1H NMR-based metabolomic identification of at-risk areas after myocardial infarction in swine

被引:30
作者
Barba, Ignasi [1 ]
Jaimez-Auguets, Ester [1 ]
Rodriguez-Sinovas, Antonio [1 ]
Garcia-Dorado, David [1 ]
机构
[1] Hosp Univ Vall Hebron, Lab Cardiol Expt, Serv Cardiol, Barcelona 08035, Spain
关键词
ischemia-reperfusion; HR-MAS; lipids; necrosis; at-risk areas;
D O I
10.1007/s10334-007-0097-8
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 [临床医学]; 100207 [影像医学与核医学]; 1009 [特种医学];
摘要
Object H-1 NMR-based metabolic profiling has been used to investigate areas of the heart after an acute myocardial infarction. Methods Tissue was obtained from control, at-risk (areas that survive within the infarct zone) and necrotic myocardium after 48 min of left anterior descending coronary artery occlusion and 2 h of reperfusion in a swine model. HR-MAS (high resolution magic angle spectroscopy) spectra from intact tissue and tissue extract spectra were obtained for each region and statistical models were built for each type of spectra allowing differentiation between control, at-risk and necrotic heart. Results At-risk and, especially, necrotic areas have a reduced concentration of NMR visible metabolites as compared to control tissue, total creatine (phosphorilated and unphosphorilated) being the single most important metabolite in the different discriminant models. Creatine concentration decreased from 18.28 +/- 0.84 mu mols/g fresh weight in controls to 12.58 +/- 2.89 (P < 0.05) and 9.96 +/- 2.21 (P < 0.01) in at-risk and necrotic areas, respectively. Taurine and myo-inositol were also involved in the discriminant models. HR-MAS spectra also showed an increase in lipid signals at 0.9 and 1.28 ppm as markers of necrotic tissue. These results support the view that the analysis of in vivo H-1 MRS may have value in differentiating normal, at-risk and infarcted myocardium.
引用
收藏
页码:265 / 271
页数:7
相关论文
共 16 条
[1]
Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging - Histopathological and displacement encoding with stimulated echoes (DENSE) functional validations [J].
Aletras, AH ;
Tilak, GS ;
Natanzon, A ;
Hsu, LY ;
Gonzalez, FM ;
Hoyt, RF ;
Arai, AE .
CIRCULATION, 2006, 113 (15) :1865-1870
[2]
Cardiac outflow of amino acids and purines during myocardial ischemia and reperfusion [J].
Bäckström, T ;
Goiny, M ;
Lockowandt, U ;
Liska, J ;
Franco-Cereceda, A .
JOURNAL OF APPLIED PHYSIOLOGY, 2003, 94 (03) :1122-1128
[3]
Barba I, 1999, CANCER RES, V59, P1861
[4]
Noninvasive localized MR quantification of creatine kinase metabolites in normal and infarcted canine myocardium [J].
Bottomley, PA ;
Weiss, RG .
RADIOLOGY, 2001, 219 (02) :411-418
[5]
ANALYSIS OF MYOCARDIAL EDEMA BY MAGNETIC-RESONANCE-IMAGING EARLY AFTER CORONARY-ARTERY OCCLUSION WITH OR WITHOUT REPERFUSION [J].
GARCIADORADO, D ;
OLIVERAS, J ;
GILI, J ;
SANZ, E ;
PEREZVILLA, F ;
BARRABES, J ;
CARRERAS, MJ ;
SOLARES, J ;
SOLERSOLER, J .
CARDIOVASCULAR RESEARCH, 1993, 27 (08) :1462-1469
[6]
Prevention of ischemic rigor contracture during coronary occlusion by inhibition of Na+-H+ exchange [J].
GarciaDorado, D ;
Gonzalez, MA ;
Barrabes, JA ;
RuizMeana, M ;
Solares, J ;
Lidon, RM ;
Blanco, J ;
Puigfel, Y ;
Piper, HM ;
SolerSoler, J .
CARDIOVASCULAR RESEARCH, 1997, 35 (01) :80-89
[7]
Metabolic profiles of dystrophin and utrophin expression in mouse models of Duchenne muscular dystrophy [J].
Griffin, JL ;
Sang, E ;
Evens, T ;
Davies, K ;
Clarke, K .
FEBS LETTERS, 2002, 530 (1-3) :109-116
[8]
GRIFFIN JL, 2003, CURR OPP CHEM BIOL, V7, P1
[9]
Horn Michael, 2006, Methods Mol Med, V124, P225
[10]
A functional analysis of mouse models of cardiac disease through metabolic profiling [J].
Jones, GLAH ;
Sang, E ;
Goddard, C ;
Mortishire-Smith, RJ ;
Sweatman, BC ;
Haselden, JN ;
Davies, K ;
Grace, AA ;
Clarke, K ;
Griffin, JL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (09) :7530-7539