Abstract: AIM: To investigate the protective effects of PL compound on experimental arrhythmias. METHODS: 3 arrhythmic animal models which inhalation of chloroform to induce ventricular fibrillation (VF) in mice, CaCl₂ to induce arrhythmia and myocardial to induce ischemia-reperfusion in rats. At the same time, the changes were observed by lead Ⅱ dynamic ECG. The activities of LDH, CK were determined, respectively. PAF receptor level in myocardial cell of rats was studied by ³HPAF radio legend binding and RT-PCR. Contents of SOD and MDA of myocardium were assayed, respectively. RESULTS: PL (0.04, 0.20, 1.00 g·kg^-1, ig)was shown to protect mice which suffering from VF induced by chloroform, decrease the incidence of VF and death induced by CaCl₂ in rats and shorten duration of ventricular arrhythmia and eliminate the incidence of VF in rats induced by myocardial ischemia-reperfusion. The activities of LDH, CK were reduced by 35.4 %, 51.8 %, 57.5 % and 22.4 %, 34.4 %, 38.4 %when compared with model group. PL compound inhibited PAF receptor level of myocardial cells in dose-dependent manner, increased the activities of SOD and decreased the contents of MDA. CONCLUTION: PL compound has obvious antiarrhythmic effects, the protective action is related to decreasing the expression of PAF receptor of myocardial cells and anti- lipid peroxydation reaction.

Key words: PL compound, arrhythmias, platelet activating factor receptor, radio legend binding assay, lipid peroxydation