ANTI ATRIAL FIBRILLATION EFFECTS OF CYCLOVIROBUXINE D AND ITS ELECTROPHYSIOLOGICAL MECHANISM STUDIED ON GUINEA PIG ATRIA

Cyclovirobuxine-D (CVB-D) was shown to produce significant and dose dependent protective effects against atrial fibrillation induced by CaCl 2 Ach in mice. On atrial fibrillation induced by aconitine, ouabain or adrenaline in isolated guinea pig atria, the effects of CVB-D were similar to those of amiodarone. CVB-D 0.3～100 μmol·L^-1 was shown to depress the automaticity of the isolated guinea pig right atria. In isolated left atria, CVB-D 0.3 μmol·L^-1 was found to inhibit the abnormal automaticity elicited by adrenaline, to prolong the duration of action potential and effective refractory period and to reduce excitability. At high concentration (30 μmol·L^-1 ), CVB-D was also found to decrease the maximal velocity of depolarization (V_max) and to elongate the conduction time of initiation. Amiodarone 0.3～30 μmol·L^-1 was shown to closely resemble CVB-D in electrophysiology without effect on V_max.