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Leifert WR, Dorian CL, Jahangiri A, et al. Dietary fish oil prevents asynchronous contractility and alters Ca(2+) handling in adult rat cardiomyocytes. J Nutr Biochem. 2001;12(6):365-376doi: 10.1016/s0955-2863(01)00151-6.
Leifert, W. R., Dorian, C. L., Jahangiri, A., & McMurchie, E. J. (2001). Dietary fish oil prevents asynchronous contractility and alters Ca(2+) handling in adult rat cardiomyocytes. The Journal of nutritional biochemistry, 12(6), 365-376. https://doi.org/10.1016/s0955-2863(01)00151-6
Leifert, W R., et al. "Dietary fish oil prevents asynchronous contractility and alters Ca(2+) handling in adult rat cardiomyocytes." The Journal of nutritional biochemistry vol. 12,6 (2001): 365-376. doi: https://doi.org/10.1016/s0955-2863(01)00151-6
Leifert WR, Dorian CL, Jahangiri A, McMurchie EJ. Dietary fish oil prevents asynchronous contractility and alters Ca(2+) handling in adult rat cardiomyocytes. J Nutr Biochem. 2001 Jun;12(6):365-376. doi: 10.1016/s0955-2863(01)00151-6. PMID: 11516641.
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J Nutr Biochem. 2001 Jun;12(6):365-376. doi: 10.1016/s0955-2863(01)00151-6.

Dietary fish oil prevents asynchronous contractility and alters Ca(2+) handling in adult rat cardiomyocytes.

The Journal of nutritional biochemistry

W R. Leifert, C L. Dorian, A Jahangiri, E J. McMurchie

Affiliations

  1. CSIRO Health Sciences and Nutrition, 5000, Adelaide, SA, Australia

PMID: 11516641 DOI: 10.1016/s0955-2863(01)00151-6

Abstract

This study examined the effects of dietary incorporation of n-3 polyunsaturated fatty acids (PUFAs) into cardiac membrane phospholipids on Ca(2+) handling (using Fura-2) and arrhythmic contractility in electrically-stimulated, adult rat ventricular cardiomyocytes. Dietary lipid supplementation with fish oil (FO) for 3 weeks significantly increased the proportion of total n-3 polyunsaturated fatty acids (in particular, docosahexaenoic acid) in ventricular membrane phospholipids compared with a saturated fat (SF) supplemented diet (26.2 +/- 0.9% vs 6.9 +/- 0.9%, respectively, P < 0.001). Cardiomyocytes isolated from the FO group were significantly (P < 0.001) less susceptible to isoproterenol-induced arrhythmic contractile activity compared with the SF group over a range of isoproterenol concentrations. Isoproterenol (0.5 &mgr;M) stimulation increased end-diastolic and systolic [Ca(2+)](i) to a similar extent in both groups. The time constant of Ca(2+) transient decay was significantly increased in the FO group compared with the SF group (98.4 +/- 2.8 ms, n = 8 and 86.9 +/- 2.1 ms, n = 8, P < 0.01, respectively). The effect of dietary n-3 PUFA incorporation into membrane phospholipids was not associated with changes in sarcoplasmic reticulum Ca(2+) content (measured by rapid application of caffeine) or membrane fluidity. The increase in the time constant of decay of Ca(2+) transients following dietary supplementation with FO may indicate altered functioning of the sarcolemmal Na(+)-Ca(2+) exchanger by n-3 PUFA incorporation into membrane phospholipids.

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