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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00855.2001
Submitted on October 2, 2001
Accepted on January 22, 2002
1 Molecular and Cellular Physiology, Louisiana State Health Sciences Center, Shreveport, LA, USA
Two strains of eNOS deficient (-/-) mice have been developed which respond differently to myocardial ischemia-reperfusion (MI-R). We evaluated both strains of eNOS-/- mice in an in vivo model of MI-R. Harvard (HAR) eNOS-/- mice (n = 12) experienced a 84% increase in myocardial necrosis compared to wild-type controls (p<0.05). University of North Carolina (UNC) eNOS-/- (n = 10) exhibited a 52% reduction in myocardial injury vs. wild-type controls (p<0.05). PCR analysis of myocardial iNOS mRNA levels revealed a significant (p<0.05) increase in the UNC eNOS-/- mice compared to wild-type and there was no significant difference between the HAR eNOS-/- and wild-type. UNC eNOS-/- mice treated with an iNOS inhibitor (1400W) exacerbated the extent of myocardial necrosis. When treated with 1400W, HAR eNOS-/- did not exhibit a significant increase in myocardial necrosis. These data demonstrate that two distinct strains of eNOS-/- mice display opposite responses to MI-R. Although the protection seen in the UNC eNOS-/- mouse may result from compensatory increases in iNOS, other genes may be involved.
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