| Objective: The test is to observe the effection of mini-pills for promoting myocardial contraction and blood circulation on Angll and mRNA expressions of AT1 acceptors and its signal transduction through the medium of PKC in rat myocardium of chronic heart failure, and to explain the mechanism of tveatmeut of the Chinese patent medicine for chronic heart failure furtherly.Methods: We had selected the SD healthy male rat whose weight is between 250g and 300g, and created chronic congestive heart failure model of deficiency of qi and blood stasis through ligation of coronary artery. Then model rats are randomly distributed into four groups: model group, Chinese medicine group with large dose, Chinese medicine group with moderate dose and Control group of west medicine, eight per group, and there is normal control group else. The content of Angll and protein kinase C in myocardium of each group rat (oncept normal control group) are detected with ABC immuno-histochemical method after the eight weeks' usage of the Chinese patent medicine. The mRNA content in AT] acceptor is deteeted by the method of PT-PCR; The ultrastructural changes of myocardinl cell are observed through transmission electron microscope(TEM).Results: The model group is contrasted with the normal control group: heart function is decreased largely (p<0.01); the content of Angll and PKC in the regional myocardium is obviously higher. Than the normal groups. (p<0.01); The mRNA expression of AT1 acceptors is also higher than the normal groupls. (p<0.05); The wltrastruction of left ventricle is more instinctly changed than the normal group. Chinese medicine group and control group are contrasted with model group: heart function is clearly improved. (p <0.05); the content of Angll and PKC in myocardium is lower than model group (p<0.01); The mRNA expression of AT1 acceptors is also lower than model group(p<0.01). The wltrastruction of left ventricle is more obviously improved than model group.Conclusion: The Chinese patent medicine may improve and rectify heart failure through decreasing Angll to inhibit RAS system, mRNA expression of AT1 acceptors and their conducting thoroughfare. |