Key result
Neutrophils and lipoxygenase metabolites accumulate during ischemia, exacerbating myocardial reperfusion injury and cardiac dysfunction.
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Demonstrates how neutrophil accumulation and arachidonic acid metabolites exacerbate myocardial reperfusion injury, indicating new therapeutic targets alongside thrombolytic therapy.
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.
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Mullane et al. (1988) conducted a review in Myocardial ischemia and reperfusion injury. Neutrophil accumulation and lipoxygenase metabolites of arachidonic acid was evaluated on Postischemic cardiac dysfunction and myocardial reperfusion injury. Neutrophils and lipoxygenase metabolites of arachidonic acid accumulate in ischemic myocardium and exacerbate postischemic cardiac dysfunction and reperfusion injury.
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