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1 Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, United States; Department of Physiology II, Nara Medical University School of Medicine, Kashihara, Nara, Japan
2 Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, United States
3 Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, United States; Massachusetts, United States
4 Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, United States; Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, Korea, Republic of
* To whom correspondence should be addressed. E-mail: hajjar{at}cvrc.mgh.harvard.edu.
The aim of this study was to examine how global cardiac gene transfer of sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) can influence left ventricular (LV) mechanical and energetic function, especially in terms of O2 cost of LV contractility, in normal rats. Normal rats were randomized to receive an adenovirus carrying either SERCA2a (SERCA) or 
-galactosidase (gal), or saline (Saline) by a catheter-based technique. LV mechanical and energetic function was measured in cross-circulated heart preparations 2-3 days after the infection. "SERCA" group showed the upward-shifted end-systolic pressure-volume relation, higher end-systolic pressure at 0.1 ml of intraballoon water volume and higher equivalent maximal elastance, i.e., the enhanced LV contractility, compared with "Normal", "gal" and "Saline" groups. Moreover, faster LV relaxation rate was found in "SERCA" group. There was no significant difference in relation between myocardial O2 consumption and systolic pressure-volume area among all groups. Finally, O2 cost of LV contractility in "SERCA" group was decreased to subnormal levels, but in "gal" and "Saline" groups it remained unchanged. This lowered O2 cost of LV contractility in "SERCA" hearts indicates energy saving in Ca2+ handling during E-C coupling. Thus, the overexpression of SERCA2a was capable of transforming the normal energy utilization into a more efficient state in Ca2+ handling, and super-inducing the supranormal contraction/relaxation due to the enhanced Ca2+ handling.
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