Studies On Anti-Myocardial Ischemia Effects And Mechanism Of Action Of Dan Xin Tong

Dan Xin Tong (DXT) is the optimal proportion defined by even-designed method and pharmacodynamics. The anti-myocardial ischemia effects and the mechanism of this medicine was preliminarily studied, the general pharmacology and acute toxicity of DXT were also studied in this paper. The results indicated T wave elevation and ST segment drift on electrocardiogram in acute myocardial ischemia rats induced by Pituitrin (Pit) and Isoprotereno (Iso) were obviously opposed by administration of DXT. The myocardial infarction areas, releasement of myocardium enzyme aspartate aminotransferase (AST),. lactic dehydrogenase (LDH), creatine phosphokinase (CPK), MB isoenzyme of creatine phosphokinase (CPK-MB) significantly increased while the superoxide dismutase (SOD) activity decreased in myocardial ischemia animals, DXT treatment prevented these effects. DXT treatment also prolonged the survival time of mice in normobaric hypoxia and duration of electrocardiograph in trachea closed mice. Those results indicated that DXT has the protection effects to ischemia myocardium. DXT administration produced significant increasment of coronary blood flow (CBF) in isolated guinea pig hearts and coronary ligated dogs. In hemodynamics studies of coronary ligated dogs, the left ventricular systolic pressure (LVSP); ventricular pressure maximal change rate (眃p/dt); cardiac output (CO); myocardial blood flow (MBF); stroke volume (SV); cardiac index (CI) and stroke work (SW) decreased, while left ventricular end diastolic pressure (LVEDP) increased aftercoronary ligation in dogs. These effects were prevented by administration of DXT, which showed that DXT ameliorated the "pump" effect of hearts in coronary ligated dogs and increased blood and oxygen supply of ischemia zone in hearts. At the same time, heart rate (HR) and systolic blood pressure (SP), coronary vascular resistance (CVR) and total peripheral vascular resistance (TPVR) were reduced by medication of DXT, these actions decreased myocardial oxygen consumption in ischemia condition. Moreover, DXT showed obvious anti- platelet aggregation and anti- thrombosis effects and significantly reduced the wet and dry thrombus weight in rabbits and the death numbers of mice in encephalic thrombus. The blood-lipid of rats with hyperlipemia, blood rheology in acute blood stasis and hyperlipemia rats could also be reduced by treatment of DXT. In other pharmacodynamics studies, DXT pretreatment provided significant reduction in writhing frequency and prolonged the time of the first writhing in acetic acid-induced pain model in mice, reduced pain reaction score in formaldehyde-induced pain model in mice. The general pharmacology studies showed the mean blood pressure (MBP); HR and respiratory frequency could be reduced by administration of DXT, while it didn't influence other indexes on electrocardiogram in anesthetized cats. DXT administration reduced independent activity frequency in mice and had synergistic action with Pentobarbital sodium, which showed some sedation effects of this medicine.In these elementary experimental studies, DXT showed anti-myocardial ischemia effects. The mechanism maybe involved in ameliorating hemodynamical indexes, increasing the superoxide dismutase (SOD) activity, stabilizing myocardial cell membrane, reducing the nitrogen monoxide (NO) and lactic acid (Lac) content in serum, anti- platelet aggregation effects, reducing blood-lipid and ameliorating blood rheology.This study provided the experimental basis to the clinical application of DXT. However, the mechanisms accounted for the effects of DXT's anti-myocardial ischemia deserve further study.