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Department of Physiology and Kimmel Cancer Center, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107
Peroxynitrite
(ONOO
), an intermediate
formed from the equimolar interaction of nitric oxide (NO) and
superoxide, is thought to be an important mediator of tissue injury in
myocardial ischemia-reperfusion. However, physiologically
relevant (i.e., maximally achievable) concentrations of
ONOO significantly
decreased neutrophil-endothelium interactions in the rat mesentery. We
therefore examined the dose-response relationship of infusion of
different concentrations of
ONOO in a feline model of
myocardial ischemia-reperfusion and provide data on the
cellular mechanisms responsible for these observed effects. Cats
subjected to 90 min of ischemia followed by 270 min of
reperfusion were infused with different concentrations of
ONOO 10 min before
reperfusion and continuing throughout reperfusion. We observed that
infusion of 2 µM ONOO
provided significant cardioprotection, whereas either 0.2 or 20 µM
ONOO did not protect.
ONOO at 2 µM also
preserved coronary endothelial function, decreased P-selectin
expression, and attenuated polymorphonuclear leukocyte (PMN) adherence
to the vascular endothelium.
ONOO did not exert its
cardioprotective effects by acting as a direct NO donor in solution.
However, in vitro, ONOO can
react with glutathione to form
S-nitrosoglutathione, which can act as
an NO carrier and exert beneficial effects. Thus only maximally
achievable concentrations of
ONOO exert significant
cardioprotective effects, in part by decreasing surface expression of
P-selectin and decreasing PMN-endothelium interactions.
endothelium; neutrophil; adherence; P-selectin; S-nitrosothiols
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