Effects of cycloprotobuxine-A on atrial fibrillation.

AIM

To study the effects of cycloprotobuxine-A (Cyc-A) on atrial fibrillation.

METHODS

Atrial fibrillations in vivo and in vitro were induced by arrhythmogenic drugs. Action potentials were measured by the standard microelectrode technique.

RESULTS

Cyc-A, similar to or slightly stronger than amiodarone (Ami), decreased incidences of atrial fibrillation elicited by CaCl2-acetylcholine in mice and increased doses of aconitine, ouabain, or adrenaline to elicit atrial fibrillation in isolated guinea pig atria. Cyc-A 0.3-100 mumol.L-1 decreased the normal automaticity and 0.3-30 mumol.L-1 attenuated or almost abolished the isoprenaline-induced abnormal increase in automaticity in sinus nodal cells. In isolated left atria, Cyc-A 0.3-30 mumol.L-1 inhibited the abnormal rhythmic activity elicited by adrenaline, prolonged action potential duration (APD) and effective refractory period, and reduced excitability. At 3-30 mumol.L-1, Cyc-A also decreased the maximal velocity of depolarization (Vmax). Cyc-A antagonized the acetylcholine-induced shortening of APD. These electrophysiologic effects were similar to those of amiodarone, but Ami did not affect the Vmax.

CONCLUSION

Cyc-A produces a protective effect against experimental atrial fibrillation via a prolongation of repolarization, a decease of automaticity, and an inhibition of excitability.