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Manganese kinetics demonstrated double contrast in acute but not in chronic infarction in a mouse model of myocardial occlusion reperfusion
Author(s) -
Delattre Bénédicte M. A.,
Braunersreuther Vincent,
Gardier Stéphany,
Hyacinthe JeanNoël,
Crowe Lindsey A.,
Mach François,
Vallée JeanPaul
Publication year - 2012
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1759
Subject(s) - infarction , coronary occlusion , myocardial infarction , washout , medicine , occlusion , cardiology , gadolinium , extracellular , ischemia , edema , pathology , chemistry , biochemistry , organic chemistry
Manganese (Mn 2+ ) is considered as a specific MRI contrast agent that enters viable cardiomyocytes through calcium pathways. Compared to extracellular gadolinium based contrast agents, it has the potential to assess cell viability. To date, only information from the washout phase after recirculation has been used for the detection and characterization of myocardial infarct. This study showed for the first time that in a mouse model of coronary occlusion‐reperfusion, Mn 2+ wash‐in kinetics are different at 24 h after surgery (acute infarction) than at eight days after surgery (chronic infarction). A fast but transient entry of Mn 2+ into the acute infarct area led to a double contrast between infarct and remote areas, whereas entry of Mn 2+ into the chronic infarct area remained reduced compared to remote regions during both wash‐in and washout phases. The main hypothesis is that extracellular space is largely enhanced in acute infarction due to cell membrane rupture and interstitial edema, whereas scar tissue is densely composed of collagen fibers that reduce the distribution volume of free Mn 2+ ions. In addition to its ability to accurately depict the infarct area during the redistribution phase, Mn 2+ is also able to discriminate acute versus chronic injury by the observation of double‐contrast kinetics in a mouse model of ischemia reperfusion. Copyright © 2011 John Wiley & Sons, Ltd.