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

• Published in: The Journal of nutritional biochemistry Vol. 12; no. 6; pp. 365 - 376
• Main Authors: Leifert, Wayne R., Dorian, Camilla L., Jahangiri, Anisa, McMurchie, Edward J.
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 2001
• Subjects: Ca 2; Docosahexaenoic acid; Fish oil; n-3 fatty acid; Ventricular myocyte; Ventricular myocyte; Docosahexaenoic acid; n-3 fatty acid; Fish oil; Ca 2
• ISSN: 0955-2863; 1873-4847
• DOI: 10.1016/S0955-2863(01)00151-6

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 μM) 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.