Activated neutrophils release mediators that may contribute to myocardial injury and dysfunction associated with ischemia and reperfusion.
Neutrophils accumulate in the ischemic myocardium and exacerbate postischemic cardiac dysfunction and injury. The formation of lipoxygenase metabolites of AA, derived either directly from the neutrophils or by interactions with other blood elements or cells, may promote neutrophil-mediated injury. Recognition of the roles played by neutrophils and AA metabolites in reperfusion injury may lead to the development of new therapies that can be used in conjunction with thrombolytic drugs to reduce the complications associated with restoring blood flow to the ischemic heart.
Mullane
K M
KM
Research Department, CIBA-GEIGY Corporation, Summit, New Jersey 07901.
Westlin
W
W
Kraemer
R
R
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D001792:Blood Platelets / Q000378:metabolism; D009202:Cardiomyopathies / Q000378:metabolism*; D003327:Coronary Disease / Q000503:physiopathology*; D004537:Eicosanoic Acids / Q000378:metabolism; D005609:Free Radicals; D006801:Humans; D008084:Lipoxygenase / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D010972:Platelet Activating Factor / Q000031:analogs & derivatives / Q000378:metabolism; D010974:Platelet Aggregation; D013189:SRS-A / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
D001095:Arachidonic Acids; D004537:Eicosanoic Acids; D005609:Free Radicals; C029271:O-deacetyl platelet activating factor; D010972:Platelet Activating Factor; D013189:SRS-A; D013481:Superoxides; D016718:Arachidonic Acid; D012701:Serotonin; D008084:Lipoxygenase; D010100:Oxygen