Objective To observe the effects of trimetazidine (TMZ) on the cardiac function and neurohormonal of heart failure model in rats.Methods Partially banding abdominal aortic artery to achieve congestive heart failure rats model.Interventricular septum thickness(IVST),left ventricular posterior wall thickness(LVPWT),left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter (LVESD),left ventricular ejection fraction(LVEF) and shortening fraction(FS) were measured by echocardiogram,Pathological changes of myocardial cells was observed,B-type natriuretic peptide (BNP)、C-type natriuretic peptide receptor (NPRC),atrial natriuretic peptide (ANP),myosin heavy chain (β-MHC) and angiotensinl (AT1) were measured by Real-Time PCR,superoxide dismutase (SOD) was measured by immunohistochemistry method.Results Trimetazidine treatment of the high-dose group and the model group compare IVST LVPWT,LVESD,LVEDD were (0.63 ± 0.05) mn,(0.73 ± 0.06) mm,(0.73 ±0.05)mm,(0.87 ±0.06)mm and (1.07 ±0.06)mm,(1.13 ±0.06) mm,(0.93 ±0.06)mm,(1.33 ±0.06) mm,was significantly reduced (P ＜ 0.05),LVEF,FS increased to (27.75 ± 1.83) ％,(11.44 ± 0.76) ％ and (11.78 ±0.56)％,(4.27 ± 0.22)％ (P ＜ 0.01),Myocardial cell structure were remarkably improved.The expression of BNP,ANP,NPRC,ATI,β-MHC were remarkably decreased.The expression of SOD was elevated.Conclusion TMZ treatment group can improve the secretion of neurohormonal of heart failure model in rats,and also obviously improve the cardiac contractility.

Objective To study the molecular mechanism of atherosclerosis induced by intravascular pressure.Methods Technic aortic coarctation (TAC) was performed in ApoE-/-mice (n＝8) and control littermate (n＝8) mice.HE staining was performed in the vessels upstream and downstream of the mice models.In vitro,hypoxia inducible factor-1a (HIF-1α),heme oxygenase,reactive oxygen species and phosphorylated AMP activated protein kinase (AMPK) were analyzed in different intravascular pressure with a myograph system that allowed independent variation of flow and pressure.Results After one month of TAC,ApoE/ mice in a normal chow diet developed occlusive plaque and accelerated atherosclerotic lesions exclusively in upstream high-pressure vessel segments.In vitro,HIF-1α was increased,heme oxygenase was higher over(2.7 ±0.6) fold,reactive oxygen species and phosphorylated AMPK were also enhanced in high intravascular pressure perfused vessel segments as compared with low intravascular pressure perfused vessel segments (all P＜0.05).Conclusions Intravascular pressure elevation can activate hypoxia and metabolism-associated pathways in the arterial wall,and predispose atherosclerosis accelerated.