Objective：To observe the protective effect and mechanism of liguzinediol on heart function in acute heart failure rats induced by propafenone. Methods：The rat model of acute heart failure was replicated by propafenone intravenous injection，and different doses of liguzinediol（5.0，10.0 and 20.0 mg/kg）and the positive drug of digilanid C（0.045 mg/kg）were given. The left ventricular pressure was recorded by the RM6240 multichannel physiological signal acquisition and processing system for 0，5，10，20，40，60，90 and 120 min. The changes of maximum ascending/ descending rate（±dp/dtmax），left ventricular systolic pressure（LVSP），mean systolic pressure（MSP），mean diastolic pressure（MDP）and heart rate（HR）were observed，and calcium transport related protein expression was used to detect the mechanism of liguzinediol by Western blot. Results：Liguzinediol 5.0，10.0 and 20.0 mg/kg could effectively increase the +dp/dtmax，-dp/dtmax，LVSP，MSP，MDP and HR in model rats. Western blot and q-PCR results showed that the expression of Ca2+/calmodulin-dependent protein kinaseⅡ（CAMKⅡ），P-CAMKⅡ，sarcoplasmic reticulum Ca2+-ATPase2a（SERCA2a）and P-phospholamban（P-PLN）increased significantly after intervention with liguzinediol. There was no significant difference in ryanodine receptor 2（RyR2） and FK506 binding protein 12.6（FKBP12.6） expression. Conclusion：Liguzinediol can increase the intracellular calcium concentration and improve heart failure，and the mechanism may be through the regulation of CAMKⅡ.