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Vol. 292, Issue 3, 912-920, March 2000
Dichotomy of Action in Crystalloid- Versus Blood-Perfused
Hearts1
Division of Emergency Medicine, Thomas Jefferson University,
Philadelphia, Pennsylvania (X.-L.M., F.G., B.L.L., T.A.C.); and
Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center of
Crawford Long Hospital and Emory University, Atlanta, Georgia (J.A.-J.)
Peroxynitrite (ONOO
) is widely recognized as a
mediator of NO· toxicity, but recent studies have indicated
that this compound may also have physiologic activity and induces
vascular relaxation as well as inhibition of platelet aggregation and
neutrophil adhesion. The present experiment was designed to determine
whether ONOO may exert different effects on postischemic
myocardial injury in a crystalloid perfusion environment versus a blood
perfusion environment and, if it does, to clarify the mechanisms
causing any differences. In Krebs-Henseleit buffer-perfused rabbit
hearts, administration of ONOO at the onset of
reperfusion enhanced myocardial injury in a concentration-dependent fashion with a significant effective concentration of 30 µM. In contrast, in blood-perfused hearts, administration of
ONOO (1 to 30 µM) significantly attenuated
postmyocardial injury as evidenced by improved cardiac function
recovery, preserved endothelial function, decreased myocardial creatine
kinase loss, and reduced necrotic size. The minimal and maximal
protective concentrations were determined to be 1 and 3 µM,
respectively. When a high concentration of ONOO (i.e.,
100 µM) was administered, a detrimental effect was observed. Administration of ONOO decreased neutrophil accumulation
in the ischemic-reperfused myocardial tissue in a
concentration-dependent manner in blood-perfused hearts and inhibited
neutrophil adhesion to cultured endothelial cells exposed to
hypoxia/reoxygenation. Taken together, these results demonstrate that
ONOO may act as a "double-edged sword" in
postischemic myocardial injury. This compound is directly toxic to the
cardiac tissue at a relatively high concentration, but it can
indirectly protect myocardial cells from neutrophil-induced injury at a
much lower concentration.
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