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Am J Physiol Heart Circ Physiol (August 8, 2002). doi:10.1152/ajpheart.01062.2001
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Articles in PresS, published online ahead of print August 8, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01062.2001
Submitted on December 4, 2001
Accepted on July 26, 2002

Overexpression of Na+/Ca2+ exchanger gene attenuatespostinfarction myocardial dysfunction

Jiang-Yong Min1, Matthew F Sullivan1, Xinhua Yan1, Xin Feng1, Victor Chu1, Ju-Feng Wang1, Ivo Amende1, James P Morgan1*, Kenneth D Philipson2, and Thomas G Hampton1

1 Cardiology Division, Beth Israel Deaconess Medical Center, Boston, MA, USA
2 Departments of Physiology and Medicine, University of California School of Medicine, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: jmorgan{at}caregroup.harvard.edu.

We monitored myocardial function in postinfarcted wild-type (WT) and transgenic mouse hearts with overexpression of the cardiac Na+/Ca2+ exchanger (TG). Five weeks after infarction, cardiac function was better maintained in TG than WT mice (LVSP, 41 ± 2 in WT vs. 58 ± 3 mmHg in TG, P < 0.05; +dP/dtmax, 3750 ± 346 in WT vs. 5075 ± 334 mmHg/s in TG, P < 0.05). The isometric contractile response to ß-adrenergic stimulation was greater in papillary muscles from TG than WT mice (13.2 ± 0.9 in WT vs. 16.3 ± 1.0 mN/mm2 in TG at 10-4 M of isoproterenol). The sarcoplasmic reticulum (SR) Ca2+ content investigated by rapid cooling contractures in papillary muscles was greater in TG than WT mouse hearts. We conclude that myocardial function is better preserved in TG mice 5 weeks after infarction, which results from enhanced SR Ca2+ content via overexpression of the Na+/Ca2+ exchanger.




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