Objective: To study the protection of Qisheng Yiqi pills on rats with myocardial infarction (MI). Method: Left coronary artery of Sprague-Dawley rats were ligated to make MI model. The rats were randomly subjected to MI model group

three different Qisheng Yiqi pills dose(15

30

45 mg·kg-1·d-1) groups

fluvastatin control group(30 mg·kg-1·d-1) and sham-operated group

each group consisted of 12 rats. The MI group and normal control group were fed 0.9% sodium chloride 30 mL·kg-1·d-1. Eight weeks later

the rats were sacrificed

blood was collected

and the serum separated was used for assaying the activity of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK). Immediately after the sacrifice

the heart was excised and homogenized. The homogenate was used for assaying the activity of antioxidant enzymes superoxide dismutase (SOD)

catalase (CAT)

glutathione-peroxidase (GPx)

and glutathione (GSH). Segmental heart samples were used for hematoxylin and eosin stain and histological evaluation. For measurement of capillary density

sections were immunohistochemically stained with a specific primary antibody. Capillary density was defined as the capillary to cardiomyocyte ratio. Apoptosis was determined using TUNEL kit. Result: Compared with the Sham-operated group

Qisheng Yiqi pills and fluvastatin group

the activities of marker enzymes

LDH

CPK in the serum of the MI group were significantly increased(P<0.05). While the activities of SOD

CAT

GPx and GSH in the heart of MI group were significant decreased than the normal control group

Qisheng Yiqi pills and fluvastatin groupP<0.05)

compared with sham operated mice

the MI group indicated compensatory cardiac hypertrophy

and the capillary density was significantly decreased(P<0.05). While in the Qisheng Yiqi pills group

the capillary density was significantly increased(P<0.05)and the number of TUNEL positive cells was significantly lower than the MI group(P<0.05). Conclusion: Qisheng Yiqi pills can significantly reduce myocardial damage

counteract the oxidative stress induced by myocardial infarction in rats

increase microvessel density

and decrease cardiomyocyte apoptosis.