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
patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the o...patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the onset to AD, indicating that AD belongs to the category of effort angina.18 patients were investigated by continuous hemodynamic monitoring. Three patients had significant increase in pulmonary artery diastolic pressure (PADP) before the onset. In the other 15 patients. PADP increased slightly in 12 and remained unchanged in 3 cases before the onset. Left ventriculography showed ejection fraction (EF)>45% in 25 of the 27 patients. These results indicate that left ventricular (LV) systolic dysfunction is not a major factor in the Pathogenesis of AD. The patients with LVEDP>12 mmHg constituted 60% of 25 patients with EF>45%, suggesting that these patients had ohvious LV diastolic dysfunction, which may be the major factor in the pathogenesis of AD.According to the results of our treatment, beta blockers may be used as the major form of tteatment in the patients with AD.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patients with angina decubitus (AD) were studied during hospitalization. These patients were found to have severe coronary artery obstructive lesions and an increase of myocardial oxygen consumption (MOC) before the onset to AD, indicating that AD belongs to the category of effort angina.18 patients were investigated by continuous hemodynamic monitoring. Three patients had significant increase in pulmonary artery diastolic pressure (PADP) before the onset. In the other 15 patients. PADP increased slightly in 12 and remained unchanged in 3 cases before the onset. Left ventriculography showed ejection fraction (EF)>45% in 25 of the 27 patients. These results indicate that left ventricular (LV) systolic dysfunction is not a major factor in the Pathogenesis of AD. The patients with LVEDP>12 mmHg constituted 60% of 25 patients with EF>45%, suggesting that these patients had ohvious LV diastolic dysfunction, which may be the major factor in the pathogenesis of AD.According to the results of our treatment, beta blockers may be used as the major form of tteatment in the patients with AD.
