Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro
Identifieur interne : 000559 ( Istex/Corpus ); précédent : 000558; suivant : 000560Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro
Auteurs : Karl Y. Hostetler ; Elisabeth J. JellisonSource :
- Molecular and Cellular Biochemistry [ 0300-8177 ] ; 1989-03-01.
English descriptors
- KwdEn :
- Teeft :
- Biochim biophys acta, Cardioprotective, Cardioprotective agents, Chloroquine, Chlorpromazine, Cytosol, Cytosolic, Cytosolic phospholipase, Diltiazem, Effective inhibitor, Experimental ischemia, Fatty acids, Heart cytosol, Heart phospholipases, Hostetler, Inhibitor, Ischemia, Ischemic, Lysosomal phospholipase, Mepacrine, Myocardial ischemia, Myocardium, Phospholipase, Phospholipases, Phospholipid, Phospholipid degradation, Reticulum, Sarcoplasmic, Sarcoplasmic reticulum, Sarcoplasmic reticulum phospholipase, Verapamil.
Abstract
Abstract: Increased breakdown of myocardial phospholipids to fatty acids and lysophosphoglycerides is an early feature of myocardial ischemic injury and many investigators believe that enhanced phospholipase action is an important factor in the process. Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. Most of the cardioprotective agents studied inhibited the heart phospholipases in vitro, providing further evidence that phospholipid degradation in ischemic myocardial injury may be modulated by pharmacologic agents.
Url:
DOI: 10.1007/BF00223427
Links to Exploration step
ISTEX:EA37684158568840D829D8AC209C2F3BBEDB0D75Le document en format XML
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Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. 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Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. 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Paper</ArticleCategory><ArticleFirstPage>77</ArticleFirstPage><ArticleLastPage>82</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>7</Month><Day>21</Day></RegistrationDate><Accepted><Year>1988</Year><Month>12</Month><Day>28</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Kluwer Academic Publishers</CopyrightHolderName><CopyrightYear>1989</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>11010</JournalID><VolumeIDStart>88</VolumeIDStart><VolumeIDEnd>88</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>2</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1 Aff2"><AuthorName DisplayOrder="Western"><GivenName>Karl</GivenName><GivenName>Y.</GivenName><FamilyName>Hostetler</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1 Aff2"><AuthorName DisplayOrder="Western"><GivenName>Elisabeth</GivenName><GivenName>J.</GivenName><FamilyName>Jellison</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>The department of Medicine, Division of Endocrinology and Metabolism</OrgDivision><OrgName>University of California</OrgName><OrgAddress><City>San Diego</City></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>Veterans Administration Medical Center</OrgName><OrgAddress><Postcode>92161</Postcode><City>San Diego</City><State>California</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Increased breakdown of myocardial phospholipids to fatty acids and lysophosphoglycerides is an early feature of myocardial ischemic injury and many investigators believe that enhanced phospholipase action is an important factor in the process. Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown <Emphasis Type="Italic">in vivo</Emphasis>. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. Most of the cardioprotective agents studied inhibited the heart phospholipases <Emphasis Type="Italic">in vitro</Emphasis>, providing further evidence that phospholipid degradation in ischemic myocardial injury may be modulated by pharmacologic agents.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>rat</Keyword><Keyword>heart</Keyword><Keyword>phospholipase A</Keyword><Keyword>mepacrine</Keyword><Keyword>verapamil</Keyword><Keyword>chloroquine</Keyword><Keyword>diltiazem</Keyword><Keyword>chlorpromazine</Keyword><Keyword>RS-87337</Keyword><Keyword>sarcoplasmic reticulum</Keyword><Keyword>cytosol</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro</title></titleInfo><name type="personal"><namePart type="given">Karl</namePart><namePart type="given">Y.</namePart><namePart type="family">Hostetler</namePart><affiliation>The department of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego</affiliation><affiliation>Veterans Administration Medical Center, 92161, San Diego, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elisabeth</namePart><namePart type="given">J.</namePart><namePart type="family">Jellison</namePart><affiliation>The department of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego</affiliation><affiliation>Veterans Administration Medical Center, 92161, San Diego, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Kluwer Academic Publishers</publisher><place><placeTerm type="text">Dordrecht</placeTerm></place><dateIssued encoding="w3cdtf">1989-03-01</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Increased breakdown of myocardial phospholipids to fatty acids and lysophosphoglycerides is an early feature of myocardial ischemic injury and many investigators believe that enhanced phospholipase action is an important factor in the process. Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. Most of the cardioprotective agents studied inhibited the heart phospholipases in vitro, providing further evidence that phospholipid degradation in ischemic myocardial injury may be modulated by pharmacologic agents.</abstract><note>Invited Paper</note><subject lang="en"><genre>Key words</genre><topic>rat</topic><topic>heart</topic><topic>phospholipase A</topic><topic>mepacrine</topic><topic>verapamil</topic><topic>chloroquine</topic><topic>diltiazem</topic><topic>chlorpromazine</topic><topic>RS-87337</topic><topic>sarcoplasmic reticulum</topic><topic>cytosol</topic></subject><relatedItem type="host"><titleInfo><title>Molecular and Cellular Biochemistry</title><subTitle>An International Journal for Chemical Biology in Health and Disease</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mol Cell Biochem</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">1989-03-01</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><subject><genre>Life Sciences</genre><topic>Cardiology</topic><topic>Medical Biochemistry</topic><topic>Oncology</topic><topic>Biochemistry, general</topic></subject><identifier type="ISSN">0300-8177</identifier><identifier type="eISSN">1573-4919</identifier><identifier type="JournalID">11010</identifier><identifier type="IssueArticleCount">30</identifier><identifier type="VolumeIssueCount">2</identifier><part><date>1989</date><detail type="volume"><number>88</number><caption>vol.</caption></detail><detail type="issue"><number>1-2</number><caption>no.</caption></detail><extent unit="pages"><start>77</start><end>82</end></extent></part><recordInfo><recordOrigin>Kluwer Academic Publishers, 1989</recordOrigin></recordInfo></relatedItem><identifier type="istex">EA37684158568840D829D8AC209C2F3BBEDB0D75</identifier><identifier type="ark">ark:/67375/1BB-BV3HXKT6-G</identifier><identifier type="DOI">10.1007/BF00223427</identifier><identifier type="ArticleID">BF00223427</identifier><identifier type="ArticleID">Art12</identifier><accessCondition type="use and reproduction" contentType="copyright">Kluwer Academic Publishers, 1989</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Kluwer Academic Publishers, 1989</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-BV3HXKT6-G/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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