Oxidative stress and heart failure
Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogene...
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Veröffentlicht in: | Molecular and cellular biochemistry 1995-06, Vol.147 (1/2), p.77-81 |
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creator | Singh, N Dhalla, A.K Seneviratne, C Singal, P.K |
description | Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent. |
doi_str_mv | 10.1007/BF00944786 |
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Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/BF00944786</identifier><identifier>PMID: 7494558</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Animals ; antioxidants ; Antioxidants - metabolism ; Cardiomegaly - metabolism ; Cardiomegaly - pathology ; free radicals ; Free Radicals - metabolism ; guinea pigs ; heart diseases ; Heart Failure - metabolism ; Heart Failure - pathology ; Heart Failure - physiopathology ; hypertrophy ; lipid peroxidation ; Microscopy, Electron ; Myocardium - metabolism ; Myocardium - ultrastructure ; oxidation ; Oxidative Stress ; rats ; stress ; Superoxide Dismutase - metabolism</subject><ispartof>Molecular and cellular biochemistry, 1995-06, Vol.147 (1/2), p.77-81</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</citedby><cites>FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7494558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Singh, N</creatorcontrib><creatorcontrib>Dhalla, A.K</creatorcontrib><creatorcontrib>Seneviratne, C</creatorcontrib><creatorcontrib>Singal, P.K</creatorcontrib><title>Oxidative stress and heart failure</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.</description><subject>Animals</subject><subject>antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomegaly - pathology</subject><subject>free radicals</subject><subject>Free Radicals - metabolism</subject><subject>guinea pigs</subject><subject>heart diseases</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - pathology</subject><subject>Heart Failure - physiopathology</subject><subject>hypertrophy</subject><subject>lipid peroxidation</subject><subject>Microscopy, Electron</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - ultrastructure</subject><subject>oxidation</subject><subject>Oxidative Stress</subject><subject>rats</subject><subject>stress</subject><subject>Superoxide Dismutase - metabolism</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LAzEQhoMotVYv3sXFgwdhdWaTbJKjFqtCoQftOaT50JVttya7ov_elS46l4F5H16Gh5BThGsEEDd3MwDFmJDlHhkjFzRnCtU-GQMFyCUKcUiOUnoH6HHEERkJphjnckwuFl-VM2316bPURp9SZjYue_MmtlkwVd1Ff0wOgqmTPxn2hCxn9y_Tx3y-eHia3s5zS6Fsc2VUCMoZjwhlQOmZ6g-WWQUFXZWMcee4kZajFZRKzhRnpXUKnC0C45JOyOWudxubj86nVq-rZH1dm41vuqRFP1go0YNXO9DGJqXog97Gam3it0bQv0L0v5AePhtau9Xauz90MNDn57s8mEab11glvXwuACkgB9F_TX8AGyFhzA</recordid><startdate>19950607</startdate><enddate>19950607</enddate><creator>Singh, N</creator><creator>Dhalla, A.K</creator><creator>Seneviratne, C</creator><creator>Singal, P.K</creator><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19950607</creationdate><title>Oxidative stress and heart failure</title><author>Singh, N ; Dhalla, A.K ; Seneviratne, C ; Singal, P.K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomegaly - pathology</topic><topic>free radicals</topic><topic>Free Radicals - metabolism</topic><topic>guinea pigs</topic><topic>heart diseases</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - pathology</topic><topic>Heart Failure - physiopathology</topic><topic>hypertrophy</topic><topic>lipid peroxidation</topic><topic>Microscopy, Electron</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - ultrastructure</topic><topic>oxidation</topic><topic>Oxidative Stress</topic><topic>rats</topic><topic>stress</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Singh, N</creatorcontrib><creatorcontrib>Dhalla, A.K</creatorcontrib><creatorcontrib>Seneviratne, C</creatorcontrib><creatorcontrib>Singal, P.K</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Singh, N</au><au>Dhalla, A.K</au><au>Seneviratne, C</au><au>Singal, P.K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress and heart failure</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>1995-06-07</date><risdate>1995</risdate><volume>147</volume><issue>1/2</issue><spage>77</spage><epage>81</epage><pages>77-81</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.</abstract><cop>Netherlands</cop><pmid>7494558</pmid><doi>10.1007/BF00944786</doi><tpages>5</tpages></addata></record> |
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subjects | Animals antioxidants Antioxidants - metabolism Cardiomegaly - metabolism Cardiomegaly - pathology free radicals Free Radicals - metabolism guinea pigs heart diseases Heart Failure - metabolism Heart Failure - pathology Heart Failure - physiopathology hypertrophy lipid peroxidation Microscopy, Electron Myocardium - metabolism Myocardium - ultrastructure oxidation Oxidative Stress rats stress Superoxide Dismutase - metabolism |
title | Oxidative stress and heart failure |
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