2009Journal of Cardiovascular and Pulmonary DiseasesRequires access

Effects of treating with carvedilol on myocardial remodeling following acute myocardial infarction in rats

Jiakai Lu

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Abstract

Objective:To observe the pathologic variation of myocardial tissue following acute myocardial infarction by earlier treating with Carvedilol. Method:Established acute myocardial infarction model by ligation of left anterior descending coronary artery(LADCA) in rats. Animals were randomly divided into sham group(without ligation of LADCA), AMI group (ligating LADCA), high-dose Carvedilol group (administrating Carvedilol with 2 mg·kg~ -1 ·d~ -1 after 2 h following AMI), low-dose Carvedilol group( administrating Carvedilol with 1 mg·kg~ -1 ·d~ -1 after 2 h following AMI). After 2 wks of Carvedilol administration, the pathologic variation of myocardial specimens of each group were examined by light microscope and transmission electron microscope and related quantitative analysis were proceed. Result:Compared with AMI group, the areas of myocardial infarction in both carvedilol groups(low-dose and high-dose) were reduced significantly,from 0.149±0.010 to 0.039±0.009 and 0.028±0.004 (P0.05), and decreased degree of abruption and disorganized of myocardial fibers in residual myocardium were also observed. Unimpaired mitochondria membranes, increased interstitium immature capillary density, mitochondria hyperplasy and swelling and enlarged cellular nucleus were found in myocardium and in myocardial cells under light microscope and electric microscope examination following carvedilol treatment. All variations above showed significant differences and were more obvious in high-dose Carvedilol group. Conclusion:The earlier treating with carvedilol for AMI rats can improve myocardial remodeling and the effects are dose dependent. We suppose that the mitochondrial protective effects of carvedilol may be one of the cellular mechanism in its effects on myocardial remodeling suppressing and AMI outcome improving.

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Objective:To observe the pathologic variation of myocardial tissue following acute myocardial infarction by earlier treating with Carvedilol. Method:Established acute myocardial infarction model by ligation of left anterior descending coronary artery(LADCA) in rats. Animals were randomly divided into sham group(without ligation of LADCA), AMI group (ligating LADCA), high-dose Carvedilol group (administrating Carvedilol with 2 mg·kg~ -1 ·d~ -1 after 2 h following AMI), low-dose Carvedilol group( administrating Carvedilol with 1 mg·kg~ -1 ·d~ -1 after 2 h following AMI). After 2 wks of Carvedilol administration, the pathologic variation of myocardial specimens of each group were examined by light microscope and transmission electron microscope and related quantitative analysis were proceed. Result:Compared with AMI group, the areas of myocardial infarction in both carvedilol groups(low-dose and high-dose) were reduced significantly,from 0.149±0.010 to 0.039±0.009 and 0.028±0.004 (P0.05), and decreased degree of abruption and disorganized of myocardial fibers in residual myocardium were also observed. Unimpaired mitochondria membranes, increased interstitium immature capillary density, mitochondria hyperplasy and swelling and enlarged cellular nucleus were found in myocardium and in myocardial cells under light microscope and electric microscope examination following carvedilol treatment. All variations above showed significant differences and were more obvious in high-dose Carvedilol group. Conclusion:The earlier treating with carvedilol for AMI rats can improve myocardial remodeling and the effects are dose dependent. We suppose that the mitochondrial protective effects of carvedilol may be one of the cellular mechanism in its effects on myocardial remodeling suppressing and AMI outcome improving.

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Available abstract

Objective:To observe the pathologic variation of myocardial tissue following acute myocardial infarction by earlier treating with Carvedilol. Method:Established acute myocardial infarction model by ligation of left anterior descending coronary artery(LADCA) in rats. Animals were randomly divided into sham group(without ligation of LADCA), AMI group (ligating LADCA), high-dose Carvedilol group (administrating Carvedilol with 2 mg·kg~ -1 ·d~ -1 after 2 h following AMI), low-dose Carvedilol group( administrating Carvedilol with 1 mg·kg~ -1 ·d~ -1 after 2 h following AMI). After 2 wks of Carvedilol administration, the pathologic variation of myocardial specimens of each group were examined by light microscope and transmission electron microscope and related quantitative analysis were proceed. Result:Compared with AMI group, the areas of myocardial infarction in both carvedilol groups(low-dose and high-dose) were reduced significantly,from 0.149±0.010 to 0.039±0.009 and 0.028±0.004 (P0.05), and decreased degree of abruption and disorganized of myocardial fibers in residual myocardium were also observed. Unimpaired mitochondria membranes, increased interstitium immature capillary density, mitochondria hyperplasy and swelling and enlarged cellular nucleus were found in myocardium and in myocardial cells under light microscope and electric microscope examination following carvedilol treatment. All variations above showed significant differences and were more obvious in high-dose Carvedilol group. Conclusion:The earlier treating with carvedilol for AMI rats can improve myocardial remodeling and the effects are dose dependent. We suppose that the mitochondrial protective effects of carvedilol may be one of the cellular mechanism in its effects on myocardial remodeling suppressing and AMI outcome improving.

Key concepts: Carvedilol, Medicine, Myocardial infarction, Cardiology, Ligation, Internal medicine, Heart failure

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