Regression of chronic hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and fibrosis: effect of enalapril
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Chronic Disease MeSH
- Enalapril therapeutic use MeSH
- Hemodynamics drug effects MeSH
- Hydroxyproline metabolism MeSH
- Hypertrophy, Right Ventricular drug therapy physiopathology MeSH
- Hypoxia complications physiopathology MeSH
- Angiotensin-Converting Enzyme Inhibitors therapeutic use MeSH
- Collagen metabolism MeSH
- Rats MeSH
- Myocardium metabolism MeSH
- Pulmonary Fibrosis drug therapy etiology MeSH
- Hypertension, Pulmonary drug therapy etiology physiopathology MeSH
- Rats, Wistar MeSH
- Body Weight drug effects physiology MeSH
- Organ Size drug effects physiology MeSH
- Altitude Sickness physiopathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Enalapril MeSH
- Hydroxyproline MeSH
- Angiotensin-Converting Enzyme Inhibitors MeSH
- Collagen 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.
References provided by Crossref.org
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
