This study evaluated the effects of early treatment with β-adrenergic blocker metoprolol on ventricular remodeling and function after acute myocardial infarction (AMI) by using high frequency ultrasound. The relationship between the efficacy and the expression level of cardiac myocardial inflammatory cytokine was examined in rats. The rat model of AMI was induced by ligating the left anterior descending artery. The surviving rats were randomly assigned to two experimental groups: MI control (MI) group and MI metoprolol (MI-B) group, with the rats undergoing sham operation serving as normal control (Sham). MI-B group was given metoprolol for 4 weeks (refer to the CCS-2 protocol) and the other two groups received equal volume of saline via intragastric (i.g.) administration. The ventricular remodeling and function were evaluated by high frequency ultrasound 4 weeks after the treatment. Then all rats were sacrificed for pathological examination and immunohistochemistrical detection of inflammatory cytokines, including IL-1β, IL-6, IL-10 and TNF-α. Compared with the MI group, the left ventricular end-systolic dimension, end-diastolic dimension, end-systolic volume and end-diastolic volume of the MI-B group were significantly decreased (P<0.01), while the left ventricular anterior wall end-diastolic thickness, ejection fraction and fractional shortening were obviously increased (P<0.01). The conspicuous improvement in the left ventricular morphology and function was coincident with the markedly reduced TNF-α and IL-1β expression and the increased IL-10 expression. We are led to conclude that early metoprolol treatment for AMI can regulate myocardial inflammatory cytokine expression to improve cardiac function and the underlying mechanism might be that it decreases the level of pro-inflammatory cytokines and increases the level of its anti-inflammatory counterparts in cardiac myocytes. Our study also showed that echocardiography is a useful technique for the structural and functional assessment of left ventricle after acute myocardial infarction.

This study evaluated the effects of early treatment with β-adrenergic blocker metoprolol on ventricular remodeling and function after acute myocardial infarction (AMI) by using high frequency ultrasound. The relationship between the efficacy and the expression level of cardiac myocardial inflammatory cytokine was examined in rats. The rat model of AMI was induced by ligating the left anterior descending artery. The surviving rats were randomly assigned to two experimental groups: MI control (MI) group and MI metoprolol (MI-B) group, with the rats undergoing sham operation serving as normal control (Sham). MI-B group was given metoprolol for 4 weeks (refer to the CCS-2 protocol) and the other two groups received equal volume of saline via intragastric (i.g.) administration. The ventricular remodeling and function were evaluated by high frequency ultrasound 4 weeks after the treatment. Then all rats were sacrificed for pathological examination and immunohistochemistrical detection of inflammatory cytokines, including IL-1β, IL-6, IL-10 and TNF-α. Compared with the MI group, the left ventricular end-systolic dimension, end-diastolic dimension, end-systolic volume and end-diastolic volume of the MI-B group were significantly decreased (P<0.01), while the left ventricular anterior wall end-diastolic thickness, ejection fraction and fractional shortening were obviously increased (P<0.01). The conspicuous improvement in the left ventricular morphology and function was coincident with the markedly reduced TNF-α and IL-1β expression and the increased IL-10 expression. We are led to conclude that early metoprolol treatment for AMI can regulate myocardial inflammatory cytokine expression to improve cardiac function and the underlying mechanism might be that it decreases the level of pro-inflammatory cytokines and increases the level of its anti-inflammatory counterparts in cardiac myocytes. Our study also showed that echocardiography is a useful technique for the structural and functional assessment of left ventricle after acute myocardial infarction.
Animals ; Cytokines ; metabolism ; Inflammation ; drug therapy ; metabolism ; Male ; Metoprolol ; pharmacology ; Myocardial Infarction ; drug therapy ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Ultrasonography ; methods