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pubmed-article:20559137pubmed:issue4lld:pubmed
pubmed-article:20559137pubmed:dateCreated2010-7-1lld:pubmed
pubmed-article:20559137pubmed:abstractTextBlood flow pulsatility can be quantified using the concept of hemodynamic energy. Because ischemia-reperfusion injury is known to affect microcirculation as well as vascular tone detrimentally, we hypothesized that vascular tone changes after ischemia-reperfusion injury would influence pulsatility of the blood vessels. We investigated the changes in pulsatility after ischemia-reperfusion injury using hemodynamic energy parameters-energy equivalent pressure (EEP) and surplus hemodynamic energy (SHE). Twenty-one New Zealand white male rabbits were divided into three groups. Ischemia group (I group, n = 7) underwent 3 hours of ischemia by clamping the abdominal aorta. Reperfusion group (I/R group, n = 7) underwent 2 hours of ischemia followed by 1 hour of reperfusion. Control group (C group, n = 7) underwent a sham procedure. Observed parameters were mean arterial pressure (MAP), mean blood flow (MBF), pulse pressure (PP), EEP, and SHE, measured at baseline, during ischemia (60 minutes after clamping), and reperfusion 5, 15, 30, and 60 minutes after clamp release. In I group, all parameters, except MBF, were higher during ischemia than at baseline. In I/R group, all except MBF were higher during ischemia. After reperfusion, MBF increased and the other parameters decreased. Interestingly, PP and EEP showed only minor changes during reperfusion (p = NS), whereas SHE decreased abruptly immediately after reperfusion and then gradually recovered to its baseline level. Surplus hemodynamic energy showed more significant changes than PP or EEP during reperfusion period (p < 0.05). In C group, no changes were noted throughout the observation period. Ischemia-reperfusion injury reduces vascular pulsatility. In this study, SHE was found to be a more sensitive hemodynamic energy parameter during ischemia-reperfusion injury than PP or EEP.lld:pubmed
pubmed-article:20559137pubmed:languageenglld:pubmed
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pubmed-article:20559137pubmed:issn1538-943Xlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:LeeSung HoSHlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:SunKyungKlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:SonHo SungHSlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:LeeJung JooJJlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:ChoiJaesoonJlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:SonKuk HuiKHlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:AhnChi BumCBlld:pubmed
pubmed-article:20559137pubmed:authorpubmed-author:JangHwan...lld:pubmed
pubmed-article:20559137pubmed:issnTypeElectroniclld:pubmed
pubmed-article:20559137pubmed:volume56lld:pubmed
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pubmed-article:20559137pubmed:authorsCompleteYlld:pubmed
pubmed-article:20559137pubmed:pagination296-300lld:pubmed
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pubmed-article:20559137pubmed:articleTitleHemodynamic energy changes after ischemia-reperfusion injury in an aortic cross-clamped rabbit model.lld:pubmed
pubmed-article:20559137pubmed:affiliationKorea Artificial Organ Center, Korea University Medical College, Seoul, South Korea.lld:pubmed
pubmed-article:20559137pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20559137pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed