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Articles in PresS, published online ahead of print November 1, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00741.2001
Submitted on August 17, 2001
Accepted on October 30, 2001
1 Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, USA
2 Department of Pediatrics, University of Virginia, Charlottesville, VA, USA
3 Department of Radiology, University of Virginia, Charlottesville, VA, USA
4 Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, USA; Department of Radiology, University of Virginia, Charlottesville, VA, USA
* To whom correspondence should be addressed. E-mail: gpm2y{at}virginia.edu.
Background: Previous studies have shown that high-level (300-fold normal) cardiac overexpression of A1-adenosine receptors (A1-ARs) in transgenic (TG) mice protects isolated hearts against ischemia/reperfusion injury. However, this high level of overexpression is associated with bradycardia and increased incidence of arrhythmia during ischemia in intact mice, which interfered with studies to determine if this line of TG mice might also be protected against myocardial infarction (MI) in vivo. For these studies, we therefore selected a line of TG mice that overexpresses the A1-AR at more moderate levels (30-fold normal) which affords cardioprotection in isolated heart, while minimizing bradycardia and arrhythmia during ischemia in intact mice. Methods and Results: Wild-type (WT, n =10) and moderate-level A1-AR TG mice (n =10) underwent 45 min of LAD occlusion followed by 24 hr reperfusion. Infarct size and region at risk were determined by TTC and phthalo blue staining, respectively. Infarct size (% region at risk) in WT mice was 52±3%, while overexpression of A1-ARs in the TG mice markedly reduced infarct size to 31±3% (P<0.05). Furthermore, contractile function (LV ejection fraction) as determined by cardiac MRI 24 hr post-MI was better preserved in TG vs. WT mice. Conclusions: Cardiac overexpression of A1-ARs reduces infarct size by 40% and preserves cardiac function in intact mice following MI.
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