Effects of carvedilol on ventricular remodeling of juvenile rats in processes of chronic heart failure and exploration of its mechanisms
Qian Yongru
Abstract
Qian Yongru
Abstract
OBJECTIVE To explore the effects and mechanisms of carvedilol in therapies for chronic heart failure(CHF) in juvenile rats. METHODS The animal model of CHF was established by constriction of abdominal aorta. After four weeks of operation, the rats were randomly divided into 3 groups: sham-operated, CHF, and carvedilol-treated group. Carvedilol was administered by direct gastric gavage. After eight-weeks of operation, the hemodynamic study, the pathologic analysis of hearts, the cardiac myocyte apoptosis, the protein level of p53 and bcl-2 were performed, and investigated serum contents of lipid peroxidation(LPO) and superoxide dismutase(SOD).RESULTS Compared with the sham-operated group, SBP, DBP, LVSP, LVEDP, LVRW, RVRW, LPO, AI, p53 were all sinificant increase (all, P_0.01) in CHF group. A significant decrease could be seen in +dp/dt _max, -dp/dt _max, SOD,Bcl-2. In comparsion with CHF group, a significant decrease could be seen in SBP, DBP, LVSP, LVEDP, LVRW, RVRW, LPO, AI, p53 in carvedilol group. While a significant increase could be seen in +dp/dt _max, -dp/dt _max(P_0.01), SOD, Bcl-2. CONCLUSION Carvedilol can prevent ventricular remodeling in chronic heart failure of juvenile rats. The inhibition of myocytes apoptosis, oxidative stress and improvement of hemodynamics may be the important mechanisms of carvedilol in the treatment of ventricular remodeling.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE To explore the effects and mechanisms of carvedilol in therapies for chronic heart failure(CHF) in juvenile rats. METHODS The animal model of CHF was established by constriction of abdominal aorta. After four weeks of operation, the rats were randomly divided into 3 groups: sham-operated, CHF, and carvedilol-treated group. Carvedilol was administered by direct gastric gavage. After eight-weeks of operation, the hemodynamic study, the pathologic analysis of hearts, the cardiac myocyte apoptosis, the protein level of p53 and bcl-2 were performed, and investigated serum contents of lipid peroxidation(LPO) and superoxide dismutase(SOD).RESULTS Compared with the sham-operated group, SBP, DBP, LVSP, LVEDP, LVRW, RVRW, LPO, AI, p53 were all sinificant increase (all, P_0.01) in CHF group. A significant decrease could be seen in +dp/dt _max, -dp/dt _max, SOD,Bcl-2. In comparsion with CHF group, a significant decrease could be seen in SBP, DBP, LVSP, LVEDP, LVRW, RVRW, LPO, AI, p53 in carvedilol group. While a significant increase could be seen in +dp/dt _max, -dp/dt _max(P_0.01), SOD, Bcl-2. CONCLUSION Carvedilol can prevent ventricular remodeling in chronic heart failure of juvenile rats. The inhibition of myocytes apoptosis, oxidative stress and improvement of hemodynamics may be the important mechanisms of carvedilol in the treatment of ventricular remodeling.
Key concepts: Carvedilol, Heart failure, Preload, Ventricular remodeling, Internal medicine, Hemodynamics, Medicine, Oxidative stress