was significantly higher than in nonsmokers. Small aggregates formed in the absence of stimulants correlated positively with the concentrations of von Willebrand factor (vWF) antigen (
r=0.2654
,
p<0.01) and of fibrinogen (
r=0.2834
,
p<0.01). The formation of these small aggregates was inhibited by monoclonal antibody against GPIIb/IIIa blocking fibrinogen binding to GPIIb/IIIa but not inhibited at all by monoclonal antibody against GPIb blocking vWF binding to GPIb. From these results, enhanced platelet aggregability in smokers was confirmed, and it was suggested that GPIIb/IIIa is concerned in platelet spontaneous aggregation, although vWF may not directly influence on the platelet spontaneous aggregation. Since the mechanism of spontaneous aggregation and the effect of increased spontaneous aggregability on the progression of atherosclerosis remains unclear, further study was considered necessary.</abstract><cop>New York, NY</cop><pub>Elsevier Ltd</pub><pmid>10093968</pmid><doi>10.1016/S0049-3848(98)00184-4</doi><tpages>8</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Fibrinogen Habitual smoker Humans Male Medical sciences Middle Aged Platelet Aggregation Platelet spontaneous aggregation Risk Factors Smoking - adverse effects Thrombosis - etiology Time Factors Tobacco, tobacco smoking Toxicology von Willbrand factor |
title | Platelet Spontaneous Aggregation in Platelet-Rich Plasma Is Increased in Habitual Smokers |
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