Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro
Identifieur interne : 003158 ( Main/Exploration ); précédent : 003157; suivant : 003159Role 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 [États-Unis] ; Elisabeth J. Jellison [États-Unis]Source :
- 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
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 000559
- to stream Istex, to step Curation: 000559
- to stream Istex, to step Checkpoint: 001F23
- to stream Main, to step Merge: 003227
- to stream Main, to step Curation: 003158
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro</title><author><name sortKey="Hostetler, Karl Y" sort="Hostetler, Karl Y" uniqKey="Hostetler K" first="Karl Y." last="Hostetler">Karl Y. Hostetler</name></author><author><name sortKey="Jellison, Elisabeth J" sort="Jellison, Elisabeth J" uniqKey="Jellison E" first="Elisabeth J." last="Jellison">Elisabeth J. Jellison</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:EA37684158568840D829D8AC209C2F3BBEDB0D75</idno><date when="1989" year="1989">1989</date><idno type="doi">10.1007/BF00223427</idno><idno type="url">https://api.istex.fr/ark:/67375/1BB-BV3HXKT6-G/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000559</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000559</idno><idno type="wicri:Area/Istex/Curation">000559</idno><idno type="wicri:Area/Istex/Checkpoint">001F23</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001F23</idno><idno type="wicri:doubleKey">0300-8177:1989:Hostetler K:role:of:phospholipases</idno><idno type="wicri:Area/Main/Merge">003227</idno><idno type="wicri:Area/Main/Curation">003158</idno><idno type="wicri:Area/Main/Exploration">003158</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro</title><author><name sortKey="Hostetler, Karl Y" sort="Hostetler, Karl Y" uniqKey="Hostetler K" first="Karl Y." last="Hostetler">Karl Y. Hostetler</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">San Diego</settlement><region type="state">Californie</region></placeName><wicri:orgArea>The department of Medicine, Division of Endocrinology and Metabolism, University of California</wicri:orgArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Veterans Administration Medical Center, 92161, San Diego, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Jellison, Elisabeth J" sort="Jellison, Elisabeth J" uniqKey="Jellison E" first="Elisabeth J." last="Jellison">Elisabeth J. Jellison</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">San Diego</settlement><region type="state">Californie</region></placeName><wicri:orgArea>The department of Medicine, Division of Endocrinology and Metabolism, University of California</wicri:orgArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Veterans Administration Medical Center, 92161, San Diego, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Molecular and Cellular Biochemistry</title><title level="j" type="sub">An International Journal for Chemical Biology in Health and Disease</title><title level="j" type="abbrev">Mol Cell Biochem</title><idno type="ISSN">0300-8177</idno><idno type="eISSN">1573-4919</idno><imprint><publisher>Kluwer Academic Publishers</publisher><pubPlace>Dordrecht</pubPlace><date type="published" when="1989-03-01">1989-03-01</date><biblScope unit="volume">88</biblScope><biblScope unit="issue">1-2</biblScope><biblScope unit="page" from="77">77</biblScope><biblScope unit="page" to="82">82</biblScope></imprint><idno type="ISSN">0300-8177</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-8177</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>RS-87337</term><term>chloroquine</term><term>chlorpromazine</term><term>cytosol</term><term>diltiazem</term><term>heart</term><term>mepacrine</term><term>phospholipase A</term><term>rat</term><term>sarcoplasmic reticulum</term><term>verapamil</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Biochim biophys acta</term><term>Cardioprotective</term><term>Cardioprotective agents</term><term>Chloroquine</term><term>Chlorpromazine</term><term>Cytosol</term><term>Cytosolic</term><term>Cytosolic phospholipase</term><term>Diltiazem</term><term>Effective inhibitor</term><term>Experimental ischemia</term><term>Fatty acids</term><term>Heart cytosol</term><term>Heart phospholipases</term><term>Hostetler</term><term>Inhibitor</term><term>Ischemia</term><term>Ischemic</term><term>Lysosomal phospholipase</term><term>Mepacrine</term><term>Myocardial ischemia</term><term>Myocardium</term><term>Phospholipase</term><term>Phospholipases</term><term>Phospholipid</term><term>Phospholipid degradation</term><term>Reticulum</term><term>Sarcoplasmic</term><term>Sarcoplasmic reticulum</term><term>Sarcoplasmic reticulum phospholipase</term><term>Verapamil</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region><settlement><li>San Diego</li></settlement></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Hostetler, Karl Y" sort="Hostetler, Karl Y" uniqKey="Hostetler K" first="Karl Y." last="Hostetler">Karl Y. Hostetler</name></region><name sortKey="Hostetler, Karl Y" sort="Hostetler, Karl Y" uniqKey="Hostetler K" first="Karl Y." last="Hostetler">Karl Y. Hostetler</name><name sortKey="Jellison, Elisabeth J" sort="Jellison, Elisabeth J" uniqKey="Jellison E" first="Elisabeth J." last="Jellison">Elisabeth J. Jellison</name><name sortKey="Jellison, Elisabeth J" sort="Jellison, Elisabeth J" uniqKey="Jellison E" first="Elisabeth J." last="Jellison">Elisabeth J. Jellison</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003158 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 003158 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:EA37684158568840D829D8AC209C2F3BBEDB0D75
|texte= Role of phospholipases in myocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro
}}
| This area was generated with Dilib version V0.6.33. |  |