Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20435
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dc.contributor.authorSamankatiwat, P.en
dc.contributor.authorSamartzis, I.en
dc.contributor.authorLertsithichai, P.en
dc.contributor.authorStefanou, D.en
dc.contributor.authorPunjabi, P. P.en
dc.contributor.authorTaylor, K. M.en
dc.contributor.authorGourlay, T.en
dc.date.accessioned2015-11-24T19:07:26Z-
dc.date.available2015-11-24T19:07:26Z-
dc.identifier.issn0267-6591-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20435-
dc.rightsDefault Licence-
dc.subjectAgeden
dc.subjectBiological Markers/blooden
dc.subjectCardiopulmonary Bypass/*adverse effects/methods/mortalityen
dc.subjectEquipment Designen
dc.subjectFemaleen
dc.subjectFiltrationen
dc.subjectHumansen
dc.subjectInflammation/prevention & controlen
dc.subjectLactoferrin/blooden
dc.subjectLymphocyte Depletion/instrumentation/*methodsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectMyocardial Reperfusion Injury/prevention & controlen
dc.subjectNeutrophil Activationen
dc.subjectTreatment Outcomeen
dc.subjectTroponin I/blooden
dc.titleLeucocyte depletion in cardiopulmonary bypass: a comparison of four strategiesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/12868787-
heal.identifier.secondaryhttp://prf.sagepub.com/content/18/2/95.full.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2003-
heal.abstractLeucocytes have been shown to play a fundamental role in the pathophysiology of inflammation. This prospective, randomized, controlled study was designed to identify the most advantageous leucocyte depletion technique in terms of reduction in systemic inflammatory response syndrome and myocardial ischaemia reperfusion injury associated with cardiopulmonary bypass (CPB). Forty consecutive patients undergoing elective coronary artery bypass graft (CABG) surgery were randomly allocated to one of four groups. The four groups consisted of a control group, a systemic leucocyte depletion (SLD) group, a cardioplegic leucocyte depletion (CLD) group and a total leucocyte depletion (TLD) group. There were 10 patients in each group. Lactoferrin (marker of neutrophil activation) and troponin-I (marker of myocardial ischaemia reperfusion injury) were measured at six time points: post induction, 5 min on CPB, 5 min before releasing the aortic crossclamp, 15 min after releasing the clamp and 1 and 24 hours after the discontinuation of CPB. Plasma lactoferrin levels increased rapidly in every group after the commencement of CPB, subsequently reached a peak after releasing the aortic crossclamp and gradually declined after the discontinuation of CPB. The lowest lactoferrin concentration was observed in the TLD (range 2.15-141.9 ng/mL) and CLD groups (7.469-114.6 ng/mL). Regarding myocardial injury, plasma cardiac troponin-I levels did not differ significantly between groups; but troponin-I concentrations rose dramatically after releasing the aortic crossclamp in all groups. Nevertheless, the CLD group had the lowest troponin-I level (1.37-5.55 ng/mL). In conclusion, it is believed that myocardial ischaemia is probably a major contributor to the inflammatory response. Although there is no clear statistical significance shown in this pilot study, the data tend to support the cardioplegic leucocyte depletion strategy as the optimal method for attenuating neutrophil activation and myocardial ischaemia reperfusion injury.en
heal.journalNamePerfusionen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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