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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/123456789/8901
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dc.contributor.authorYao, D. C.en
dc.contributor.authorVlessidis, A. G.en
dc.contributor.authorEvmiridis, N. P.en
dc.contributor.authorSiminelakis, S.en
dc.contributor.authorDimitra, M.en
dc.date.accessioned2015-11-24T16:45:15Z-
dc.date.available2015-11-24T16:45:15Z-
dc.identifier.issn0003-2670-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/8901-
dc.rightsDefault Licence-
dc.subjectacute myocardial infarctionen
dc.subjectnitric oxideen
dc.subjecttotal antioxidant activityen
dc.subjectnitric oxide synthaseen
dc.subjectsuperoxide dismutaseen
dc.subjectchemiluminescenceen
dc.subjectflow injectionen
dc.subjecttotal antioxidant capacityen
dc.subjectsuperoxide-dismutase activityen
dc.subjectin-vivoen
dc.subjectmn-superoxideen
dc.subjectsynthaseen
dc.subjectserumen
dc.subjectaciden
dc.titlePossible mechanism for nitric oxide and oxidative stress induced pathophysiological variance in acute myocardial infarction development - A study by a flow injection-chemiluminescence methoden
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primaryDoi 10.1016/S0003-2670(02)01536-2-
heal.identifier.secondary<Go to ISI>://000189102800017-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0003267002015362/1-s2.0-S0003267002015362-main.pdf?_tid=c22c97f4-356a-11e3-b756-00000aacb35e&acdnat=1381822019_9335cc54a038688bb109948ccaab9d2d-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.publicationDate2004-
heal.abstractThe acute myocardial infarction (AMI) model was established through rabbits, and this kind of model was used to investigate the possible mechanism for the AMI mediated damage, induced by NO release and oxidative stress. The biomedical parameters nitric oxide (NO), total antioxidant capacity (TAC) variation in vivo and the enzymatic activity of nitric oxide synthase (NOS) and superoxide dismutase (SOD), which are considered as the major markers for pathophysiological variation, were detected. The results obtained gave evidence that AMI can lead to the NO excess release and compensation by excess cellular respiration, and both of them can result in oxidative stress and further generation of reactive oxygen species (ROS). The latter can bring a series of damages to the organism, including decrease of the TAC value, and NOS and SOD activity. (C) 2002 Elsevier Science B.V. All rights reserved.en
heal.publisherElsevier Massonen
heal.journalNameAnalytica Chimica Actaen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
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