Effects of cycloprotobuxine-A on atrial fibrillation.
Abstract
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.
Keywords:
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.