Effect of Ramipril and Furosemide Treatment on Interstitial Remodeling in Post-Infarction Heart Failure Rat Hearts

Seeland, Ute; Kouchi, Ichiro; Zolk, Oliver; Itter, Gabi; Linz, Wolfgang; Böhm, Michael

doi:10.1006/jmcc.2001.1497

Cited by 52 publications

(44 citation statements)

References 25 publications

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“…[12][13][14] However, none of in vivo results fully showed whether the effect of ACE inhibition on MMPs was a cause for or a result of the prevention of the LV geometrical and hemodynamic deteri- oration. In this study, the administration of ACE inhibitor at a subdepressor dose suppressed gene expression and gelatinolytic activity of MMPs even at the predilatation stage and prevented LV dilatation in the hypertensive HF model.…”

Section: Effect Of Ace Inhibition On Mmp Activitymentioning

confidence: 99%

“…Previous in vitro studies showed that ACE inhibition attenuated MMP activity, 7,11 and long-term ACE inhibition decreased MMP activity with attenuation of LV dilatation in animal studies. [12][13][14] However, it is unclear whether the suppression of MMP activity by ACE inhibition is causative of or secondary to prevention of LV dilatation in vivo. We aimed to investigate gene expression and gelatinolytic activity of MMPs just before and after the development of LV remodeling in a hypertensive HF model 15 and to elucidate the effects of ACE inhibition in vivo.…”

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confidence: 99%

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Activation of Matrix Metalloproteinases Precedes Left Ventricular Remodeling in Hypertensive Heart Failure Rats

et al. 2004

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Background-Matrix metalloproteinases (MMPs) are activated in dilated failing hearts, and angiotensin-converting enzyme (ACE) inhibition prevents left ventricular (LV) dilatation. However, it remains unclear whether activation of MMPs precedes or is secondary to LV remodeling, and an effect of ACE inhibition on MMPs is unknown. Methods and Results-Dahl salt-sensitive rats fed a high-salt diet from 8 weeks served as the hypertensive heart failure (HF) model. LV echo, histological study, measurement of mRNA levels, and gelatin zymography were performed before (at 23 weeks) and after (at 26 weeks) the development of LV dilatation and pulmonary edema. The same procedures were conducted in the HF model rats treated with a subdepressor dose of ACE inhibitor (enalapril 5 mg · kg Ϫ1 · d

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Section: Effect Of Ace Inhibition On Mmp Activitymentioning

confidence: 99%

mentioning

confidence: 99%

Activation of Matrix Metalloproteinases Precedes Left Ventricular Remodeling in Hypertensive Heart Failure Rats

et al. 2004

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“…Upregulated MMP gene expression paralleled by increased ECM deposition has been previously reported in decompensated ischaemic and dilated cardiomyopathies (Munger et al 1996;Seeland et al 2002Seeland et al , 2007. Justification of this phenomenon is based on the premise that the catalytic activities of MMPs are influenced by substrate product stoichiometry (Chadwick et al 1998).…”

Section: Transforming Growth Factor β1 In Fibrotic Remodellingmentioning

confidence: 99%

Left ventricle structural remodelling in the prediabetic Goto-Kakizaki rat

D’Souza

Howarth

Yanni

et al. 2011

Experimental Physiology

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This study tested the hypothesis that experimental prediabetes can elicit structural remodelling in the left ventricle (LV). Left ventricles isolated from 8-week-old male Goto-Kakizaki (GK) rats and age-matched male Wistar control rats were used to assess remodelling changes and underlying transforming growth factor β1 (TGFβ1) activity, prohypertrophic Akt-p70S6K1 signalling and gene expression profile of the extracellular matrix (ECM) using histological, immunohistochemical, immunoblotting and quantitative gene expression analyses. Prediabetes in GK rats was confirmed by impaired glucose tolerance and modestly elevated fasting blood glucose. Left ventricle remodelling in the GK rat presented with marked hypertrophy of cardiomyocytes and increased ECM deposition that together translated into increased heart size in the absence of ultrastructural changes or fibre disarray. Molecular derangements underlying this phenotype included recapitulation of the fetal gene phenotype markers B-type natriuretic peptide and α-skeletal muscle actin, activation of the Akt-p70S6K1 pathway and altered gene expression profile of key components (collagen 1α and fibronectin) and modulators of the ECM (matrix metalloproteinases 2 and 9 and connective tissue growth factor). These changes were correlated with parallel findings of increased TGFβ1 transcription and activation in the LV and elevated active TGFβ1 in plasma of GK rats compared with control animals (Student's t test, P < 0.05 versus age-matched Wistar control animals for all parameters). This is the first report to describe LV structural remodelling in experimental prediabetes. The results suggest that ventricular decompensation pathognomonic of advanced diabetic cardiomyopathy may have possible origins in profibrotic and prohypertrophic mechanisms triggered before the onset of type 2 diabetes mellitus.

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“…Previous studies demonstrated that pharmacological inhibition of MMPs resulted in suppression of cardiac remodeling in animal models of CHF (7,36,37). In addition, there is evidence that the beneficial effects of angiotensinconverting enzyme inhibitors on cardiac remodeling is due to the inhibition of collagen synthesis as well as the influence on MMPs, particularly MMP-2 (38). Taking these findings into account, there is no doubt that MMPs play a crucial role in promoting cardiac remodeling.…”

Section: Discussionmentioning

confidence: 99%

Ethanol extract from Epimedium brevicornum attenuates left ventricular dysfunction and cardiac remodeling through down-regulating matrix metalloproteinase-2 and -9 activity and myocardial apoptosis in rats with congestive heart failure

Song

Li²,

Chen³

et al. 2008

Int J Mol Med

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Abstract. Epimedium, a traditional Chinese herb, has been used for the remedy of coronary heart disease, impotence and osteoporosis in traditional oriental medicine. However, despite extensive pharmacological studies, the molecular mechanism of the anti-heart failure effect of epimedium is little known. In the present study, we investigated the pharmacological action mechanism of ethanol extract of epimedium (EPI-ext) on isoproterenol-induced congestive heart failure (CHF) in rats. Isoproterenol administration resulted in severe heart failure, as shown by the increased levels of left ventricular (LV) weight index and heart rate, as well as LV end diastolic pressure, and by the decreased levels of LV systolic pressure, maximal rate of LV pressure rise, and maximal rate of LV pressure decline. EPI-ext dose-dependently reversed the changes of these cardiac morphometric and hemodynamic parameters. In addition, EPI-ext significantly inhibited the serum levels of tumor necrosis factor α, norepinephrine, angiotensin II and brain natriuretic peptide in rats with CHF and improved the histological changes including cadiocyte hypertrophy, cadiocyte degeneration, inflammatory infiltration, and cardiac desmoplasia. Furthermore, the expression and activities of matrix metalloproteinase-2 and -9, which regulate collagen production, were also blocked by EPI-ext. Moreover, myocardial apoptosis was remarkably attenuated by EPI-ext through the regulating Bcl-2/Bax axle. In conclusion, EPI-ext ameliorates LV dysfunction and cardiac remodeling through down-regulating matrix metalloproteinase-2 and -9 activity and myocardial apoptosis in rats with CHF.

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Effect of Ramipril and Furosemide Treatment on Interstitial Remodeling in Post-Infarction Heart Failure Rat Hearts

Cited by 52 publications

References 25 publications

Activation of Matrix Metalloproteinases Precedes Left Ventricular Remodeling in Hypertensive Heart Failure Rats

Activation of Matrix Metalloproteinases Precedes Left Ventricular Remodeling in Hypertensive Heart Failure Rats

Left ventricle structural remodelling in the prediabetic Goto-Kakizaki rat

Ethanol extract from Epimedium brevicornum attenuates left ventricular dysfunction and cardiac remodeling through down-regulating matrix metalloproteinase-2 and -9 activity and myocardial apoptosis in rats with congestive heart failure

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