Influence and mechanism of Xindakang on cardiac functions of isolated frog heart / 中国药理学与毒理学杂志

ABSTRACT

OBJECTIVE To evaluate the effects of flavonoids from Xindakang (Hippophae Fructus flavone) on myo?cardial systolic and diastolic functions of isolated frog hearts and explore the possible mechanism, and provide experi?mental basis for improving the effect and efficacy of Xindakang on cardiac function. METHODS The isolated frog heart perfusion specimens were prepared by Yagi's method, and the effects of different concentrations of Xindakang on myo?cardial contractility (0.0125, 0.025, 0.05, 0.1 and 0.2 g·L-1), heart rate and cardiac output of isolated frog heart were stud?ied. Acetylcholine, atropine and epinephrine were administered successively to analyze the effects of Xindakang on car?diac systolic function of isolated frogs under the action of different drugs, and compared with propranolol. The effect of extracellular calcium ion concentration on the action of Xindakang was studied by using low calcium concentration, high cal?cium concentration and normal Ren's solution. To study the effect and possible mechanism of Xindakang on cardiac systolic function of frog. RESULTS The concentration of Xindakang in the range of 0.0125-0.1 g·L-1 could weaken the contractility of isolated frog heart and increase the concentration of Xindakang. The inhibitory effect of Xindakang on con?tractility of isolated frog heart was enhanced, and showed obvious dose-effect relationship. Cardiac output was signifi?cantly decreased by Xindakang (P<0.01), slow heart rate (P<0.05); M receptor blocker atropine could not antagonize the contractile effect of Xindakang, and Xindakang could not completely antagonize the contractile effect of adrenalin. Xindakang could inhibit the isolated frog heart in low calcium concentration, high calcium concentration and normal Ren's solution, and increased with the increase of extracellular calcium concentration (P<0.01). CONCLUSION Xinda?kang has inhibitory effect on isolated frog heart, which may be achieved by blocking the calcium channel on myocardial cell membrane and reducing the calcium concentration in myocardial cells.