Regression of chronic hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and fibrosis: effect of enalapril
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
9140694
DOI
10.1023/a:1007788915732
Knihovny.cz E-zdroje
- MeSH
- chronická nemoc MeSH
- enalapril terapeutické užití MeSH
- hemodynamika účinky léků MeSH
- hydroxyprolin metabolismus MeSH
- hypertrofie pravé komory srdeční farmakoterapie patofyziologie MeSH
- hypoxie komplikace patofyziologie MeSH
- inhibitory ACE terapeutické užití MeSH
- kolagen metabolismus MeSH
- krysa rodu Rattus MeSH
- myokard metabolismus MeSH
- plicní fibróza farmakoterapie etiologie MeSH
- plicní hypertenze farmakoterapie etiologie patofyziologie MeSH
- potkani Wistar MeSH
- tělesná hmotnost účinky léků fyziologie MeSH
- velikost orgánu účinky léků fyziologie MeSH
- výšková nemoc patofyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- enalapril MeSH
- hydroxyprolin MeSH
- inhibitory ACE MeSH
- kolagen MeSH
Chronic hypoxia induces pulmonary hypertension and right ventricular hypertrophy. These changes are completely reversible, except for persistent myocardial fibrosis. The aim of the present study was to determine whether treatment with the angiotensin-converting enzyme (ACE) inhibitor enalapril can reduce the ventricular collagen content in animals recovering from chronic hypoxia. Adult male Wistar rats were exposed to intermittent high-altitude hypoxia simulated in a barochamber (7000 m, 8 hr/day, 5 days a week, 24 exposures), then transferred to normoxia and divided into two groups: (a) treated with enalapril (0.1 g/kg/day for 60 days) and (b) without treatment. The corresponding control groups were kept under normoxic conditions. Enalapril significantly decreased the heart rate, systemic arterial pressure, and absolute left and right ventricular weights in both hypoxic and control rats; on the other hand, the pulmonary blood pressure was unchanged. The content and concentration of collagen was reduced in both ventricles of enalapril-treated hypoxic and control animals by 10-26% compared with the corresponding untreated groups. These data suggest that the partial regression of cardiac fibrosis due to enalapril may be independent of the pressure load.
Citace poskytuje Crossref.org
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