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  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά). ΧΗΜ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/8875
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dc.contributor.authorGoudevenos, J.en
dc.contributor.authorTselepis, A. D.en
dc.contributor.authorVini, M. P.en
dc.contributor.authorMichalis, L.en
dc.contributor.authorTsoukatos, D. C.en
dc.contributor.authorElisaf, M.en
dc.contributor.authorNinio, E.en
dc.contributor.authorSideris, D. A.en
dc.date.accessioned2015-11-24T16:45:03Z-
dc.date.available2015-11-24T16:45:03Z-
dc.identifier.issn0014-2972-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/8875-
dc.rightsDefault Licence-
dc.subjectanginaen
dc.subjectangioplastyen
dc.subjectplatelet-activating factoren
dc.subjectpaf-acetylhydrolaseen
dc.subjectplateletsen
dc.subjectactivating-factor acetylhydrolaseen
dc.subjectcoronary-artery diseaseen
dc.subjectmyocardial-ischemiaen
dc.subjecthuman-plasmaen
dc.subjectheart-diseaseen
dc.subjectneutrophilen
dc.subjectreperfusionen
dc.subjectadhesionen
dc.subjectinjuryen
dc.subjectpathogenesisen
dc.titlePlatelet-associated and secreted PAF-acetylhydrolase activity in patients with stable angina: sequential changes of the enzyme activity after angioplastyen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondary<Go to ISI>://000166660200005-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1046/j.1365-2362.2001.00782.x/asset/j.1365-2362.2001.00782.x.pdf?v=1&t=h0f942dg&s=463a0f7601231b752345a78922e8e135b86424ca-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.publicationDate2001-
heal.abstractBackground Platelet-activating factor (PAF), the lipid mediator of inflammation and potent platelet agonist, can be hydrolysed and inactivated by PAF-acetylhydrolase (PAF-AH). We investigated the PAF-AH activity in relation to PAF formation in platelets from patients with stable angina undergoing elective percutaneous transluminal coronary angioplasty (PTCA). Design Twenty-seven patients with stable angina, undergoing PTCA, and 30 age- and sex-matched controls were studied. The platelet-associated and secreted PAF-AH activity was measured, before PTCA, as well as at 4 h, 48 h and 6 months afterwards. PAF formation by thrombin-stimulated platelets and the platelet aggregation responses to PAF and ADP were also determined. Results The PAF-AH activity secreted by thrombin-stimulated platelets before PTCA (in pmol/10(9) cells/h) was significantly higher compared to controls (892 +/- 222 vs. 624 +/- 144, P < 0.001). The enzyme activity was not altered at 4 h after PTCA, but was significantly increased at 48 h (1284 +/- 312, P < 0.005) to return to the levels observed in the control group 6 months afterwards. Detectable levels of PAF in thrombin-stimulated platelets were found only at 6 months after PTCA. Furthermore, the cell-associated enzyme activity in resting platelets before PTCA was significantly lower compared with controls. Unlike in controls, the platelet-associated enzyme activity in the patient group was not increased after stimulation with thrombin and it was associated by a platelet hyperaggregability to PAF. Both the intact cell-associated activity and the platelet hyper-reactivity to PAF were restored at 6 months after PTCA. Conclusions Alterations in the platelet PAF-AH activity, which affect the PAF formation in thrombin-stimulated platelets and are associated by an increased aggregatory response to PAF, are observed in patients with stable angina and are completely restored after PTCA.en
heal.journalNameEur J Clin Investen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
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