The impact of night-shift work on platelet function in healthy medical staff
[Abstract] : [Objectives] : Rotating shift work has been reported to increase the risk of cardiovascular diseases. Vascular endothelial dysfunction and platelet activation are among the leading causes of thrombus formation in patients with myocardial infarction or stroke. Endothelial function has be...
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Veröffentlicht in: | Journal of Occupational Health 2018-07, Vol.60 (4), p.324-332 |
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creator | Nakao, Tomoko Yasumoto, Atsushi Tokuoka, Suzumi Kita, Yoshihiro Kawahara, Takuya Daimon, Masao Yatomi, Yutaka |
description | [Abstract] : [Objectives] : Rotating shift work has been reported to increase the risk of cardiovascular diseases. Vascular endothelial dysfunction and platelet activation are among the leading causes of thrombus formation in patients with myocardial infarction or stroke. Endothelial function has been shown to be impaired immediately after night-shift work ; however, it is not known whether platelets are also activated. The aim of this study was to investigate the acute impact of night-shift work on platelet function. [Methods] : This observational study included 11 healthy medical staff members (seven women, median age 32 years) . We examined each subject's platelet aggregation rates and the serum concentrations of eicosanoid mediators after night-shift work and on dayshift work without preceding night-shift work (baseline) . [Results] : Platelet aggregation did not differ from baseline levels after night-shift work. However, serum cyclooxygenase (COX)-metabolized eicosanoid mediators, particularly thromboxane (Tx) B2 (a stable metabolite of TxA2 and the most important marker of platelet activation) , were significantly higher after the night-shift than at baseline (median 65.3 vs 180.4 ng/ml) . [Conclusions] : Although platelet aggregation did not increase, there was an increase in serum COX-metabolized eicosanoid mediators such as TxB2 in healthy medical staff after nightshift work. This platelet hypersensitivity may be one of the mechanisms underlying the significant association between night-shift work and adverse cardiovascular outcomes. |
doi_str_mv | 10.1539/joh.2018-0027-FS |
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Vascular endothelial dysfunction and platelet activation are among the leading causes of thrombus formation in patients with myocardial infarction or stroke. Endothelial function has been shown to be impaired immediately after night-shift work ; however, it is not known whether platelets are also activated. The aim of this study was to investigate the acute impact of night-shift work on platelet function. [Methods] : This observational study included 11 healthy medical staff members (seven women, median age 32 years) . We examined each subject's platelet aggregation rates and the serum concentrations of eicosanoid mediators after night-shift work and on dayshift work without preceding night-shift work (baseline) . [Results] : Platelet aggregation did not differ from baseline levels after night-shift work. However, serum cyclooxygenase (COX)-metabolized eicosanoid mediators, particularly thromboxane (Tx) B2 (a stable metabolite of TxA2 and the most important marker of platelet activation) , were significantly higher after the night-shift than at baseline (median 65.3 vs 180.4 ng/ml) . [Conclusions] : Although platelet aggregation did not increase, there was an increase in serum COX-metabolized eicosanoid mediators such as TxB2 in healthy medical staff after nightshift work. This platelet hypersensitivity may be one of the mechanisms underlying the significant association between night-shift work and adverse cardiovascular outcomes.</description><identifier>ISSN: 1341-9145</identifier><identifier>ISSN: 1348-9585</identifier><identifier>EISSN: 1348-9585</identifier><identifier>DOI: 10.1539/joh.2018-0027-FS</identifier><identifier>PMID: 29669967</identifier><language>eng</language><publisher>Japan: JAPAN SOCIETY FOR OCCUPATIONAL HEALTH</publisher><subject>Activation ; Adult ; Agglomeration ; Blood Platelets - physiology ; Cardiovascular diseases ; Cerebral infarction ; Cyclooxygenase ; Eicosanoids ; Female ; Field Study ; Health risks ; Healthy Volunteers ; Heart diseases ; Humans ; Hypersensitivity ; Male ; Medical personnel ; Medical Staff, Hospital ; Myocardial infarction ; Night ; Occupational health ; Platelet Activation ; Platelet Aggregation ; Platelets ; Prostaglandin endoperoxide synthase ; Shift work ; Shift Work Schedule ; Sleep deprivation ; Thrombosis ; Thromboxane B2 ; Thromboxane B2 - blood ; Working conditions</subject><ispartof>Journal of Occupational Health, 2018-07, Vol.60 (4), p.324-332</ispartof><rights>2018 Article author(s)</rights><rights>Copyright Japan Science and Technology Agency 2018</rights><rights>Article author (s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c7898-6599b12c5b41108fa688f2d0afd4adb6cc3e31166fe199e1dc116c25214757593</citedby><cites>FETCH-LOGICAL-c7898-6599b12c5b41108fa688f2d0afd4adb6cc3e31166fe199e1dc116c25214757593</cites><orcidid>0000-0003-1719-4297</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078842/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078842/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,27901,27902,45550,45551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29669967$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakao, Tomoko</creatorcontrib><creatorcontrib>Yasumoto, Atsushi</creatorcontrib><creatorcontrib>Tokuoka, Suzumi</creatorcontrib><creatorcontrib>Kita, Yoshihiro</creatorcontrib><creatorcontrib>Kawahara, Takuya</creatorcontrib><creatorcontrib>Daimon, Masao</creatorcontrib><creatorcontrib>Yatomi, Yutaka</creatorcontrib><creatorcontrib>Department of Lipidomics</creatorcontrib><creatorcontrib>Biostatistics Division</creatorcontrib><creatorcontrib>Clinical Research Support Center</creatorcontrib><creatorcontrib>The University of Tokyo Hospital</creatorcontrib><creatorcontrib>The University of Tokyo</creatorcontrib><creatorcontrib>Department of Clinical Laboratory</creatorcontrib><creatorcontrib>Graduate School of Medicine</creatorcontrib><title>The impact of night-shift work on platelet function in healthy medical staff</title><title>Journal of Occupational Health</title><addtitle>J Occup Health</addtitle><description>[Abstract] : [Objectives] : Rotating shift work has been reported to increase the risk of cardiovascular diseases. Vascular endothelial dysfunction and platelet activation are among the leading causes of thrombus formation in patients with myocardial infarction or stroke. Endothelial function has been shown to be impaired immediately after night-shift work ; however, it is not known whether platelets are also activated. The aim of this study was to investigate the acute impact of night-shift work on platelet function. [Methods] : This observational study included 11 healthy medical staff members (seven women, median age 32 years) . We examined each subject's platelet aggregation rates and the serum concentrations of eicosanoid mediators after night-shift work and on dayshift work without preceding night-shift work (baseline) . [Results] : Platelet aggregation did not differ from baseline levels after night-shift work. However, serum cyclooxygenase (COX)-metabolized eicosanoid mediators, particularly thromboxane (Tx) B2 (a stable metabolite of TxA2 and the most important marker of platelet activation) , were significantly higher after the night-shift than at baseline (median 65.3 vs 180.4 ng/ml) . [Conclusions] : Although platelet aggregation did not increase, there was an increase in serum COX-metabolized eicosanoid mediators such as TxB2 in healthy medical staff after nightshift work. This platelet hypersensitivity may be one of the mechanisms underlying the significant association between night-shift work and adverse cardiovascular outcomes.</description><subject>Activation</subject><subject>Adult</subject><subject>Agglomeration</subject><subject>Blood Platelets - physiology</subject><subject>Cardiovascular diseases</subject><subject>Cerebral infarction</subject><subject>Cyclooxygenase</subject><subject>Eicosanoids</subject><subject>Female</subject><subject>Field Study</subject><subject>Health risks</subject><subject>Healthy Volunteers</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Hypersensitivity</subject><subject>Male</subject><subject>Medical personnel</subject><subject>Medical Staff, Hospital</subject><subject>Myocardial infarction</subject><subject>Night</subject><subject>Occupational health</subject><subject>Platelet Activation</subject><subject>Platelet Aggregation</subject><subject>Platelets</subject><subject>Prostaglandin endoperoxide synthase</subject><subject>Shift work</subject><subject>Shift Work Schedule</subject><subject>Sleep deprivation</subject><subject>Thrombosis</subject><subject>Thromboxane B2</subject><subject>Thromboxane B2 - blood</subject><subject>Working conditions</subject><issn>1341-9145</issn><issn>1348-9585</issn><issn>1348-9585</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNqFUs9vFCEYnRiNbWrvngyJFy9T-WBgICYmpnFbzSY9tJ4Jw0KHysI6MDb738t2t_XHxdP3Ae-9vO97NM1rwGfAqHx_l8YzgkG0GJO-XVw_a46BdqKVTLDnDz20Ejp21Jzm7AdMKLAeOH3ZHBHJuZS8P26WN6NFfr3RpqDkUPS3Y2nz6F1B92n6jlJEm6CLDbYgN0dTfL3xEY1WhzJu0dquvNEB5aKde9W8cDpke3qoJ823xeeb88t2eXXx5fzTsjW9kKLlTMoBiGFDB4CF01wIR1ZYu1WnVwM3hloKwLmzIKWFlakHQxiBrmc9k_Sk-bjX3cxDNWBsLJMOajP5tZ62Kmmv_n6JflS36afiuBeiI1Xg3UFgSj9mm4ta-2xsCDraNGdF6kY5xnV5Ffr2H-hdmqdYx1OEUNoLTMVOEO9RZko5T9Y9mQGsdmlV1qh2aaldWmpxXSlv_hziifCYTQV82APufbDb_wqqr1eXBFfXuMNYVPbFnn1IKMXgo_1t3rj-oX_UqMSultpSUhtK63chBDDQXwWauG4</recordid><startdate>201807</startdate><enddate>201807</enddate><creator>Nakao, Tomoko</creator><creator>Yasumoto, Atsushi</creator><creator>Tokuoka, Suzumi</creator><creator>Kita, Yoshihiro</creator><creator>Kawahara, Takuya</creator><creator>Daimon, Masao</creator><creator>Yatomi, Yutaka</creator><general>JAPAN SOCIETY FOR OCCUPATIONAL HEALTH</general><general>John Wiley & Sons, Inc</general><general>Japan Society for Occupational Health</general><scope>24P</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>7T2</scope><scope>7TA</scope><scope>7TB</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>JG9</scope><scope>KR7</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1719-4297</orcidid></search><sort><creationdate>201807</creationdate><title>The impact of night-shift work on platelet function in healthy medical staff</title><author>Nakao, Tomoko ; 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Vascular endothelial dysfunction and platelet activation are among the leading causes of thrombus formation in patients with myocardial infarction or stroke. Endothelial function has been shown to be impaired immediately after night-shift work ; however, it is not known whether platelets are also activated. The aim of this study was to investigate the acute impact of night-shift work on platelet function. [Methods] : This observational study included 11 healthy medical staff members (seven women, median age 32 years) . We examined each subject's platelet aggregation rates and the serum concentrations of eicosanoid mediators after night-shift work and on dayshift work without preceding night-shift work (baseline) . [Results] : Platelet aggregation did not differ from baseline levels after night-shift work. However, serum cyclooxygenase (COX)-metabolized eicosanoid mediators, particularly thromboxane (Tx) B2 (a stable metabolite of TxA2 and the most important marker of platelet activation) , were significantly higher after the night-shift than at baseline (median 65.3 vs 180.4 ng/ml) . [Conclusions] : Although platelet aggregation did not increase, there was an increase in serum COX-metabolized eicosanoid mediators such as TxB2 in healthy medical staff after nightshift work. This platelet hypersensitivity may be one of the mechanisms underlying the significant association between night-shift work and adverse cardiovascular outcomes.</abstract><cop>Japan</cop><pub>JAPAN SOCIETY FOR OCCUPATIONAL HEALTH</pub><pmid>29669967</pmid><doi>10.1539/joh.2018-0027-FS</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-1719-4297</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Activation Adult Agglomeration Blood Platelets - physiology Cardiovascular diseases Cerebral infarction Cyclooxygenase Eicosanoids Female Field Study Health risks Healthy Volunteers Heart diseases Humans Hypersensitivity Male Medical personnel Medical Staff, Hospital Myocardial infarction Night Occupational health Platelet Activation Platelet Aggregation Platelets Prostaglandin endoperoxide synthase Shift work Shift Work Schedule Sleep deprivation Thrombosis Thromboxane B2 Thromboxane B2 - blood Working conditions |
title | The impact of night-shift work on platelet function in healthy medical staff |
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