The Protective Effect Of1,2,3,4,5,6,7,8-octohydro-9-phenyl-acetamido Acridine And Its Hydrochloride On Experimental Arrhythmia

Cardiacarrhythmia is that the site of the origin of heart. Heart rate, rhythm andimpulse conduction when any one of those occurs exception. Cardiacarrhythmia isan important disease which is harmful to human health. Myocardial ischemicarrhythmia is a very high incidence of myocardial ischemia and arrhythmias are themost common ventricular arrhythmias, including ventricular contractions,ventricular tachycardia, ventricular fibrillation and so on.The purpose of this paper is to explore how OPAA and OPAA·HCl play a rolein the treatment of cardiovascular diseases and observe whether they havearrhythmia antagonism or not. Select the drug (Aconitine, Uabaina) and coronaryartery ligation in rats induced experimental arrhythmia model to observe theprotective effect of OPAA and OPAA·HCl to experimental arrhythmia.Preparated experimental arrhythmia induced by Aconitine and Uabainarespectively in rats and guinea pig. OPAA and OPAA·HCl (in dosage of100,200mg/kg) were given to the rats, and the dose of positive drug propranolol was10mg/kg. Control group was given0.5%sodium carboxymethyl cellulose, andevery group was gavaged one time. Recorded to the occurrence time of VP, VT, VFand CA in arrhythmia rats induced by Aconitine; and observed the dosage ofUabaina when the guinea pigs appeared VP, VT, VF and CA.The results of drug-induced experimental arrhythmia: the low and high dosegroup in rats of OPAA and OPAA·HCl induced by Aconitine has significantantiarrhythmic effect, and also improved significantly the dosage of Uabaina whenthe guinea pigs appeared VP, VT, VF and CA. Its role was equal to positive drugpropranolol. And the effect of OPAA·HCl was slightly higher than OPAA.Preparated experimental arrhythmia model induced by Ischemic in rats. OPAAand OPAA·HCl (in dosage of50,100,200mg/kg) were given to the rats, and the doseof positive drug verapamil was50mg/kg. Control group was given0.5%sodiumcarboxymethyl cellulose, and every group was gavaged one time. Recorded to theoccurrence time and the incidence of VP, VT, VF and CA in arrhythmia rats afterligation.The results of coronary artery ligation-induced experimental arrhythmia: Compared with sham group, the occurrence time of VP, VT, VF and CA in modelgroup rats was significantly shortened. Compared with model group, the occurrencetime of VP, VT, VF and CA in OPAA high-dose group were significantly prolonged,and the occurrence time of VP and CA in the middle and low-dose group weresignificantly prolong; the occurrence time of VP, VT, VF and CA in OPAA·HClmiddle and high-dose group were significantly prolonged, and the occurrence timeof VP and CA in the low-dose group were significantly prolong. The effect ofOPAA·HCl high-dose group was quite to positive drug verapamil. In addition,compared with sham group, the incidence of VT, VF and CA in model rats weresignificantly increased. Compared with model group, OPAA high dose groupsignificantly reduced the incidence of VT and CA, but in the middle and low-dosegroup had no significant impact on the incidence of VT, VF and CA. OPAA·HClmiddle and high dose group could significantly reduce the incidence of VT, VF andCA, but in the low-dose group had no significant impact on the incidence of VT, VFand CA. The effect of OPAA·HCl high-dose group was the equivalent to positivedrug verapamil.OPAA and OPAA·HCl had the role of anti-drug arrhythmogenic. and alsoimproved significantly the dosage of Uabaina when the guinea pigs appeared VP, VT,VF and CA.OPAA·HCl is equal to positive drug propranolol; OPAA and OPAA·HClhad the effect of anti-experimental arrhythmia induced by coronary artery ligation inrats. OPAA·HCl was the equivalent to positive drug verapamil. They are worthy offurther development and utilization, and the anti-arrhythmic mechanism of them hasyet to be elucidating.