Abstract
Carvedilol is a nonselective β-blocker with α1-adrenergic blocking and antioxidant properties. A number of preclinical experiments and clinical trials have demonstrated that carvedilol provides prominent benefit in heart failure. However, less research has been done in the area of animal models of viral myocarditis. This paper reviews the use of carvedilol in animal models of viral myocarditis. The experimental evidence strongly suggests that carvedilol, but not metoprolol (a selective β1-adrenergic blocking agent), protects against viral myocarditis and the superior cardioprotection effect of carvedilol to metoprolol may be due to its upregulating the production of antiinflammatory cytokines, downregulating the production of proinflammatory cytokines, antioxidative effects, the suppression of matrix metalloproteinases production, and positive hemodynamic effects.
Keywords: Carvedilol, viral myocarditis, cytokines, antioxidants, hemodynamics, nonselective -blocker, heart failure, metoprolol, matrix metalloproteinases production, viral injury
Current Pharmaceutical Design
Title:The Mechanism of Carvedilol in Experimental Viral Myocarditis
Volume: 18 Issue: 12
Author(s): Li Yue-Chun, Ge Li-Sha, Guan Xue-Qiang, Lin Jia-Feng
Affiliation:
Keywords: Carvedilol, viral myocarditis, cytokines, antioxidants, hemodynamics, nonselective -blocker, heart failure, metoprolol, matrix metalloproteinases production, viral injury
Abstract: Carvedilol is a nonselective β-blocker with α1-adrenergic blocking and antioxidant properties. A number of preclinical experiments and clinical trials have demonstrated that carvedilol provides prominent benefit in heart failure. However, less research has been done in the area of animal models of viral myocarditis. This paper reviews the use of carvedilol in animal models of viral myocarditis. The experimental evidence strongly suggests that carvedilol, but not metoprolol (a selective β1-adrenergic blocking agent), protects against viral myocarditis and the superior cardioprotection effect of carvedilol to metoprolol may be due to its upregulating the production of antiinflammatory cytokines, downregulating the production of proinflammatory cytokines, antioxidative effects, the suppression of matrix metalloproteinases production, and positive hemodynamic effects.
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Cite this article as:
Li Yue-Chun, Ge Li-Sha, Guan Xue-Qiang, Lin Jia-Feng , The Mechanism of Carvedilol in Experimental Viral Myocarditis , Current Pharmaceutical Design 2012; 18 (12) . https://dx.doi.org/10.2174/138161212799958530
DOI https://dx.doi.org/10.2174/138161212799958530 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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