Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced...Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups: 1 ) AMI control group (n =19), 2) losartan group (n= 22, 3 mg @ kg - 1 @ d - 1 ), 3 ) enalapril group (n = 20, 1 mg @ kg - 1 @ d - 1 ), 4) losartan - enalapril combinative group (n = 22, 3 and 1 mg @ kg- 1 @ d - 1 respectively). 5 ) sham-operated group ( n =10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1 ) AMI controls (n = 11 ), 2) losartan group (n = 10), 3 ) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11 ),5) sham - operated group (n = 6) and 6) normal controls (n=8). Results. There were no significant differences among the 4 AMI groups in MI size (41.7% ~ 43.4%, all P> 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW)in AMI group were all significantly increased ( P <0.05 ~ 0. 001 ); whereas the maximum left ventricular pressure rising and droping rates ( + dp/dt) and their corrected values by LV systolic pressure ( + dp/dt/LVSP)were significantly reduced (all P <0.001 ), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group , LVEDP, LVV, LVAW and LVRW were all significantly decreased (P <0.05~0.001 ); while + dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P <0.05~0.001 ) except -dp/dt/LVSP in losartan group (P> 0. 05 ). There were no significant differences in the above indices among the 3 treatment groups (all P> 0.05). Conclusion. Both losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.展开更多
OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs)...OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P展开更多
文摘Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups: 1 ) AMI control group (n =19), 2) losartan group (n= 22, 3 mg @ kg - 1 @ d - 1 ), 3 ) enalapril group (n = 20, 1 mg @ kg - 1 @ d - 1 ), 4) losartan - enalapril combinative group (n = 22, 3 and 1 mg @ kg- 1 @ d - 1 respectively). 5 ) sham-operated group ( n =10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1 ) AMI controls (n = 11 ), 2) losartan group (n = 10), 3 ) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11 ),5) sham - operated group (n = 6) and 6) normal controls (n=8). Results. There were no significant differences among the 4 AMI groups in MI size (41.7% ~ 43.4%, all P> 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW)in AMI group were all significantly increased ( P <0.05 ~ 0. 001 ); whereas the maximum left ventricular pressure rising and droping rates ( + dp/dt) and their corrected values by LV systolic pressure ( + dp/dt/LVSP)were significantly reduced (all P <0.001 ), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group , LVEDP, LVV, LVAW and LVRW were all significantly decreased (P <0.05~0.001 ); while + dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P <0.05~0.001 ) except -dp/dt/LVSP in losartan group (P> 0. 05 ). There were no significant differences in the above indices among the 3 treatment groups (all P> 0.05). Conclusion. Both losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.
文摘OBJECTIVE: To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. METHODS: Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. RESULTS: Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P