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BACKGROUND: Ischemia-reperfusion injury (IRI) is damage to ischemic myocardium after blood flow is restored. This is most pronounced in cardiac transplantation when there is prolonged global cardiac ischemia followed by reperfusion with oxygen rich blood. The generation of reactive oxygen species in subsequent reperfusion results in lipid peroxidation. However, there has been no investigation to identify the specific phospholipid oxidation products generated during cardiac ischemia-reperfusion and their correlation with cardiac function. Utilizing a swine model of global ischemia, our goal was to determine the particular species of myocardial derived oxidized phosphatidylcholines (OxPC) and their correlation to myocardial damage and inflammation as potential mediators of IRI. METHODS: A group of domestic pigs were subjected to a hypoxemic cardiac arrest and a 15-minute warm ischemic standoff period. Hearts were subsequently perfused ex vivo for 90 minutes and then orthotopically transplanted into recipient animals then pressure/volume loops were observed for posttransplant function. Myocardial biopsies were taken from hearts under normoxic conditions Lipids from myocardial tissue were extracted by Folch extraction method in the presence of internal standards. Extracts were separated using a normal phase liquid chromatography and quantified by an electrospray ionization tandem mass spectrometer. Formalin fixed, paraffin embedded sections of anterior left ventricle were stained with hematoxylin and eosin, then assessed for evidence of IRI and assigned a semiqualitative score of on a score of 0-3 by a blinded clinical …