Abstract
BACKGROUND: Fish oil reduces the incidence of sudden cardiac death
in postmyocardial infarction patients. Triggered activity is the
principal mechanism of arrhythmogenesis under these conditions. OBJECTIVE:
The purpose of this study was to test whether dietary fish oil in
pigs inhibits Ca2+ overload-induced triggered activity. METHODS:
Pigs were fed a diet of fish oil or sunflower oil for 8 weeks. Ventricular
myocytes (omega3: fish oil, n = 11; control: sunflower oil, n = 8)
were isolated by enzymatic dissociation and used for patch clamp
studies and intracellular Ca2+ recordings. Triggered activity was
induced by rapid pacing in the presence of norepinephrine. RESULTS:
Dietary fish oil reduced the incidence of triggered action potentials
and delayed afterdepolarizations compared to control (9.1\% in omega3
and 84.6\% in control, P <.05), concomitant with a reduction in spontaneous
Ca2+ release. Dietary fish oil prevented Ca2+ overload and reduced
action potential prolongation in response to norepinephrine (DeltaAPD(90):
23.2 +/- 8.5 ms in omega3 and 107.4 +/- 15.9 in control, P <.05).
omega3 myocytes displayed decreased sarcoplasmic reticulum Ca2+ content,
reduced L-type Ca2+ current (I(Ca,L)), and less recruitment of the
Na+/Ca2+ exchange current (I(NCX)) in response to norepinephrine
compared to control. In the absence of norepinephrine, the slow component
of the delayed rectifier current (I(Ks)) was larger in omega3 myocytes.
In the presence of norepinephrine, I(Ks) increased to the same level
in omega3 and control myocytes. CONCLUSION: Dietary fish oil reduces
the incidence of triggered activity and prevents Ca2+ overload and
AP prolongation in response to norepinephrine. Fish oil may prevent
arrhythmias in patients with heart failure.
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