RESUMO
AIM: The effect of decreasing infarct area and stimulating angiogenesis of Shexiangbaoxin Pills in rat with coronary occlusion were studied. METHODS: 44 rats with ligation of the left coronary artery were randomly divided into 4 roups:11 rats were treated with small dose Shexiangbaoxin Pills (group 1), 11 rats were treated with high dose Shexiangbaoxin Pills (group 2), 11 rats were treated with Beifuji and heparin (group 3), 11 rats were treated with 0.9% normal saline (group 4). 18 rats were randomly divided into 2 control groups:10 sham operated rats (group 5) and 8 normal rats (group 6). Infarct area and vascular density in the edge of infarct section were measured after treating for 8 weeks. RESULTS: Infarct area in group 1,2 and 3 was obviously less than that in group 4. The difference was not significant between group 1 and group 3 but group 2 was better than group 3. The difference was significant between group 1 and group 2. The vascular density in group 1,2 and 3 were significanly increased in comparison with those in group 4. The difference was not significant between group 2 with 3. CONCLUSION: Shexiangbaoxin Pills could decrease infarct area and stimulate angiogenesis of the experimental myocardial infarction rat. The effect of Shexiangbaoxin Pills was equal to the group treated with Beifuji and heparin. Shexiangbaoxin Pills had a dose response relationship.
RESUMO
AIM: We observed the expression of KDR/Flk1 in post-myocardiac ischemia(MI) SD rats in order to explain the effect of captopril and its relationship with myocardium angiogenesis after long-term administration.METHODS: The MI model was made by LAD ligation.Captopril was administered for 6 weeks.Immuohistological method and FQ-PCR were used to test the myocardium KDR/Flk-1 expression.RESULTS: In captopril group,no inhibitory effect was observed in myocardium factor VIII expression,but KDR/Flk-1 decreased.The copies of KDR/Flk-1 mRNA reduced dramatically when compared to control group,false-operation and normal group(P0.05).CONCLUSION: ACEI down-regulates KDR/Flk-1 and its mRNA expression in ischemic rat myocardium after long-term administration of captopril,but does not inhibit angiogenesis.So we suspect that some other pathways exist,which can not affect by ACEI,or that ACEI just reduces abnormal angiogenesis.