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Articles in PresS, published online ahead of print April 4, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00790.2001
Submitted on September 6, 2001
Accepted on December 31, 1969
1 Pathology, Duke University Medical Center, Durham, NC, USA
2 Laboratory of Signal Transduction, NIEHS, Research Triangle Park, NC, USA
* To whom correspondence should be addressed. E-mail: cross017{at}mc.duke.edu.
To compare ischemia/reperfusion injury in males vs. females under hypercontractile conditions, perfused hearts from 129J-mice pretreated with 3 mmol/L Ca2+ or 10-8 mol/L isoproterenol ± 10-6 mol/L L-NAME were subjected to 20 min ischemia and 40 min reperfusion while 31P NMR spectra were acquired. Basal contractility increased equivalently in female vs. male hearts with isoproterenol or Ca2+-treatment. Injury was equivalent in untreated male vs. female hearts, but was greater in isoproterenol or Ca2+-treated male than female hearts, as indicated by lower post-ischemic contractile function, ATP and PCr. eNOS expression was higher in female than male hearts, nNOS did not differ, iNOS was undetectable. Ischemic NO production was higher in female than male hearts and L-NAME increased injury in female isoproterenol-treated hearts. In summary, isoproterenol or high Ca2+ pretreatment increased ischemia/reperfusion injury in males more than females. eNOS expression and NO production were higher in female than male hearts and L-NAME blocked female protection. Females were therefore protected from the detrimental effects of adrenergic stimulation and Ca2+-loading, via a NOS-mediated mechanism.
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