Artikel
Prevention of left ventricular dysfunction by non-selective beta-blocker Carvedilol in CVB-3-Induced acute myocarditis
Prävention der links ventrikulären Dysfunktion durch nicht-selektiven beta-Blocker Carvedilol in CVB-3-induzierter akuter Myokarditis
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Veröffentlicht: | 11. November 2004 |
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Gliederung
Text
Myocardial collagen network supports the structural integrity of the heart and extracellular matrix remodeling contributes to left ventricular dysfunction and dilatation. Proinflammatoric cytokines like IL-1beta and matrix metalloproteinases like MMP-8 play crucial role during myocardial remodeling. beta-adrenergic receptor stimulation by catecholamines influences the production of cytokines heralding the possibility of modulating cytokine production by beta-adrenergic blockers. Carvedilol, a non selective beta-blocker has in addition to the non selective adrenergic actions antioxidative and antiinflammatoric capacity. However, the effects of Carvedilol with the regulation of the MMP/TIMP system in acute myocarditis are still unclear. This study was designed to investigate the mRNA expression of myocardial IL-1-beta. TGF- beta as well as MMP-8 and MMP-9 in a murine myocarditis model under treatment with Carvedilol (10mg/d). Moreover the left ventricular function was characterized by haemodynamic parameters (tip catheter). CVB-3 infected BALB/c mice showed a marked decrease in body weight and a ruffled fur. The significant impairment of LV-function was improved in all parameters with the treatment of Carvedilol with reduced expression of proinflammatoric cytokines and matrixmetalloproteinases.
The reduced expression of proinflammatoric cytokines and metalloproteinases may contribute to reduced matrix degradation with a better structural integrity of the heart. This overall beneficial effect might be due to the wide range of biological activities beside the antiadrenergic potential (antioxidative, antiinflammatoric).