Pharmacologic modulation of PAF-induced mortality in mice
Identifieur interne : 001681 ( Istex/Corpus ); précédent : 001680; suivant : 001682Pharmacologic modulation of PAF-induced mortality in mice
Auteurs : R. P. Carlson ; L. O'Neill-Davis ; J. ChangSource :
- Agents and Actions [ 0065-4299 ] ; 1987-08-01.
English descriptors
- Teeft :
- Antagonist, Antioxidant, Antioxidant activity, Dapsone, Diphenyldisulfide, Dose survival, Drug class, Indomethacin, Inhibitor, Inhibitory activity, Isobutylmethylxanthine, Kadsurenone, Lethality, Leukotriene, Mediator antagonists, Mortality model, Ndga, Pharmacologic, Pla2 inhibitor, Platelet, Specific inhibitors, Steroid, Survival rate, Uricosuric agent.
Abstract
Abstract: The effect of antiinflammatory drugs, phosphodiesterase inhibitors, leukotriene and mediator antagonists and other drug classes were evaluated in a PAF-induced mortality model in mice. By the oral route of administration (−1 hr), dapsone (ED50=25 mg/kg), BW 755C (ED50=29 mg/kg), theophylline (ED50=30 mg/kg) and LY-171,883 (ED50=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.
Url:
DOI: 10.1007/BF01966521
Links to Exploration step
ISTEX:C57AAFF52790233C7BEFC59181C7EC1740150BFBLe document en format XML
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Carlson</name><affiliation><mods:affiliation>Immunopharmacology Subdivision, Division of Experimental Therapeutics, Wyeth Laboratories, Inc., P.O. Box 8299, 19101, Philadelphia, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="O Neill Davis, L" sort="O Neill Davis, L" uniqKey="O Neill Davis L" first="L." last="O'Neill-Davis">L. O'Neill-Davis</name><affiliation><mods:affiliation>Immunopharmacology Subdivision, Division of Experimental Therapeutics, Wyeth Laboratories, Inc., P.O. Box 8299, 19101, Philadelphia, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Chang, J" sort="Chang, J" uniqKey="Chang J" first="J." last="Chang">J. Chang</name><affiliation><mods:affiliation>Immunopharmacology Subdivision, Division of Experimental Therapeutics, Wyeth Laboratories, Inc., P.O. 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By the oral route of administration (−1 hr), dapsone (ED50=25 mg/kg), BW 755C (ED50=29 mg/kg), theophylline (ED50=30 mg/kg) and LY-171,883 (ED50=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.</div></front></TEI><istex><corpusName>springer-journals</corpusName><keywords><teeft><json:string>inhibitor</json:string><json:string>pharmacologic</json:string><json:string>antioxidant</json:string><json:string>diphenyldisulfide</json:string><json:string>dapsone</json:string><json:string>isobutylmethylxanthine</json:string><json:string>ndga</json:string><json:string>kadsurenone</json:string><json:string>leukotriene</json:string><json:string>platelet</json:string><json:string>indomethacin</json:string><json:string>antioxidant activity</json:string><json:string>mortality model</json:string><json:string>survival rate</json:string><json:string>inhibitory activity</json:string><json:string>lethality</json:string><json:string>mediator antagonists</json:string><json:string>dose survival</json:string><json:string>specific inhibitors</json:string><json:string>uricosuric agent</json:string><json:string>pla2 inhibitor</json:string><json:string>drug class</json:string><json:string>antagonist</json:string><json:string>steroid</json:string></teeft></keywords><author><json:item><name>R. 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Box 8299, 19101, Philadelphia, PA, USA</affiliation></author><idno type="istex">C57AAFF52790233C7BEFC59181C7EC1740150BFB</idno><idno type="ark">ark:/67375/1BB-R47J7Q39-Q</idno><idno type="DOI">10.1007/BF01966521</idno><idno type="article-id">BF01966521</idno><idno type="article-id">Art48</idno></analytic><monogr><title level="j">Agents and Actions</title><title level="j" type="abbrev">Agents and Actions</title><idno type="pISSN">0065-4299</idno><idno type="eISSN">1420-908X</idno><idno type="journal-ID">true</idno><idno type="issue-article-count">55</idno><idno type="volume-issue-count">4</idno><imprint><publisher>Birkhäuser-Verlag</publisher><pubPlace>Basel</pubPlace><date type="published" when="1987-08-01"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">3-4</biblScope><biblScope unit="page" from="379">379</biblScope><biblScope unit="page" to="381">381</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1987</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The effect of antiinflammatory drugs, phosphodiesterase inhibitors, leukotriene and mediator antagonists and other drug classes were evaluated in a PAF-induced mortality model in mice. By the oral route of administration (−1 hr), dapsone (ED50=25 mg/kg), BW 755C (ED50=29 mg/kg), theophylline (ED50=30 mg/kg) and LY-171,883 (ED50=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Immunology</term></item><item><term>Pharmacology/Toxicology</term></item><item><term>Allergology</term></item><item><term>Dermatology</term></item><item><term>Neurology</term></item><item><term>Rheumatology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1987-08-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-R47J7Q39-Q/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Birkhäuser-Verlag</PublisherName><PublisherLocation>Basel</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>11</JournalID><JournalPrintISSN>0065-4299</JournalPrintISSN><JournalElectronicISSN>1420-908X</JournalElectronicISSN><JournalTitle>Agents and Actions</JournalTitle><JournalAbbreviatedTitle>Agents and Actions</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Biomedicine</JournalSubject><JournalSubject Type="Secondary">Immunology</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Allergology</JournalSubject><JournalSubject Type="Secondary">Dermatology</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject><JournalSubject Type="Secondary">Rheumatology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>21</VolumeIDStart><VolumeIDEnd>21</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Combined"><IssueInfo TocLevels="0"><IssueIDStart>3</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueArticleCount>55</IssueArticleCount><IssueHistory><CoverDate><Year>1987</Year><Month>8</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Birkhäuser-Verlag</CopyrightHolderName><CopyrightYear>1987</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art48"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01966521</ArticleID><ArticleDOI>10.1007/BF01966521</ArticleDOI><ArticleSequenceNumber>48</ArticleSequenceNumber><ArticleTitle Language="En">Pharmacologic modulation of PAF-induced mortality in mice</ArticleTitle><ArticleCategory>Mediators of Acute Inflammation</ArticleCategory><ArticleFirstPage>379</ArticleFirstPage><ArticleLastPage>381</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>7</Month><Day>5</Day></RegistrationDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Birkhäuser Verlag</CopyrightHolderName><CopyrightYear>1987</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>11</JournalID><VolumeIDStart>21</VolumeIDStart><VolumeIDEnd>21</VolumeIDEnd><IssueIDStart>3</IssueIDStart><IssueIDEnd>4</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>R.</GivenName><GivenName>P.</GivenName><FamilyName>Carlson</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>L.</GivenName><FamilyName>O'Neill-Davis</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>J.</GivenName><FamilyName>Chang</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Immunopharmacology Subdivision, Division of Experimental Therapeutics</OrgDivision><OrgName>Wyeth Laboratories, Inc.</OrgName><OrgAddress><Postbox>P.O. Box 8299</Postbox><Postcode>19101</Postcode><City>Philadelphia</City><State>PA</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>The effect of antiinflammatory drugs, phosphodiesterase inhibitors, leukotriene and mediator antagonists and other drug classes were evaluated in a PAF-induced mortality model in mice. By the oral route of administration (−1 hr), dapsone (ED<Subscript>50</Subscript>=25 mg/kg), BW 755C (ED<Subscript>50</Subscript>=29 mg/kg), theophylline (ED<Subscript>50</Subscript>=30 mg/kg) and LY-171,883 (ED<Subscript>50</Subscript>=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.</Para></Abstract></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Pharmacologic modulation of PAF-induced mortality in mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Pharmacologic modulation of PAF-induced mortality in mice</title></titleInfo><name type="personal"><namePart type="given">R.</namePart><namePart type="given">P.</namePart><namePart type="family">Carlson</namePart><affiliation>Immunopharmacology Subdivision, Division of Experimental Therapeutics, Wyeth Laboratories, Inc., P.O. Box 8299, 19101, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">O'Neill-Davis</namePart><affiliation>Immunopharmacology Subdivision, Division of Experimental Therapeutics, Wyeth Laboratories, Inc., P.O. Box 8299, 19101, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Chang</namePart><affiliation>Immunopharmacology Subdivision, Division of Experimental Therapeutics, Wyeth Laboratories, Inc., P.O. Box 8299, 19101, Philadelphia, PA, 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>Birkhäuser-Verlag</publisher><place><placeTerm type="text">Basel</placeTerm></place><dateIssued encoding="w3cdtf">1987-08-01</dateIssued><copyrightDate encoding="w3cdtf">1987</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: The effect of antiinflammatory drugs, phosphodiesterase inhibitors, leukotriene and mediator antagonists and other drug classes were evaluated in a PAF-induced mortality model in mice. By the oral route of administration (−1 hr), dapsone (ED50=25 mg/kg), BW 755C (ED50=29 mg/kg), theophylline (ED50=30 mg/kg) and LY-171,883 (ED50=50 mg/kg) protected against PAF-induced lethality in the mouse. Other drugs that afforded protection when given at various dosing schedules and routes were NDGA (100 mg/kg, −18 hr p.o.), diphenyldisulfide (200 mg/kg, −18 hr p.o.), dexamethasone (1 mg/kg, −3 hr p.o.), dipyridamole (2 mg/kg, −2 min i.v.) and kadsurenone (10 mg/kg, −2 min i.v.). Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin were inactive and the combination of AA-861, a putative 5-LO inhibitor, and indomethacin also failed to prevent PAF-induced lethality. Therefore, our pharmacological data do not consistently support the notion that PAF-induced lethality is due unequivocally to leukotrienes derived from 5-lipoxygenase metabolism.</abstract><note>Mediators of Acute Inflammation</note><relatedItem type="host"><titleInfo><title>Agents and Actions</title></titleInfo><titleInfo type="abbreviated"><title>Agents and Actions</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">1987-08-01</dateIssued><copyrightDate encoding="w3cdtf">1987</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Immunology</topic><topic>Pharmacology/Toxicology</topic><topic>Allergology</topic><topic>Dermatology</topic><topic>Neurology</topic><topic>Rheumatology</topic></subject><identifier type="ISSN">0065-4299</identifier><identifier type="eISSN">1420-908X</identifier><identifier type="JournalID">11</identifier><identifier type="IssueArticleCount">55</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>1987</date><detail type="volume"><number>21</number><caption>vol.</caption></detail><detail type="issue"><number>3-4</number><caption>no.</caption></detail><extent unit="pages"><start>379</start><end>381</end></extent></part><recordInfo><recordOrigin>Birkhäuser-Verlag, 1987</recordOrigin></recordInfo></relatedItem><identifier type="istex">C57AAFF52790233C7BEFC59181C7EC1740150BFB</identifier><identifier type="ark">ark:/67375/1BB-R47J7Q39-Q</identifier><identifier type="DOI">10.1007/BF01966521</identifier><identifier type="ArticleID">BF01966521</identifier><identifier type="ArticleID">Art48</identifier><accessCondition type="use and reproduction" contentType="copyright">Birkhäuser Verlag, 1987</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>Birkhäuser Verlag, 1987</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-R47J7Q39-Q/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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