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dc.contributor.author Korkmaz S
dc.contributor.author Barnucz E
dc.contributor.author Loganathan S
dc.contributor.author Li S
dc.contributor.author Radovits Tamás
dc.contributor.author Puskás László
dc.contributor.author Faragó Nóra
dc.contributor.author Gyuris Márió
dc.contributor.author Merkely Béla Péter
dc.date.accessioned 2014-11-14T09:09:56Z
dc.date.available 2014-11-14T09:09:56Z
dc.date.issued 2013
dc.identifier 84879366548
dc.identifier.citation pagination=1817-1826; journalVolume=77; journalIssueNumber=7; journalTitle=CIRCULATION JOURNAL;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/527
dc.identifier.uri doi:10.1253/circj.CJ-12-1162
dc.description.abstract Background: Reperfusion of ischemic myocardium may contribute to substantial cardiac tissue damage, but the addition of iron chelators, zinc or zinc complexes has been shown to prevent heart from reperfusion injury. We investigated the possible beneficial effects of an iron-chelating and zinc-complexing agent, Q50, in rat models of ischemia/reperfusion (I/R)-induced myocardial infarction and on global reversible myocardial I/R injury after heart transplantation. Methods and Results: Rats underwent 45-min myocardial ischemia by left anterior descending coronary artery ligation followed by 24h reperfusion. Vehicle or Q50 (10mg/kg, IV) were given 5min before reperfusion. In a heart transplantation model, donor rats received vehicle or Q50 (30mg/kg, IV) 1h before the onset of ischemia. In myocardial infarcted rats, increased left ventricular end-systolic and end-diastolic volumes were significantly decreased by Q50 post treatment as compared with the sham group. Moreover, in I/R rat hearts, the decreased dP/dtmax and load-independent contractility parameters were significantly increased after Q50. However, Q50 treatment did not reduce infarct size or have any effect on increased plasma cardiac troponin-T-levels. In the rat model of heart transplantation, 1h after reperfusion, decreased left ventricular systolic pressure, dP/dtmax, dP/dtmin and myocardial ATP content were significantly increased and myocardial protein expression of superoxide dismutase-1 was upregulated after Q50 treatment. Conclusions: In 2 experimental models of I/R, administration of Q50 improved myocardial function. Its mechanisms of action implicate in part the restoration of myocardial high-energy phosphates and upregulation of antioxidant enzymes.
dc.relation.ispartof urn:issn:1346-9843
dc.title Q50, an Iron-Chelating and Zinc-Complexing Agent, Improves Cardiac Function in Rat Models of Ischemia/Reperfusion-Induced Myocardial Injury.
dc.type Journal Article
dc.date.updated 2014-11-14T09:09:21Z
dc.language.rfc3066 en
dc.identifier.mtmt 2263860
dc.identifier.wos 000321405000026
dc.identifier.pubmed 23575364
dc.contributor.department SE/ÁOK/K/Kardiológiai Központ, Kardiológia Tanszék (névváltozás: 2012-től Kardiológiai Tanszék-Kardiológiai Központ)
dc.contributor.institution Semmelweis Egyetem


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