In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction
The in vivo production of prostacyclin and thromboxane was monitored by measuring their major urinary metabolites 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in ten patients with acute myocardial infarction, five on standard treatment and five receiving prostacyclin infusion...
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| Veröffentlicht in: | British Heart Journal 1986-06, Vol.55 (6), p.543-548 |
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| container_title | British Heart Journal |
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| creator | Henriksson, P Wennmalm, A Edhag, O Vesterqvist, O Green, K |
| description | The in vivo production of prostacyclin and thromboxane was monitored by measuring their major urinary metabolites 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in ten patients with acute myocardial infarction, five on standard treatment and five receiving prostacyclin infusion. During acute myocardial infarction excretion of 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha, measured by a gas chromatography-mass spectrometry method with deuterated internal standards, was significantly increased. This indicates that thromboxane and prostacyclin synthesis are increased during the development of acute myocardial infarction. The excretion data for 2,3-dinor-thromboxane B2 showed that after administration of aspirin there was less pronounced and more variable inhibition than expected. Prostacyclin infusion did not markedly affect the excretion of the thromboxane metabolite. |
| doi_str_mv | 10.1136/hrt.55.6.543 |
| format | Article |
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During acute myocardial infarction excretion of 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha, measured by a gas chromatography-mass spectrometry method with deuterated internal standards, was significantly increased. This indicates that thromboxane and prostacyclin synthesis are increased during the development of acute myocardial infarction. The excretion data for 2,3-dinor-thromboxane B2 showed that after administration of aspirin there was less pronounced and more variable inhibition than expected. Prostacyclin infusion did not markedly affect the excretion of the thromboxane metabolite.</description><identifier>ISSN: 0007-0769</identifier><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>EISSN: 2053-5864</identifier><identifier>DOI: 10.1136/hrt.55.6.543</identifier><identifier>PMID: 3521690</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>6-Ketoprostaglandin F1 alpha - analogs & derivatives ; 6-Ketoprostaglandin F1 alpha - urine ; Epoprostenol - administration & dosage ; Epoprostenol - biosynthesis ; Humans ; Infusions, Parenteral ; Myocardial Infarction - metabolism ; Myocardial Infarction - urine ; Thromboxane B2 - analogs & derivatives ; Thromboxane B2 - urine ; Thromboxanes - biosynthesis</subject><ispartof>British Heart Journal, 1986-06, Vol.55 (6), p.543-548</ispartof><rights>Copyright BMJ Publishing Group LTD Jun 1986</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b3923-67387bfaaaaa131a8ded2e6ee8d672a5509d83f9984b8fc2f76b9473fa9fbe083</citedby><cites>FETCH-LOGICAL-b3923-67387bfaaaaa131a8ded2e6ee8d672a5509d83f9984b8fc2f76b9473fa9fbe083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1236759/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1236759/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3521690$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Henriksson, P</creatorcontrib><creatorcontrib>Wennmalm, A</creatorcontrib><creatorcontrib>Edhag, O</creatorcontrib><creatorcontrib>Vesterqvist, O</creatorcontrib><creatorcontrib>Green, K</creatorcontrib><title>In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction</title><title>British Heart Journal</title><addtitle>Br Heart J</addtitle><description>The in vivo production of prostacyclin and thromboxane was monitored by measuring their major urinary metabolites 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in ten patients with acute myocardial infarction, five on standard treatment and five receiving prostacyclin infusion. During acute myocardial infarction excretion of 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha, measured by a gas chromatography-mass spectrometry method with deuterated internal standards, was significantly increased. This indicates that thromboxane and prostacyclin synthesis are increased during the development of acute myocardial infarction. The excretion data for 2,3-dinor-thromboxane B2 showed that after administration of aspirin there was less pronounced and more variable inhibition than expected. Prostacyclin infusion did not markedly affect the excretion of the thromboxane metabolite.</description><subject>6-Ketoprostaglandin F1 alpha - analogs & derivatives</subject><subject>6-Ketoprostaglandin F1 alpha - urine</subject><subject>Epoprostenol - administration & dosage</subject><subject>Epoprostenol - biosynthesis</subject><subject>Humans</subject><subject>Infusions, Parenteral</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - urine</subject><subject>Thromboxane B2 - analogs & derivatives</subject><subject>Thromboxane B2 - urine</subject><subject>Thromboxanes - biosynthesis</subject><issn>0007-0769</issn><issn>1355-6037</issn><issn>1468-201X</issn><issn>2053-5864</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1vEzEQxS0EKqFw44pkCYle2GCv118XJBSVtlJVLlD1Znm9NnHYXae2NzT_PU4TRcChvljj99PzzDwA3mI0x5iwT8uY55TO2Zw25BmY4YaJqkb47jmYIYR4hTiTL8GrlFalbKRgJ-CE0BoziWZAXY1w4zcBrmPoJpN9GGFwuyplbbam9yPUYwfzMoahDQ96tLA8rXX2dswJ_vZ5CbWZsoXDNhgdO6_7QjgdH81egxdO98m-Odyn4MfX8--Ly-r628XV4st11RJZk4pxInjr9O5ggrXobFdbZq3oGK81pUh2gjgpRdMKZ2rHWSsbTpyWrrVIkFPwee-7ntrBdqY0F3Wv1tEPOm5V0F79q4x-qX6GjcI1YZzKYvDhYBDD_WRTVoNPxvZ9mThMSXEmBEdkB77_D1yFKY5lOIU5RxihsthCfdxTpmwyReuOrWCkdrGpEpuiVDFVYiv4u7_bP8KHnIpe7XWfsn04yjr-UmV1nKqb24VqJBaLu9tGXRT-bM-3w-rpn_8ADVqx_g</recordid><startdate>19860601</startdate><enddate>19860601</enddate><creator>Henriksson, P</creator><creator>Wennmalm, A</creator><creator>Edhag, O</creator><creator>Vesterqvist, O</creator><creator>Green, K</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19860601</creationdate><title>In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction</title><author>Henriksson, P ; Wennmalm, A ; Edhag, O ; Vesterqvist, O ; Green, K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b3923-67387bfaaaaa131a8ded2e6ee8d672a5509d83f9984b8fc2f76b9473fa9fbe083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>6-Ketoprostaglandin F1 alpha - analogs & derivatives</topic><topic>6-Ketoprostaglandin F1 alpha - urine</topic><topic>Epoprostenol - administration & dosage</topic><topic>Epoprostenol - biosynthesis</topic><topic>Humans</topic><topic>Infusions, Parenteral</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - urine</topic><topic>Thromboxane B2 - analogs & derivatives</topic><topic>Thromboxane B2 - urine</topic><topic>Thromboxanes - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Henriksson, P</creatorcontrib><creatorcontrib>Wennmalm, A</creatorcontrib><creatorcontrib>Edhag, O</creatorcontrib><creatorcontrib>Vesterqvist, O</creatorcontrib><creatorcontrib>Green, K</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British Heart Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Henriksson, P</au><au>Wennmalm, A</au><au>Edhag, O</au><au>Vesterqvist, O</au><au>Green, K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction</atitle><jtitle>British Heart Journal</jtitle><addtitle>Br Heart J</addtitle><date>1986-06-01</date><risdate>1986</risdate><volume>55</volume><issue>6</issue><spage>543</spage><epage>548</epage><pages>543-548</pages><issn>0007-0769</issn><issn>1355-6037</issn><eissn>1468-201X</eissn><eissn>2053-5864</eissn><abstract>The in vivo production of prostacyclin and thromboxane was monitored by measuring their major urinary metabolites 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in ten patients with acute myocardial infarction, five on standard treatment and five receiving prostacyclin infusion. During acute myocardial infarction excretion of 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha, measured by a gas chromatography-mass spectrometry method with deuterated internal standards, was significantly increased. This indicates that thromboxane and prostacyclin synthesis are increased during the development of acute myocardial infarction. The excretion data for 2,3-dinor-thromboxane B2 showed that after administration of aspirin there was less pronounced and more variable inhibition than expected. Prostacyclin infusion did not markedly affect the excretion of the thromboxane metabolite.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>3521690</pmid><doi>10.1136/hrt.55.6.543</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British Heart Journal, 1986-06, Vol.55 (6), p.543-548 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | 6-Ketoprostaglandin F1 alpha - analogs & derivatives 6-Ketoprostaglandin F1 alpha - urine Epoprostenol - administration & dosage Epoprostenol - biosynthesis Humans Infusions, Parenteral Myocardial Infarction - metabolism Myocardial Infarction - urine Thromboxane B2 - analogs & derivatives Thromboxane B2 - urine Thromboxanes - biosynthesis |
| title | In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction |
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