EFFECTS OF CYCLOPROTOBUXINE-A ON ATRIAL-FIBRILLATION

AIM: To study the effects of cycloprotobuxine-A (Cyc-A) on atrial fibr illation. METHODS: Atrial fibrillations in vivo, and in vitro were ind uced by arrhythmogenic drugs. Action potentials were measured by the s tandard microelectrode technique. RESULTS: Cyc-A, similar to or slight ly stronger than amiodarone (Ami), decreased incidences of atrial fibr illation elicited by CaCl2-acetylcholine in mice and increased doses o f aconitine, ouabain, or adrenaline to elicit atrial fibrillation in i solated guinea pig atria. Cyc-A 0.3 - 100 mu mol.L-1 decreased the nor mal automaticity and 0.3 - 30 mu mol.L-1 attenuated or almost abolishe d the isoprenaline-induced abnormal increase in automaticity in sinus nodal cells. In isolated left atria, Cyc-A 0.3 - 30 mu mol.L-1 inhibit ed the abnormal rhythmic activity elicited by adrenaline, prolonged ac tion potential duration (APD) and effective refractory period, and red uced excitability. At 3 - 30 mu mol.L-1, Cyc-A also decreased the maxi mal velocity of depolarization (V-max). Cyc-A antagonized the acetylch oline-induced shortening of APD. These electrophysiologic effects were similar to those of amiodarone, but Ami did not affect the V-max. CON CLUSION: Cyc-A produces a protective effect against experimental atria l fibrillation via a prolongation of repolarization, a decease of auto maticity, and an inhibition of excitability.