Effects of Ligustrazine Structural Modification Product Liguzinediol on Hemodynamics of Chronic Heart Failure Model Rats Induced by Adriamycin / 中国药房

ABSTRACT

OBJECTIVE： To investigate the effects of ligustrazine structural modification product Liguzinediol on hemodynamics in chronic heart failure （CHF） model rats induced by adriamycin. METHODS： SD rats were given intraperitoneal injection of adriamycin （2 mg/kg） to induce CHF model. Model rats were randomly divided into normal saline group， positive control group （Deacetyl tricyanidin injection， 0.022 5 mg/kg） and Liguzinediol low-dose， medium-dose and high-dose groups （5， 10， 20        mg/kg）， with 8 rats in each group. Other 8 normal rats were selected as blank control group （normal saline）. Each group was given relevant medicine intravenously. The left ventricular systolic pressure （LVSP）， maximal rate of rise or drop of left ventricular     （±dp/dtmax）， systolic pressure （SP）， diastolic pressure （DP）， heart rate （HR） and other hemodynamic indexes were recorded by multichannel physiological recorder at 1， 5， 10， 20， 40， 60， 90， 120 min after medication. RESULTS： Compared with blank control group， LVSP， +dp/dtmax， │－dp/dtmax│， SP， HR and DP at 120 min after medication of normal saline group were decreased significantly （P＜0.05）. Compared with normal saline group， LVSP at 5-60 min after medication， +dp/dtmax at 40-90 min after medication， SP at 10-40 min after medication were increased significantly in Liguzinediol low-dose group （P＜0.05 or P＜0.01）. LVSP at 5-90 min after medication， SP at 10-60 min after medication， DP at 10-60 min （except for 20 min） after medication were increased significantly in Liguzinediol medium-dose group （P＜0.05 or P＜0.01）. LVSP at 1-120 min after medication， +dp/dtmax at 5-90 min after medication， │－dp/dtmax│， and SP at 5-60 min after medication， DP at 40-60 min after medication were increased significantly in Liguzinediol high-dose group （P＜0.05 or P＜0.01）. CONCLUSIONS： Single intravenous injection of Liguzinediol can significantly enhance ventricular systolic function of CHF model rats so as to control or relieve CHF.