Distinctive Effects of Carvedilol in the Non-Infarct Zone: Remodelling of the Ligated Rat Heart Linked to Oxidative Stress
Autor: | Haochen Wang, X F Zhuang, Chengzeng Yin, Ning Ling Sun |
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Rok vydání: | 2009 |
Předmět: |
Vasodilator Agents
Myocardial Infarction Electrophoretic Mobility Shift Assay Pharmacology medicine.disease_cause Biochemistry Antioxidants Propanolamines Rats Sprague-Dawley Myocardial infarction Carvedilol Metoprolol Reverse Transcriptase Polymerase Chain Reaction NF-kappa B Heart General Medicine Drug Combinations Matrix Metalloproteinase 8 medicine.anatomical_structure Acute Disease Female Inflammation Mediators medicine.drug medicine.medical_specialty Bunazosin Blotting Western Carbazoles Alpha (ethology) Internal medicine Matrix Metalloproteinase 13 medicine Animals RNA Messenger cardiovascular diseases Ligation Tissue Inhibitor of Metalloproteinase-1 business.industry Biochemistry (medical) Cell Biology medicine.disease Rats Oxidative Stress Endocrinology Ventricle Heart failure Quinazolines business Oxidative stress |
Zdroj: | Journal of International Medical Research. 37:1354-1364 |
ISSN: | 1473-2300 0300-0605 |
DOI: | 10.1177/147323000903700510 |
Popis: | In this study, an experimental rat ligated heart model was used to observe the effect of treatment with carvedilol, metoprolol and metoprolol plus a highly selective α1-adrenergic blocking agent, bunazosin, after acute myocardial infarction (MI). Compared with an untreated MI group, all drug-treated groups demonstrated attenuation of inflammatory mediators, activation of nuclear factor-κB (NF-κB), and increased levels of mRNA and active protein for the collagenases matrix metallopeptidase (MMP)-8 and MMP-13 in the non-infarct zone of the ventricle, as well as inhibition of the increase of left ventricular end-diastolic pressure. Supplementation of metoprolol with bunazosin did not add greatly to the effects of metoprolol alone. Of the three drug treatments, carvedilol showed a uniquely potent antioxidant activity that may strengthen its capacity to inhibit oxidative stress, the release of inflammatory mediators and activation of NF-κB. This study may help provide a mechanistic explanation for the greater benefits shown by carvedilol compared with metoprolol in treating heart failure. |
Databáze: | OpenAIRE |
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