Pulmonary vasomotor dysfunction is produced with chronically high pulmonary blood flow
This study examined the hypothesis that chronic high pulmonary blood flow produces dysfunction of the mechanisms of pulmonary vasorelaxation. A 3:1 left-to-right shunt was created in dogs by bilateral femoral artery–femoral vein shunts with use of 6 mm polytetrafluoroethylene grafts. Isolated pulmon...
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| Veröffentlicht in: | The Journal of thoracic and cardiovascular surgery 1996, Vol.111 (1), p.190-197 |
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| creator | Fullerton, David A. Mitchell, Max B. Jones, Darrell N. Maki, A. McIntyre, Robert C. |
| description | This study examined the hypothesis that chronic high pulmonary blood flow produces dysfunction of the mechanisms of pulmonary vasorelaxation. A 3:1 left-to-right shunt was created in dogs by bilateral femoral artery–femoral vein shunts with use of 6 mm polytetrafluoroethylene grafts. Isolated pulmonary artery rings were studied at the following times: 3 days (
n = 2), 2 weeks (
n = 4), and 5 months (
n = 6). Control animals had no shunt. The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings (4 rings from each dog): (1) endothelium-dependent cyclic guanosine monophosphate–mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate–mediated relaxation (response to sodium nitroprusside), and (3) β-adrenergic cyclic adenosine monophosphate–mediated relaxation (response to isoproterenol). Stastical analysis was done by analysis of variance. This model of high pulmonary flow did not produce an increase in pulmonary arterial pressure or transpulmonary gradient. However, chronic high pulmonary flow produced progressive dysfunction of all three of these mechanisms of pulmonary vasorelaxation. By 5 months of high pulmonary flow, acetylcholine produced only 36% ± 6% relaxation versus 95% ± 5% in control animals (
p < 0.05). Likewise, sodium nitroprusside produced only 69% ± 6% relaxation versus 100% in control animals (
p < 0.05). Finally, isoproterenol produced only 55% ± 5% relaxation versus 94% ± 6% in control animals (
p < 0.05). We conclude that dysfunction of the mechanisms of pulmonary vasorelaxation may contribute to exaggerated perioperative pulmonary vasoconstriction in the setting of chronic high pulmonary blood flow. (J T
HORAC C
ARDIOVASC S
URG 1996;111:190-7) |
| doi_str_mv | 10.1016/S0022-5223(96)70416-6 |
| format | Article |
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n = 2), 2 weeks (
n = 4), and 5 months (
n = 6). Control animals had no shunt. The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings (4 rings from each dog): (1) endothelium-dependent cyclic guanosine monophosphate–mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate–mediated relaxation (response to sodium nitroprusside), and (3) β-adrenergic cyclic adenosine monophosphate–mediated relaxation (response to isoproterenol). Stastical analysis was done by analysis of variance. This model of high pulmonary flow did not produce an increase in pulmonary arterial pressure or transpulmonary gradient. However, chronic high pulmonary flow produced progressive dysfunction of all three of these mechanisms of pulmonary vasorelaxation. By 5 months of high pulmonary flow, acetylcholine produced only 36% ± 6% relaxation versus 95% ± 5% in control animals (
p < 0.05). Likewise, sodium nitroprusside produced only 69% ± 6% relaxation versus 100% in control animals (
p < 0.05). Finally, isoproterenol produced only 55% ± 5% relaxation versus 94% ± 6% in control animals (
p < 0.05). We conclude that dysfunction of the mechanisms of pulmonary vasorelaxation may contribute to exaggerated perioperative pulmonary vasoconstriction in the setting of chronic high pulmonary blood flow. (J T
HORAC C
ARDIOVASC S
URG 1996;111:190-7)</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1016/S0022-5223(96)70416-6</identifier><identifier>PMID: 8551766</identifier><identifier>CODEN: JTCSAQ</identifier><language>eng</language><publisher>Philadelphia, PA: Mosby, Inc</publisher><subject>Acetylcholine - pharmacology ; Adrenergic beta-Agonists - pharmacology ; Animals ; Arteriovenous Shunt, Surgical ; Biological and medical sciences ; Blood Vessel Prosthesis ; Cardiovascular system ; Cyclic AMP - physiology ; Cyclic GMP - physiology ; Dogs ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Femoral Artery - surgery ; Femoral Vein - surgery ; Hypertension, Pulmonary - etiology ; Investigative techniques, diagnostic techniques (general aspects) ; Isoproterenol - pharmacology ; Male ; Medical sciences ; Nitroprusside - pharmacology ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Polytetrafluoroethylene ; Pulmonary Artery - drug effects ; Pulmonary Artery - physiopathology ; Pulmonary Circulation ; Time Factors ; Vasoconstriction - physiology ; Vasodilator Agents - pharmacology ; Vasomotor System - drug effects ; Vasomotor System - physiopathology</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 1996, Vol.111 (1), p.190-197</ispartof><rights>1996 Mosby, Inc.</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-5e78b3c3db8166d578874ecd80ab4120188e941d305ce7b4bbe1bfe8c33106d13</citedby><cites>FETCH-LOGICAL-c468t-5e78b3c3db8166d578874ecd80ab4120188e941d305ce7b4bbe1bfe8c33106d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0022-5223(96)70416-6$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2976481$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8551766$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fullerton, David A.</creatorcontrib><creatorcontrib>Mitchell, Max B.</creatorcontrib><creatorcontrib>Jones, Darrell N.</creatorcontrib><creatorcontrib>Maki, A.</creatorcontrib><creatorcontrib>McIntyre, Robert C.</creatorcontrib><title>Pulmonary vasomotor dysfunction is produced with chronically high pulmonary blood flow</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>This study examined the hypothesis that chronic high pulmonary blood flow produces dysfunction of the mechanisms of pulmonary vasorelaxation. A 3:1 left-to-right shunt was created in dogs by bilateral femoral artery–femoral vein shunts with use of 6 mm polytetrafluoroethylene grafts. Isolated pulmonary artery rings were studied at the following times: 3 days (
n = 2), 2 weeks (
n = 4), and 5 months (
n = 6). Control animals had no shunt. The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings (4 rings from each dog): (1) endothelium-dependent cyclic guanosine monophosphate–mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate–mediated relaxation (response to sodium nitroprusside), and (3) β-adrenergic cyclic adenosine monophosphate–mediated relaxation (response to isoproterenol). Stastical analysis was done by analysis of variance. This model of high pulmonary flow did not produce an increase in pulmonary arterial pressure or transpulmonary gradient. However, chronic high pulmonary flow produced progressive dysfunction of all three of these mechanisms of pulmonary vasorelaxation. By 5 months of high pulmonary flow, acetylcholine produced only 36% ± 6% relaxation versus 95% ± 5% in control animals (
p < 0.05). Likewise, sodium nitroprusside produced only 69% ± 6% relaxation versus 100% in control animals (
p < 0.05). Finally, isoproterenol produced only 55% ± 5% relaxation versus 94% ± 6% in control animals (
p < 0.05). We conclude that dysfunction of the mechanisms of pulmonary vasorelaxation may contribute to exaggerated perioperative pulmonary vasoconstriction in the setting of chronic high pulmonary blood flow. (J T
HORAC C
ARDIOVASC S
URG 1996;111:190-7)</description><subject>Acetylcholine - pharmacology</subject><subject>Adrenergic beta-Agonists - pharmacology</subject><subject>Animals</subject><subject>Arteriovenous Shunt, Surgical</subject><subject>Biological and medical sciences</subject><subject>Blood Vessel Prosthesis</subject><subject>Cardiovascular system</subject><subject>Cyclic AMP - physiology</subject><subject>Cyclic GMP - physiology</subject><subject>Dogs</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Femoral Artery - surgery</subject><subject>Femoral Vein - surgery</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Isoproterenol - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nitroprusside - pharmacology</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Polytetrafluoroethylene</subject><subject>Pulmonary Artery - drug effects</subject><subject>Pulmonary Artery - physiopathology</subject><subject>Pulmonary Circulation</subject><subject>Time Factors</subject><subject>Vasoconstriction - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasomotor System - drug effects</subject><subject>Vasomotor System - physiopathology</subject><issn>0022-5223</issn><issn>1097-685X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFq3DAQhkVoSbdJHiGgQ2nag1ONZUvyqYTQNoVACk1LbsKSxlkF29pKdpZ9-2qzy16DDnOY7x_9fIScA7sEBuLLb8bKsqjLkn9qxGfJKhCFOCILYI0shKof3pDFAXlH3qf0xBiTDJpjcqzqGqQQC_L319wPYWzjhj63KQxhCpG6Term0U4-jNQnuorBzRYdXftpSe0yhtHbtu83dOkfl3R1uGD6EBzt-rA-JW-7tk94tp8n5M_3b_fXN8Xt3Y-f11e3ha2EmooapTLccmcUCOFqqZSs0DrFWlNByUApbCpwnNUWpamMQTAdKss5MOGAn5CPu7u5478Z06QHnyz2fTtimJOWsskqOM9gvQNtDClF7PQq-iGX1sD01qd-8am3snQj9ItPLXLufP_BbAZ0h9ReYN5_2O_blJ10sR2tTwesbKSo1LbnxQ7bGlv7iDoN2WA-CvppsgkAdH4Ny-TXHYlZ27PHqJP1OGb9OWUn7YJ_pfJ_iJ-grA</recordid><startdate>1996</startdate><enddate>1996</enddate><creator>Fullerton, David A.</creator><creator>Mitchell, Max B.</creator><creator>Jones, Darrell N.</creator><creator>Maki, A.</creator><creator>McIntyre, Robert C.</creator><general>Mosby, Inc</general><general>AATS/WTSA</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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></search><sort><creationdate>1996</creationdate><title>Pulmonary vasomotor dysfunction is produced with chronically high pulmonary blood flow</title><author>Fullerton, David A. ; Mitchell, Max B. ; Jones, Darrell N. ; Maki, A. ; McIntyre, Robert C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-5e78b3c3db8166d578874ecd80ab4120188e941d305ce7b4bbe1bfe8c33106d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adrenergic beta-Agonists - pharmacology</topic><topic>Animals</topic><topic>Arteriovenous Shunt, Surgical</topic><topic>Biological and medical sciences</topic><topic>Blood Vessel Prosthesis</topic><topic>Cardiovascular system</topic><topic>Cyclic AMP - physiology</topic><topic>Cyclic GMP - physiology</topic><topic>Dogs</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Femoral Artery - surgery</topic><topic>Femoral Vein - surgery</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Isoproterenol - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nitroprusside - pharmacology</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Polytetrafluoroethylene</topic><topic>Pulmonary Artery - drug effects</topic><topic>Pulmonary Artery - physiopathology</topic><topic>Pulmonary Circulation</topic><topic>Time Factors</topic><topic>Vasoconstriction - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasomotor System - drug effects</topic><topic>Vasomotor System - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fullerton, David A.</creatorcontrib><creatorcontrib>Mitchell, Max B.</creatorcontrib><creatorcontrib>Jones, Darrell N.</creatorcontrib><creatorcontrib>Maki, A.</creatorcontrib><creatorcontrib>McIntyre, Robert C.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fullerton, David A.</au><au>Mitchell, Max B.</au><au>Jones, Darrell N.</au><au>Maki, A.</au><au>McIntyre, Robert C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pulmonary vasomotor dysfunction is produced with chronically high pulmonary blood flow</atitle><jtitle>The Journal of thoracic and cardiovascular surgery</jtitle><addtitle>J Thorac Cardiovasc Surg</addtitle><date>1996</date><risdate>1996</risdate><volume>111</volume><issue>1</issue><spage>190</spage><epage>197</epage><pages>190-197</pages><issn>0022-5223</issn><eissn>1097-685X</eissn><coden>JTCSAQ</coden><abstract>This study examined the hypothesis that chronic high pulmonary blood flow produces dysfunction of the mechanisms of pulmonary vasorelaxation. A 3:1 left-to-right shunt was created in dogs by bilateral femoral artery–femoral vein shunts with use of 6 mm polytetrafluoroethylene grafts. Isolated pulmonary artery rings were studied at the following times: 3 days (
n = 2), 2 weeks (
n = 4), and 5 months (
n = 6). Control animals had no shunt. The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings (4 rings from each dog): (1) endothelium-dependent cyclic guanosine monophosphate–mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate–mediated relaxation (response to sodium nitroprusside), and (3) β-adrenergic cyclic adenosine monophosphate–mediated relaxation (response to isoproterenol). Stastical analysis was done by analysis of variance. This model of high pulmonary flow did not produce an increase in pulmonary arterial pressure or transpulmonary gradient. However, chronic high pulmonary flow produced progressive dysfunction of all three of these mechanisms of pulmonary vasorelaxation. By 5 months of high pulmonary flow, acetylcholine produced only 36% ± 6% relaxation versus 95% ± 5% in control animals (
p < 0.05). Likewise, sodium nitroprusside produced only 69% ± 6% relaxation versus 100% in control animals (
p < 0.05). Finally, isoproterenol produced only 55% ± 5% relaxation versus 94% ± 6% in control animals (
p < 0.05). We conclude that dysfunction of the mechanisms of pulmonary vasorelaxation may contribute to exaggerated perioperative pulmonary vasoconstriction in the setting of chronic high pulmonary blood flow. (J T
HORAC C
ARDIOVASC S
URG 1996;111:190-7)</abstract><cop>Philadelphia, PA</cop><pub>Mosby, Inc</pub><pmid>8551766</pmid><doi>10.1016/S0022-5223(96)70416-6</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of thoracic and cardiovascular surgery, 1996, Vol.111 (1), p.190-197 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Acetylcholine - pharmacology Adrenergic beta-Agonists - pharmacology Animals Arteriovenous Shunt, Surgical Biological and medical sciences Blood Vessel Prosthesis Cardiovascular system Cyclic AMP - physiology Cyclic GMP - physiology Dogs Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Femoral Artery - surgery Femoral Vein - surgery Hypertension, Pulmonary - etiology Investigative techniques, diagnostic techniques (general aspects) Isoproterenol - pharmacology Male Medical sciences Nitroprusside - pharmacology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Polytetrafluoroethylene Pulmonary Artery - drug effects Pulmonary Artery - physiopathology Pulmonary Circulation Time Factors Vasoconstriction - physiology Vasodilator Agents - pharmacology Vasomotor System - drug effects Vasomotor System - physiopathology |
| title | Pulmonary vasomotor dysfunction is produced with chronically high pulmonary blood flow |
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