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Am J Physiol Heart Circ Physiol 283: H2466-H2471, 2002. First published August 8, 2002; doi:10.1152/ajpheart.01062.2001
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Vol. 283, Issue 6, H2466-H2471, December 2002

Overexpression of Na+/Ca2+ exchanger gene attenuates postinfarction 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 Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02115; and 2 Departments of Physiology and Medicine, University of California School of Medicine, Los Angeles, California 90095

We monitored myocardial function in postinfarcted wild-type (WT) and transgenic (TG) mouse hearts with overexpression of the cardiac Na+/Ca2+ exchanger. Five weeks after infarction, cardiac function was better maintained in TG than WT mice [left ventricular (LV) systolic pressure: WT, 41 ± 2; TG, 58 ± 3 mmHg; P < 0.05; maximum rising rate of LV pressure (+dP/dtmax): WT, 3,750 ± 346; TG, 5,075 ± 334 mmHg/s; P < 0.05]. The isometric contractile response to beta -adrenergic stimulation was greater in papillary muscles from TG than WT mice (WT, 13.2 ± 0.9; TG, 16.3 ± 1.0 mN/mm2 at 10-4 M 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 wk after infarction, which results from enhanced SR Ca2+ content via overexpression of the Na+/Ca2+ exchanger.

cardiac function; transgenic mice


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