| pubmed-article:2618724 | pubmed:abstractText | Cycloprotobuxine-A (CPB-A) 1-4 mg/kg (1/100-1/25 LD50) produced therapeutic and prophylactic effects which were found to be dose-dependent on experimental arrhythmias induced by BaCl2, aconitine and chloroform. Given at equitoxic doses, the anti-arrhythmic action of CPB-A was as potent as cyclovirobuxine-D (CVB-D) and amiodarone (Amio). However, its therapeutic index (LD50/ED50) was 1.8 times that of CVB-D and 1.2 times that of Amio. The most pronounced effects of CPB-A (0.3-30 mumol/L) on the electrophysiology of ventricular muscle of guinea pig were the lengthening of APD50, APD90 and ERP. This may contribute to its anti-arrhythmic action and suggests that CPB-A most likely belongs to class III anti-arrhythmic drugs (prolongation of APD). Perfused with the same concentration (3 mumol/L), CPB-A brought about more significant increases in APD50, APD90 and ERP than CVB-D and Amio did. | lld:pubmed |
