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Articles in PresS, published online ahead of print October 3, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00567.2002
Submitted on July 8, 2002
Accepted on September 30, 2002
1 Department of Pathology, Duke University Medical Center, Durham, NC, USA
2 National Institute of Environmental Health Sciences, Triangle Park, NC, USA
3 Department of Pharmacology and Cell Biophysics, University of Cincinnati, College of Medicine, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: cross017{at}mc.duke.edu.
Recent studies suggest a role for phospholamban phosphorylation during ischemia and reperfusion. The role of phospholamban in ischemia was studied by subjecting hearts from male and female wild-type (MWT/FWT) and phospholamban-knockout (MKO/FKO) mice to 20 min ischemia/40 min reperfusion while 31P-NMR spectra were acquired. ATP and pH fell lower during ischemia, and post-ischemic contractility was less, in MKO and FKO vs WT-hearts. After shorter ischemia, 15 min, recoveries of contraction, ATP and pH were greater in FKO than MKO-hearts. To examine the role of nitric oxide synthases (NOS) in the protection in FKO vs. MKO-hearts, we utilized 1 µM L-NAME, a NOS-inhibitor, or 100 µM SNAP, an NO-donor. Recoveries of function, ATP and pH were less in L-NAME-treated FKO than untreated FKO-hearts and greater in SNAP-treated MKO than untreated MKO-hearts. In conclusion, phospholamban ablation increased ischemic injury in both males and females, however, female hearts were less susceptible than males. Protection in females was decreased by a NOS-inhibitor and mimicked in males by an NO-donor, implying that protection was NOS-mediated.
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