Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/24575
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dc.contributor.authorSağdilek, Engin-
dc.contributor.authorKorkmaz, Ahmet-
dc.contributor.authorÖter, Şükrü-
dc.contributor.authorAvcu, Ferit-
dc.contributor.authorTopal, Turgut-
dc.contributor.authorÖzler, Mehmet-
dc.contributor.authorUysal, Bülent-
dc.contributor.authorNevruz, Oral-
dc.contributor.authorBeyan, Cengiz-
dc.date.accessioned2022-02-22T07:14:11Z-
dc.date.available2022-02-22T07:14:11Z-
dc.date.issued2011-04-
dc.identifier.citationSağdilek, E. vd. (2011). "The similarity between aspirin treatment and the lack of response to epinephrine and the frequency of aspirin resistance in healthy males". Clinical and Applied Thrombosis-Hemostasis, 17(2), 202-207.en_US
dc.identifier.issn1076-0296-
dc.identifier.urihttps://doi.org/10.1177/1076029609356425-
dc.identifier.urihttps://pubmed.ncbi.nlm.nih.gov/20460337/-
dc.identifier.urihttp://hdl.handle.net/11452/24575-
dc.descriptionBu çalışma, 05-07 Mayıs 2006 tarihleri arasında İzmir[Türkiye]’da düzenlenen 6. National Congress of Thrombosis, Haemostasis and Angiology’da bildiri olarak sunulmuştur.tr_TR
dc.description.abstractObjectives: The lack of response of platelets against epinephrine has been discovered with a frequency of 14% to 40% in previous studies. There are studies that have demonstrated the effect of aspirin on platelets may resemble the lack of response to epinephrine. In this study, the extent of the effects of aspirin treatment on aggregation and secretion in healthy males with a lack of response to epinephrine and the frequency of aspirin resistance were investigated. Methods: Blood samples were collected at the beginning and at the end of a 10-day aspirin usage in 52 healthy males. Epinephrine, adenosine diphosphate (ADP), collagen, arachidonic acid (AA) and thrombin aggregations, and adenosine triphosphate (ATP) secretion were studied. Participants were assigned to nonresponder (< 20%), semiresponder (20%-60%), and responder (> 60%) groups, depending on their maximum aggregation responses to epinephrine. Participants who displayed an aggregation to AA at the end of the aspirin treatment were accepted to be aspirin resistant. Results: Of the 52 participants, 4 were found to be nonresponders and 3 of 52 of the participants were found to be semiresponders. Although the lack of response to epinephrine and aspirin treatment displayed similarities in aggregations using epinephrine, ADP, collagen, and thrombin, they differed in aggregations using AA and for ATP secretion. The ratio of aspirin resistance was determined to be 4:52. Conclusions: The observation of AA aggregation in the participants with a lack of response to epinephrine demonstrates that epinephrine nonresponse cannot substitute aspirin treatment. The fact that aspirin resistance is observed in healthy males supports the view that aspirin resistance exists even before the first usage.en_US
dc.language.isoenen_US
dc.publisherSage Publicationsen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAtıf Gayri Ticari Türetilemez 4.0 Uluslararasıtr_TR
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectHematologyen_US
dc.subjectCardiovascular system & cardiologyen_US
dc.subjectPlateletsen_US
dc.subjectOptical aggregometeren_US
dc.subjectEpinephrineen_US
dc.subjectAspirin resistanceen_US
dc.subjectPlatelet-functionen_US
dc.subjectIn-vitroen_US
dc.subjectResponsivenessen_US
dc.subjectPrevalenceen_US
dc.subjectDiseaseen_US
dc.subjectDrugsen_US
dc.subject.meshAdrenergic alpha-agonistsen_US
dc.subject.meshAdulten_US
dc.subject.meshAspirinen_US
dc.subject.meshDrug resistanceen_US
dc.subject.meshEpinephrineen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshPlatelet aggregationen_US
dc.subject.meshPlatelet aggregation inhibitorsen_US
dc.subject.meshTime factorsen_US
dc.titleThe similarity between aspirin treatment and the lack of response to epinephrine and the frequency of aspirin resistance in healthy malesen_US
dc.typeArticleen_US
dc.typeProceedings Paperen_US
dc.identifier.wos000288463500012tr_TR
dc.identifier.scopus2-s2.0-79952810810tr_TR
dc.relation.publicationcategoryKonferans Öğesi - Uluslararasıtr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.tr_TR
dc.identifier.startpage202tr_TR
dc.identifier.endpage207tr_TR
dc.identifier.volume17tr_TR
dc.identifier.issue2tr_TR
dc.relation.journalClinical and Applied Thrombosis-Hemostasisen_US
dc.contributor.buuauthorÖzlük, Kasım-
dc.relation.collaborationYurt içitr_TR
dc.identifier.pubmed20460337tr_TR
dc.subject.wosHematologyen_US
dc.subject.wosPeripheral vascular diseaseen_US
dc.indexed.wosSCIEen_US
dc.indexed.wosCPCISen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubmeden_US
dc.wos.quartileQ4en_US
dc.contributor.scopusid6602676331tr_TR
dc.subject.scopusAdrenergic Agents; Epinephrine; Blood Plateletsen_US
dc.subject.emtreeAcetylsalicylic aciden_US
dc.subject.emtreeAcetylsalicylic acid calciumen_US
dc.subject.emtreeAdenosine diphosphateen_US
dc.subject.emtreeAdenosine triphosphateen_US
dc.subject.emtreeAdrenalinen_US
dc.subject.emtreeArachidonic aciden_US
dc.subject.emtreeCollagenen_US
dc.subject.emtreeThrombinen_US
dc.subject.emtreeAdulten_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeBlood samplingen_US
dc.subject.emtreeControlled studyen_US
dc.subject.emtreeDrug effecten_US
dc.subject.emtreeDrug resistanceen_US
dc.subject.emtreeHumanen_US
dc.subject.emtreeHuman experimenten_US
dc.subject.emtreeLoading drug doseen_US
dc.subject.emtreeMaleen_US
dc.subject.emtreeNormal humanen_US
dc.subject.emtreePriority journalen_US
dc.subject.emtreeThrombocyte aggregationen_US
dc.subject.emtreeThrombocyte release reactionen_US
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