ISSN:
1573-4919
Keywords:
atrial fibrillation
;
atrial myocytes
;
n-3 polyunsaturated fatty acids
;
membrane fluidity
;
docosahexaenoic acid
;
eicosapentaenoic acid
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
Notes:
Abstract A protective effect of the n-3 polyunsaturated fatty acids (PUFAs) in preventing ventricular fibrillation in experimental animals and cultured cardiomyocytes has been demonstrated in a number of studies. In this study, a possible role for the n-3 PUFAs in the treatment of atrial fibrillation (AF) was investigated at the cellular level using atrial myocytes isolated from young adult rats as the experimental model. Electrically-stimulated, synchronously-contracting myocytes were induced to contract asynchronously by the addition of 10 μM isoproterenol. Asynchronous contractile activity was reduced following acute addition of the n-3 PUFAs docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) at 10 μM, compared with no fatty acid addition (from 99.0 ±: 1.0% to 30.7 ± 5.2% (p 〈 0.05) for DHA and 23.8 ± 2.8% (p 〈 0.01) for EPA), while the saturated fatty acid, docosanoic acid (DA) and the methyl ester of DHA (DHA m.e.) did not exert a significant effect on asynchronous contractile activity. Asynchronous contractile activity was also reduced to 1.7 ± 1.7% in the presence of the membrane fluidising agent, benzyl alcohol (p 〈 0.001 vs no fatty acid addition). Cell membrane fluidity was determined by steady state fluorescence anisotropy using the fluorescent probe, TMAP-DPH. Addition of DHA, EPA or benzyl alcohol significantly increased sarcolemmal membrane fluidity (decreased anisotropy, rss) of atrial myocytes compared with no addition of fatty acid (control) (from rss = 0.203 ±0.004 to 0.159 ± 0.004 (p 〈 0.01) for DHA, 0.166 ± 0.001 (p 〈 0.01) for EPA and 0.186 ±0.003 (p 〈 0.05) for benzyl alcohol, while DA and DHA m.e. were without effect. It is concluded that the n-3 PUFAs exert anti-asynchronous effects in rat atrial myocytes by a mechanism which may involve changes in membrane fluidity.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1007025007403
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