Carbon monoxide and pulmonary circulation in an ovine model
The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or rig...
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| Veröffentlicht in: | Journal of burn care & rehabilitation 1992-11, Vol.13 (6), p.623-627 |
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| container_title | Journal of burn care & rehabilitation |
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| creator | THEISSEN, J. L LOICK, H. M TRABER, L. D HERNDON, D. N TRABER, D. L |
| description | The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output. |
| doi_str_mv | 10.1097/00004630-199211000-00003 |
| format | Article |
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L ; LOICK, H. M ; TRABER, L. D ; HERNDON, D. N ; TRABER, D. L</creator><creatorcontrib>THEISSEN, J. L ; LOICK, H. M ; TRABER, L. D ; HERNDON, D. N ; TRABER, D. L</creatorcontrib><description>The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.</description><identifier>ISSN: 0273-8481</identifier><identifier>EISSN: 1534-5939</identifier><identifier>DOI: 10.1097/00004630-199211000-00003</identifier><identifier>PMID: 1469025</identifier><identifier>CODEN: JBCRD2</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Carbon Monoxide Poisoning - physiopathology ; Carboxyhemoglobin - metabolism ; Cardiac Output - physiology ; Chemical and industrial products toxicology. Toxic occupational diseases ; Gas, fumes ; Medical sciences ; Pulmonary Artery - physiopathology ; Pulmonary Circulation - physiology ; Pulmonary Veins - physiopathology ; Pulmonary Wedge Pressure - physiology ; Sheep ; Toxicology ; Vascular Resistance - physiology ; Vasoconstriction - physiology</subject><ispartof>Journal of burn care & rehabilitation, 1992-11, Vol.13 (6), p.623-627</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c254t-bac38af3bf1e7dad5d981f91d01610ecb246a64c356b3df0ebc6dc7b60eb4ba13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4458531$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1469025$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>THEISSEN, J. L</creatorcontrib><creatorcontrib>LOICK, H. M</creatorcontrib><creatorcontrib>TRABER, L. D</creatorcontrib><creatorcontrib>HERNDON, D. N</creatorcontrib><creatorcontrib>TRABER, D. L</creatorcontrib><title>Carbon monoxide and pulmonary circulation in an ovine model</title><title>Journal of burn care & rehabilitation</title><addtitle>J Burn Care Rehabil</addtitle><description>The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carbon Monoxide Poisoning - physiopathology</subject><subject>Carboxyhemoglobin - metabolism</subject><subject>Cardiac Output - physiology</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Gas, fumes</subject><subject>Medical sciences</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Pulmonary Circulation - physiology</subject><subject>Pulmonary Veins - physiopathology</subject><subject>Pulmonary Wedge Pressure - physiology</subject><subject>Sheep</subject><subject>Toxicology</subject><subject>Vascular Resistance - physiology</subject><subject>Vasoconstriction - physiology</subject><issn>0273-8481</issn><issn>1534-5939</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUE1LAzEQDaLUWv0Jwh68RjObj93gSYpVoeBFz8vkCyLb3ZK0ov_e1NY6l_l47w0zj5AK2C0w3dyxEkJxRkHrGqB0dDfiJ2QKkgsqNdenZMrqhtNWtHBOLnL-YAx0o-SETEAozWo5JfdzTGYcqtU4jF_R-QoHV623fekxfVc2JrvtcRMLJQ4FrMbPOPhCd76_JGcB--yvDnlG3hePb_Nnunx9epk_LKmtpdhQg5a3GLgJ4BuHTjrdQtDgGChg3ppaKFTCcqkMd4F5Y5WzjVGlEgaBz0i732vTmHPyoVunuCrndcC6nR3dnx3d0Y7fES_S6710vTUr7_6F-_8LfnPAMVvsQ8LBxnykCSFbyYH_ADpSaDc</recordid><startdate>199211</startdate><enddate>199211</enddate><creator>THEISSEN, J. 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L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c254t-bac38af3bf1e7dad5d981f91d01610ecb246a64c356b3df0ebc6dc7b60eb4ba13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carbon Monoxide Poisoning - physiopathology</topic><topic>Carboxyhemoglobin - metabolism</topic><topic>Cardiac Output - physiology</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Gas, fumes</topic><topic>Medical sciences</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Pulmonary Circulation - physiology</topic><topic>Pulmonary Veins - physiopathology</topic><topic>Pulmonary Wedge Pressure - physiology</topic><topic>Sheep</topic><topic>Toxicology</topic><topic>Vascular Resistance - physiology</topic><topic>Vasoconstriction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>THEISSEN, J. L</creatorcontrib><creatorcontrib>LOICK, H. M</creatorcontrib><creatorcontrib>TRABER, L. D</creatorcontrib><creatorcontrib>HERNDON, D. N</creatorcontrib><creatorcontrib>TRABER, D. 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L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Carbon monoxide and pulmonary circulation in an ovine model</atitle><jtitle>Journal of burn care & rehabilitation</jtitle><addtitle>J Burn Care Rehabil</addtitle><date>1992-11</date><risdate>1992</risdate><volume>13</volume><issue>6</issue><spage>623</spage><epage>627</epage><pages>623-627</pages><issn>0273-8481</issn><eissn>1534-5939</eissn><coden>JBCRD2</coden><abstract>The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>1469025</pmid><doi>10.1097/00004630-199211000-00003</doi><tpages>5</tpages></addata></record> |
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| ispartof | Journal of burn care & rehabilitation, 1992-11, Vol.13 (6), p.623-627 |
| issn | 0273-8481 1534-5939 |
| language | eng |
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| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Carbon Monoxide Poisoning - physiopathology Carboxyhemoglobin - metabolism Cardiac Output - physiology Chemical and industrial products toxicology. Toxic occupational diseases Gas, fumes Medical sciences Pulmonary Artery - physiopathology Pulmonary Circulation - physiology Pulmonary Veins - physiopathology Pulmonary Wedge Pressure - physiology Sheep Toxicology Vascular Resistance - physiology Vasoconstriction - physiology |
| title | Carbon monoxide and pulmonary circulation in an ovine model |
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