(Circulation. 1997;96:1386-1389.)
© 1997 American Heart Association, Inc.
Articles |
by Human Mononuclear Cells
From the Department of Cardiovascular Medicine, Kyoto University, Japan.
Correspondence to Akira Matsumori, MD, PhD, Department of Cardiovascular Medicine, Kyoto University, 54 Kawaracho Shogoin, Sakyo-ku, Kyoto 606, Japan. E-mail amat{at}kuhp.kyoto-u.ac.jp
Background Recent studies suggest that
cytokines such as tumor necrosis factor (TNF)-
and
interleukins (ILs) are capable of modulating
cardiovascular function and that drugs used in the
treatment of heart failure have various modulatory effects on the
production of cytokines. This study was performed to
examine the effects of amiodarone (a drug shown to be
beneficial in some patients suffering from heart failure) versus other
antiarrhythmic agents on the production of cytokines in
vitro.
Methods and Results Human peripheral blood
mononuclear cells (PBMC) were obtained from healthy volunteers. PBMC
were cultured with 0.1, 1, and 10 µmol/L of amiodarone,
quinidine, disopyramide, and lidocaine in the presence of
lipopolysaccharide. After 24 hours' incubation, TNF-
,
IL-1ß, and IL-6 were measured in the culture supernatants by an
enzyme-linked immunosorbent assay. TNF-
production was
inhibited by amiodarone but stimulated by quinidine in a
concentration-dependent manner. Disopyramide and lidocaine
tended to increase TNF-
production. IL-6 production
was decreased by amiodarone in all concentrations but was
increased significantly by disopyramide. Modulation of
IL-1ß production by amiodarone was biphasic and
significantly increased at a concentration of 10 µmol/L.
Conclusions These previously unrecognized immunomodulatory effects of amiodarone may contribute to its beneficial effects in heart failure patients.
Key Words: amiodarone heart failure immune system interleukins
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