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Regression of chronic hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and fibrosis : Effect of enalapril
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 r...
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Published in: | Cardiovascular drugs and therapy 1997-04, Vol.11 (2), p.177-185 |
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creator | PELOUCH, V KOLAR, F OST'ADAL, B MILEROVA, M CIHAK, R WIDIMSKY, J |
description | 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. |
doi_str_mv | 10.1023/A:1007788915732 |
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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.</description><identifier>ISSN: 0920-3206</identifier><identifier>EISSN: 1573-7241</identifier><identifier>DOI: 10.1023/A:1007788915732</identifier><identifier>PMID: 9140694</identifier><identifier>CODEN: CDTHET</identifier><language>eng</language><publisher>Dordrecht: Springer</publisher><subject>Altitude Sickness - physiopathology ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Animals ; Antihypertensive agents ; Biological and medical sciences ; Body Weight - drug effects ; Body Weight - physiology ; Cardiovascular system ; Chronic Disease ; Collagen - metabolism ; Enalapril - therapeutic use ; Hemodynamics - drug effects ; Hydroxyproline - metabolism ; Hypertension, Pulmonary - drug therapy ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - physiopathology ; Hypertrophy, Right Ventricular - drug therapy ; Hypertrophy, Right Ventricular - physiopathology ; Hypoxia - complications ; Hypoxia - physiopathology ; Male ; Medical sciences ; Myocardium - metabolism ; Organ Size - drug effects ; Organ Size - physiology ; Pharmacology. 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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.</description><subject>Altitude Sickness - physiopathology</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Animals</subject><subject>Antihypertensive agents</subject><subject>Biological and medical sciences</subject><subject>Body Weight - drug effects</subject><subject>Body Weight - physiology</subject><subject>Cardiovascular system</subject><subject>Chronic Disease</subject><subject>Collagen - metabolism</subject><subject>Enalapril - therapeutic use</subject><subject>Hemodynamics - drug effects</subject><subject>Hydroxyproline - metabolism</subject><subject>Hypertension, Pulmonary - drug therapy</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Hypertrophy, Right Ventricular - drug therapy</subject><subject>Hypertrophy, Right Ventricular - physiopathology</subject><subject>Hypoxia - complications</subject><subject>Hypoxia - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardium - metabolism</subject><subject>Organ Size - drug effects</subject><subject>Organ Size - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pulmonary Fibrosis - drug therapy</subject><subject>Pulmonary Fibrosis - etiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Space life sciences</subject><issn>0920-3206</issn><issn>1573-7241</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><recordid>eNo9kD1PwzAQhi0EKqUwMyF5QEwNnO00ybFVVfmQKiEhmCvHsVuj1A52gujEXycVEdMNz3Mf7xFyyeCWARd383sGkOdFgWyWC35Exoea5Dxlx2QMyCERHLJTchbjB_QqYjEiI2QpZJiOyc-r3gQdo_WOekPVNnhnFd3uG_9tZWJd1Sld0aard97JsD8QHVrtDh1TGuxm29Iv7dpgVVfLMPDgm-1-SqWrqLFl8NFGek-XxmjVHvZoJ2vZBFufkxMj66gvhjoh7w_Lt8VTsnp5fF7MV4niBWuTEiRiHyxTKVaY4mxWGYEIM64qyTVoqUVVlnlpCshYmho0IAAyYKXATKRiQm7-5jbBf3Y6tuudjUrXtXTad3GdF4g5FrwXrwaxK3e6WvdH7vrc6-FjPb8euIxK1iZIp2z813iWASIXv_jrfEk</recordid><startdate>19970401</startdate><enddate>19970401</enddate><creator>PELOUCH, V</creator><creator>KOLAR, F</creator><creator>OST'ADAL, B</creator><creator>MILEROVA, M</creator><creator>CIHAK, R</creator><creator>WIDIMSKY, J</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19970401</creationdate><title>Regression of chronic hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and fibrosis : Effect of enalapril</title><author>PELOUCH, V ; KOLAR, F ; OST'ADAL, B ; MILEROVA, M ; CIHAK, R ; WIDIMSKY, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c281t-b0a995736c49d94955df399052cda2e0eae3dbb7bf806144f9f0300601b396343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Altitude Sickness - physiopathology</topic><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>Animals</topic><topic>Antihypertensive agents</topic><topic>Biological and medical sciences</topic><topic>Body Weight - drug effects</topic><topic>Body Weight - physiology</topic><topic>Cardiovascular system</topic><topic>Chronic Disease</topic><topic>Collagen - metabolism</topic><topic>Enalapril - therapeutic use</topic><topic>Hemodynamics - drug effects</topic><topic>Hydroxyproline - metabolism</topic><topic>Hypertension, Pulmonary - drug therapy</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>Hypertrophy, Right Ventricular - drug therapy</topic><topic>Hypertrophy, Right Ventricular - physiopathology</topic><topic>Hypoxia - complications</topic><topic>Hypoxia - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardium - metabolism</topic><topic>Organ Size - drug effects</topic><topic>Organ Size - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pulmonary Fibrosis - drug therapy</topic><topic>Pulmonary Fibrosis - etiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Space life sciences</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PELOUCH, V</creatorcontrib><creatorcontrib>KOLAR, F</creatorcontrib><creatorcontrib>OST'ADAL, B</creatorcontrib><creatorcontrib>MILEROVA, M</creatorcontrib><creatorcontrib>CIHAK, R</creatorcontrib><creatorcontrib>WIDIMSKY, J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular drugs and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>PELOUCH, V</au><au>KOLAR, F</au><au>OST'ADAL, B</au><au>MILEROVA, M</au><au>CIHAK, R</au><au>WIDIMSKY, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regression of chronic hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and fibrosis : Effect of enalapril</atitle><jtitle>Cardiovascular drugs and therapy</jtitle><addtitle>Cardiovasc Drugs Ther</addtitle><date>1997-04-01</date><risdate>1997</risdate><volume>11</volume><issue>2</issue><spage>177</spage><epage>185</epage><pages>177-185</pages><issn>0920-3206</issn><eissn>1573-7241</eissn><coden>CDTHET</coden><abstract>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.</abstract><cop>Dordrecht</cop><pub>Springer</pub><pmid>9140694</pmid><doi>10.1023/A:1007788915732</doi><tpages>9</tpages></addata></record> |
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subjects | Altitude Sickness - physiopathology Angiotensin-Converting Enzyme Inhibitors - therapeutic use Animals Antihypertensive agents Biological and medical sciences Body Weight - drug effects Body Weight - physiology Cardiovascular system Chronic Disease Collagen - metabolism Enalapril - therapeutic use Hemodynamics - drug effects Hydroxyproline - metabolism Hypertension, Pulmonary - drug therapy Hypertension, Pulmonary - etiology Hypertension, Pulmonary - physiopathology Hypertrophy, Right Ventricular - drug therapy Hypertrophy, Right Ventricular - physiopathology Hypoxia - complications Hypoxia - physiopathology Male Medical sciences Myocardium - metabolism Organ Size - drug effects Organ Size - physiology Pharmacology. Drug treatments Pulmonary Fibrosis - drug therapy Pulmonary Fibrosis - etiology Rats Rats, Wistar Space life sciences |
title | Regression of chronic hypoxia-induced pulmonary hypertension, right ventricular hypertrophy, and fibrosis : Effect of enalapril |
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