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The impact of phosphodiesterase-5 inhibition or angiotensin-converting enzyme inhibition on right and left ventricular remodeling in heart failure due to chronic volume overload
T. Tykvartova, M. Miklovic, M. Kotrc, P. Skaroupkova, L. Kazdova, J. Trnovska, V. Skop, M. Kolar, J. Novotny, V. Melenovsky
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
Grantová podpora
304121
Grant Agency of Charles University (GAUK)
NU20-02-00052
Ministry of Health of the Czech Republic
NU22-02-00161
Ministry of Health of the Czech Republic
LX22NPO5104
Project National Institute for Research of Metabolic and Cardiovascular Diseases (Programme EXCELES), funded by the European Union-Next Generation EU
NLK
Directory of Open Access Journals
od 2013
Free Medical Journals
od 2013
PubMed Central
od 2013
ProQuest Central
od 2013-10-01
Open Access Digital Library
od 2013-01-01
Open Access Digital Library
od 2013-01-01
Health & Medicine (ProQuest)
od 2013-10-01
Wiley-Blackwell Open Access Titles
od 2013
ROAD: Directory of Open Access Scholarly Resources
od 2013
PubMed
38284173
DOI
10.1002/prp2.1172
Knihovny.cz E-zdroje
- MeSH
- inhibitory ACE * farmakologie MeSH
- inhibitory fosfodiesterasy 5 * farmakologie MeSH
- kardiomegalie farmakoterapie MeSH
- krysa rodu rattus MeSH
- remodelace komor * MeSH
- srdeční selhání * farmakoterapie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
While phosphodiesterase-5 inhibition (PED5i) may prevent hypertrophy and failure in pressure-overloaded heart in an experimental model, the impact of PDE5i on volume-overload (VO)-induced hypertrophy is unknown. It is also unclear whether the hypertrophied right ventricle (RV) and left ventricle (LV) differ in their responsiveness to long-term PDE5i and if this therapy affects renal function. The goal of this study was to elucidate the effect of PDE5i treatment in VO due to aorto-caval fistula (ACF) and to compare PDE5i treatment with standard heart failure (HF) therapy with angiotensin-converting enzyme inhibitor (ACEi). ACF/sham procedure was performed on male HanSD rats aged 8 weeks. ACF animals were randomized for PDE5i sildenafil, ACEi trandolapril, or placebo treatments. After 20 weeks, RV and LV function (echocardiography, pressure-volume analysis), myocardial gene expression, and renal function were studied. Separate rat cohorts served for survival analysis. ACF led to biventricular eccentric hypertrophy (LV: +68%, RV: +145%), increased stroke work (LV: 3.6-fold, RV: 6.7-fold), and reduced load-independent systolic function (PRSW, LV: -54%, RV: -51%). Both ACF ventricles exhibited upregulation of the genes of myocardial stress and glucose metabolism. ACEi but not PDE5i attenuated pulmonary congestion, LV remodeling, albuminuria, and improved survival (median survival in ACF/ACEi was 41 weeks vs. 35 weeks in ACF/placebo, p = .02). PDE5i increased cyclic guanosine monophosphate levels in the lungs, but not in the RV, LV, or kidney. PDE5i did not improve survival rate and cardiac and renal function in ACF rats, in contrast to ACEi. VO-induced HF is not responsive to PDE5i therapy.
Department of Pathophysiology 2nd Faculty of Medicine Charles University Prague Czech Republic
Institute for Clinical and Experimental Medicine IKEM Prague Czech Republic
Citace poskytuje Crossref.org
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