AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 279: H2846-H2854, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H2846-H2854, December 2000

Enhanced gene expression of Na+/Ca2+ exchanger attenuates ischemic and hypoxic contractile dysfunction

Thomas G. Hampton1, Ju-Feng Wang1, Joseph DeAngelis1, Ivo Amende1, Kenneth D. Philipson2, and James P. Morgan1

1 Charles A. Dana Research Institute and Harvard-Thorndike Laboratories, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215; and 2 Departments of Physiology and Medicine, University of California School of Medicine, University of California, Los Angeles, California 90095

Enhanced gene expression of the Na+/Ca2+ exchanger in failing hearts may be a compensatory mechanism to promote influx and efflux of Ca2+, despite impairment of the sarcoplasmic reticulum (SR). To explore this, we monitored intracellular calcium (Cai2+) and cardiac function in mouse hearts engineered to overexpress the Na+/Ca2+ exchanger and subjected to ischemia and hypoxia, conditions known to impair SR Cai2+ transport and contractility. Although baseline Cai2+ and function were similar between transgenic and wild-type hearts, significant differences were observed during ischemia and hypoxia. During early ischemia, Cai2+ was preserved in transgenic hearts but significantly altered in wild-type hearts. Transgenic hearts maintained 40% of pressure-generating capacity during early ischemia, whereas wild-type hearts maintained only 25% (P < 0.01). During hypoxia, neither peak nor diastolic Cai2+ decreased in transgenic hearts. In contrast, both peak and diastolic Cai2+ decreased significantly in wild-type hearts. The decline of Cai2+ was abbreviated in hypoxic transgenic hearts but prolonged in wild-type hearts. Peak systolic pressure decreased by nearly 10% in hypoxic transgenic hearts and >25% in wild-type hearts (P < 0.001). These data demonstrate that enhanced gene expression of the Na+/Ca2+ exchanger preserves Cai2+ homeostasis during ischemia and hypoxia, thereby preserving cardiac function in the acutely failing heart.

ischemia; hypoxia; sodium; calcium; heart failure; excitation-contraction


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