Amplification by Hyperoxia of Coronary Vasodilation Induced by Propofol
We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10–300 μM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (Pao2 = 137 ± 16 mm Hg, n = 12) or in the presence (Pao2 = 541 ± 138 mm Hg, n = 12) of hyperoxia....
Gespeichert in:
| Veröffentlicht in: | Anesthesia and analgesia 2004-03, Vol.98 (3), p.595-603 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 603 |
|---|---|
| container_issue | 3 |
| container_start_page | 595 |
| container_title | Anesthesia and analgesia |
| container_volume | 98 |
| creator | Ouattara, Alexandre Boccara, Gilles Lecomte, Patrick Souktani, Rachid Le Cosquer, Philippe Mouren, Stéphane Coriat, Pierre Riou, Bruno |
| description | We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10–300 μM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (Pao2 = 137 ± 16 mm Hg, n = 12) or in the presence (Pao2 = 541 ± 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (−13% ± 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 μM) and cromakalim (0.5 μM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (−16% ± 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 μM both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. |
| doi_str_mv | 10.1213/01.ANE.0000100681.15355.AC |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_04439746v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>80182055</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4767-109b77f5686f75115c56ddf9f0440c95e18e13f787bc86699e528b284f6cce5f3</originalsourceid><addsrcrecordid>eNpF0E2P0zAQBmALgdiy8BdQhAQSh4RxHH9xi6Jlu1IFHICr5Ti2GnDjYjcs_fe4TUV9sTx6ZsZ6EXqDocI1Jh8AV-3nuwrywQBM4ApTQmnVdk_QCtOalZxK8RStMiBlLaW8QS9S-nn2gj1HN7iRAiQ0K3Tf7vZ-dKPRhzFMRX8s1se9jeHvqIvgii7EMOl4LH7oFIbRL-phGmZjh5P-GsM-uOBfomdO-2RfXe5b9P3T3bduXW6-3D907aY0DWe8xCB7zh1lgjlOMaaGsmFw0kHTgJHUYmExcVzw3gjGpLS0Fn0tGseMsdSRW_R-mbvVXu3juMufU0GPat1u1KmWBxHJG_YHZ_tusfsYfs82HdRuTMZ6rycb5qQEYFEDpRl-XKCJIaVo3f_JGNQpcgVY5cjVNXJ1jly1XW5-fdky9zs7XFsvGWfw9gJ0Mtq7qCczpqujlLGaQHbN4h6DP9iYfvn50Ua1tdoftufVQIksa4AGSH6Upwon_wDen5ex</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>80182055</pqid></control><display><type>article</type><title>Amplification by Hyperoxia of Coronary Vasodilation Induced by Propofol</title><source>MEDLINE</source><source>Journals@Ovid LWW Legacy Archive</source><source>Journals@Ovid Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Ouattara, Alexandre ; Boccara, Gilles ; Lecomte, Patrick ; Souktani, Rachid ; Le Cosquer, Philippe ; Mouren, Stéphane ; Coriat, Pierre ; Riou, Bruno</creator><creatorcontrib>Ouattara, Alexandre ; Boccara, Gilles ; Lecomte, Patrick ; Souktani, Rachid ; Le Cosquer, Philippe ; Mouren, Stéphane ; Coriat, Pierre ; Riou, Bruno</creatorcontrib><description>We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10–300 μM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (Pao2 = 137 ± 16 mm Hg, n = 12) or in the presence (Pao2 = 541 ± 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (−13% ± 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 μM) and cromakalim (0.5 μM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (−16% ± 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 μM both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia.</description><identifier>ISSN: 0003-2999</identifier><identifier>EISSN: 1526-7598</identifier><identifier>DOI: 10.1213/01.ANE.0000100681.15355.AC</identifier><identifier>PMID: 14980904</identifier><identifier>CODEN: AACRAT</identifier><language>eng</language><publisher>Hagerstown, MD: International Anesthesia Research Society</publisher><subject>Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Anesthetics, Intravenous - pharmacology ; Animals ; ATP-Binding Cassette Transporters ; Biological and medical sciences ; Blood Gas Analysis ; Coronary Circulation - drug effects ; Coronary Vessels - drug effects ; Coronary Vessels - metabolism ; Coronary Vessels - physiopathology ; Cromakalim - pharmacology ; Electrolytes - blood ; Glyburide - pharmacology ; Hyperoxia - physiopathology ; In Vitro Techniques ; KATP Channels ; Life Sciences ; Medical sciences ; Myocardial Contraction - drug effects ; Myocardium - metabolism ; Oxygen - blood ; Perfusion ; Potassium Channel Blockers - pharmacology ; Potassium Channels - agonists ; Potassium Channels - drug effects ; Potassium Channels, Inwardly Rectifying ; Propofol - pharmacology ; Rabbits ; Vasodilation - drug effects ; Vasodilation - physiology</subject><ispartof>Anesthesia and analgesia, 2004-03, Vol.98 (3), p.595-603</ispartof><rights>International Anesthesia Research Society</rights><rights>2004 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4767-109b77f5686f75115c56ddf9f0440c95e18e13f787bc86699e528b284f6cce5f3</citedby><cites>FETCH-LOGICAL-c4767-109b77f5686f75115c56ddf9f0440c95e18e13f787bc86699e528b284f6cce5f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf><![CDATA[$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&PDF=y&D=ovft&AN=00000539-200403000-00007$$EPDF$$P50$$Gwolterskluwer$$H]]></linktopdf><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00000539-200403000-00007$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>230,315,781,785,886,4610,27929,27930,64671,65466</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15566230$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14980904$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04439746$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Ouattara, Alexandre</creatorcontrib><creatorcontrib>Boccara, Gilles</creatorcontrib><creatorcontrib>Lecomte, Patrick</creatorcontrib><creatorcontrib>Souktani, Rachid</creatorcontrib><creatorcontrib>Le Cosquer, Philippe</creatorcontrib><creatorcontrib>Mouren, Stéphane</creatorcontrib><creatorcontrib>Coriat, Pierre</creatorcontrib><creatorcontrib>Riou, Bruno</creatorcontrib><title>Amplification by Hyperoxia of Coronary Vasodilation Induced by Propofol</title><title>Anesthesia and analgesia</title><addtitle>Anesth Analg</addtitle><description>We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10–300 μM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (Pao2 = 137 ± 16 mm Hg, n = 12) or in the presence (Pao2 = 541 ± 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (−13% ± 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 μM) and cromakalim (0.5 μM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (−16% ± 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 μM both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia.</description><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Anesthetics, Intravenous - pharmacology</subject><subject>Animals</subject><subject>ATP-Binding Cassette Transporters</subject><subject>Biological and medical sciences</subject><subject>Blood Gas Analysis</subject><subject>Coronary Circulation - drug effects</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - metabolism</subject><subject>Coronary Vessels - physiopathology</subject><subject>Cromakalim - pharmacology</subject><subject>Electrolytes - blood</subject><subject>Glyburide - pharmacology</subject><subject>Hyperoxia - physiopathology</subject><subject>In Vitro Techniques</subject><subject>KATP Channels</subject><subject>Life Sciences</subject><subject>Medical sciences</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardium - metabolism</subject><subject>Oxygen - blood</subject><subject>Perfusion</subject><subject>Potassium Channel Blockers - pharmacology</subject><subject>Potassium Channels - agonists</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels, Inwardly Rectifying</subject><subject>Propofol - pharmacology</subject><subject>Rabbits</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><issn>0003-2999</issn><issn>1526-7598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0E2P0zAQBmALgdiy8BdQhAQSh4RxHH9xi6Jlu1IFHICr5Ti2GnDjYjcs_fe4TUV9sTx6ZsZ6EXqDocI1Jh8AV-3nuwrywQBM4ApTQmnVdk_QCtOalZxK8RStMiBlLaW8QS9S-nn2gj1HN7iRAiQ0K3Tf7vZ-dKPRhzFMRX8s1se9jeHvqIvgii7EMOl4LH7oFIbRL-phGmZjh5P-GsM-uOBfomdO-2RfXe5b9P3T3bduXW6-3D907aY0DWe8xCB7zh1lgjlOMaaGsmFw0kHTgJHUYmExcVzw3gjGpLS0Fn0tGseMsdSRW_R-mbvVXu3juMufU0GPat1u1KmWBxHJG_YHZ_tusfsYfs82HdRuTMZ6rycb5qQEYFEDpRl-XKCJIaVo3f_JGNQpcgVY5cjVNXJ1jly1XW5-fdky9zs7XFsvGWfw9gJ0Mtq7qCczpqujlLGaQHbN4h6DP9iYfvn50Ua1tdoftufVQIksa4AGSH6Upwon_wDen5ex</recordid><startdate>200403</startdate><enddate>200403</enddate><creator>Ouattara, Alexandre</creator><creator>Boccara, Gilles</creator><creator>Lecomte, Patrick</creator><creator>Souktani, Rachid</creator><creator>Le Cosquer, Philippe</creator><creator>Mouren, Stéphane</creator><creator>Coriat, Pierre</creator><creator>Riou, Bruno</creator><general>International Anesthesia Research Society</general><general>Lippincott</general><general>Lippincott, Williams & Wilkins</general><scope>IQODW</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><scope>1XC</scope></search><sort><creationdate>200403</creationdate><title>Amplification by Hyperoxia of Coronary Vasodilation Induced by Propofol</title><author>Ouattara, Alexandre ; Boccara, Gilles ; Lecomte, Patrick ; Souktani, Rachid ; Le Cosquer, Philippe ; Mouren, Stéphane ; Coriat, Pierre ; Riou, Bruno</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4767-109b77f5686f75115c56ddf9f0440c95e18e13f787bc86699e528b284f6cce5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Anesthetics, Intravenous - pharmacology</topic><topic>Animals</topic><topic>ATP-Binding Cassette Transporters</topic><topic>Biological and medical sciences</topic><topic>Blood Gas Analysis</topic><topic>Coronary Circulation - drug effects</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - metabolism</topic><topic>Coronary Vessels - physiopathology</topic><topic>Cromakalim - pharmacology</topic><topic>Electrolytes - blood</topic><topic>Glyburide - pharmacology</topic><topic>Hyperoxia - physiopathology</topic><topic>In Vitro Techniques</topic><topic>KATP Channels</topic><topic>Life Sciences</topic><topic>Medical sciences</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardium - metabolism</topic><topic>Oxygen - blood</topic><topic>Perfusion</topic><topic>Potassium Channel Blockers - pharmacology</topic><topic>Potassium Channels - agonists</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels, Inwardly Rectifying</topic><topic>Propofol - pharmacology</topic><topic>Rabbits</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ouattara, Alexandre</creatorcontrib><creatorcontrib>Boccara, Gilles</creatorcontrib><creatorcontrib>Lecomte, Patrick</creatorcontrib><creatorcontrib>Souktani, Rachid</creatorcontrib><creatorcontrib>Le Cosquer, Philippe</creatorcontrib><creatorcontrib>Mouren, Stéphane</creatorcontrib><creatorcontrib>Coriat, Pierre</creatorcontrib><creatorcontrib>Riou, Bruno</creatorcontrib><collection>Pascal-Francis</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><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Anesthesia and analgesia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ouattara, Alexandre</au><au>Boccara, Gilles</au><au>Lecomte, Patrick</au><au>Souktani, Rachid</au><au>Le Cosquer, Philippe</au><au>Mouren, Stéphane</au><au>Coriat, Pierre</au><au>Riou, Bruno</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amplification by Hyperoxia of Coronary Vasodilation Induced by Propofol</atitle><jtitle>Anesthesia and analgesia</jtitle><addtitle>Anesth Analg</addtitle><date>2004-03</date><risdate>2004</risdate><volume>98</volume><issue>3</issue><spage>595</spage><epage>603</epage><pages>595-603</pages><issn>0003-2999</issn><eissn>1526-7598</eissn><coden>AACRAT</coden><abstract>We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10–300 μM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (Pao2 = 137 ± 16 mm Hg, n = 12) or in the presence (Pao2 = 541 ± 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (−13% ± 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 μM) and cromakalim (0.5 μM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (−16% ± 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 μM both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia.</abstract><cop>Hagerstown, MD</cop><pub>International Anesthesia Research Society</pub><pmid>14980904</pmid><doi>10.1213/01.ANE.0000100681.15355.AC</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0003-2999 |
| ispartof | Anesthesia and analgesia, 2004-03, Vol.98 (3), p.595-603 |
| issn | 0003-2999 1526-7598 |
| language | eng |
| recordid | cdi_hal_primary_oai_HAL_hal_04439746v1 |
| source | MEDLINE; Journals@Ovid LWW Legacy Archive; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Anesthetics, Intravenous - pharmacology Animals ATP-Binding Cassette Transporters Biological and medical sciences Blood Gas Analysis Coronary Circulation - drug effects Coronary Vessels - drug effects Coronary Vessels - metabolism Coronary Vessels - physiopathology Cromakalim - pharmacology Electrolytes - blood Glyburide - pharmacology Hyperoxia - physiopathology In Vitro Techniques KATP Channels Life Sciences Medical sciences Myocardial Contraction - drug effects Myocardium - metabolism Oxygen - blood Perfusion Potassium Channel Blockers - pharmacology Potassium Channels - agonists Potassium Channels - drug effects Potassium Channels, Inwardly Rectifying Propofol - pharmacology Rabbits Vasodilation - drug effects Vasodilation - physiology |
| title | Amplification by Hyperoxia of Coronary Vasodilation Induced by Propofol |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-14T20%3A58%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_hal_p&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Amplification%20by%20Hyperoxia%20of%20Coronary%20Vasodilation%20Induced%20by%20Propofol&rft.jtitle=Anesthesia%20and%20analgesia&rft.au=Ouattara,%20Alexandre&rft.date=2004-03&rft.volume=98&rft.issue=3&rft.spage=595&rft.epage=603&rft.pages=595-603&rft.issn=0003-2999&rft.eissn=1526-7598&rft.coden=AACRAT&rft_id=info:doi/10.1213/01.ANE.0000100681.15355.AC&rft_dat=%3Cproquest_hal_p%3E80182055%3C/proquest_hal_p%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=80182055&rft_id=info:pmid/14980904&rfr_iscdi=true |