Antibody-Mediated Neutrophil Depletion Preserves Pulmonary Vasomotor Function
Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mec...
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creator | Sheridan, Brett C. McIntyre, Jr, Robert C. Meldrum, Daniel R. Cleveland, Jr, Joseph C. Agrafojo, Jeanette Eisenach, John H. Harken, Alden H. Fullerton, David A. |
description | Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor-dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia ( |
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However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor-dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia (<75 neutrophils/μl) was induced with anti-neutrophil antibody serum 24 hr prior to lung harvest in five rats. Saline-injected rats were controls (n= 5). Dose–response curves to ACh, A23187, and SNP were generated in isolated pulmonary artery rings preconstricted with phenylepherine. Statistical comparison was performed using one-way ANOVA with post-hoc Bonferroni–Dunn, andP< 0.05 was accepted as significant. Relaxation to ACh, A23187, and SNP was complete in both control and neutropenic rats. Thus, antibody-mediated depletion does not impair endothelial-dependent or -independent cGMP-mediated pulmonary vasorelaxation.</description><identifier>ISSN: 0022-4804</identifier><identifier>EISSN: 1095-8673</identifier><identifier>DOI: 10.1006/jsre.1996.0176</identifier><identifier>PMID: 8606514</identifier><identifier>CODEN: JSGRA2</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Acetylcholine - pharmacology ; Animals ; Biological and medical sciences ; Blood vessels and receptors ; Calcimycin - pharmacology ; Cyclic GMP - physiology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Fundamental and applied biological sciences. Psychology ; Immune Sera ; Lung - blood supply ; Male ; Muscle Relaxation - drug effects ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; Neutropenia ; Neutrophils - immunology ; Neutrophils - physiology ; Nitroprusside - pharmacology ; Rats ; Rats, Sprague-Dawley ; Vasomotor System - physiology ; Vertebrates: cardiovascular system</subject><ispartof>The Journal of surgical research, 1996-04, Vol.62 (1), p.74-78</ispartof><rights>1996 Academic Press</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-ab4432bd112df30b42f7c3505dcec2dd963b3eac35681ca2f5f6c345f4c181483</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/jsre.1996.0176$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3052399$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8606514$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sheridan, Brett C.</creatorcontrib><creatorcontrib>McIntyre, Jr, Robert C.</creatorcontrib><creatorcontrib>Meldrum, Daniel R.</creatorcontrib><creatorcontrib>Cleveland, Jr, Joseph C.</creatorcontrib><creatorcontrib>Agrafojo, Jeanette</creatorcontrib><creatorcontrib>Eisenach, John H.</creatorcontrib><creatorcontrib>Harken, Alden H.</creatorcontrib><creatorcontrib>Fullerton, David A.</creatorcontrib><title>Antibody-Mediated Neutrophil Depletion Preserves Pulmonary Vasomotor Function</title><title>The Journal of surgical research</title><addtitle>J Surg Res</addtitle><description>Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor-dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia (<75 neutrophils/μl) was induced with anti-neutrophil antibody serum 24 hr prior to lung harvest in five rats. Saline-injected rats were controls (n= 5). Dose–response curves to ACh, A23187, and SNP were generated in isolated pulmonary artery rings preconstricted with phenylepherine. Statistical comparison was performed using one-way ANOVA with post-hoc Bonferroni–Dunn, andP< 0.05 was accepted as significant. Relaxation to ACh, A23187, and SNP was complete in both control and neutropenic rats. Thus, antibody-mediated depletion does not impair endothelial-dependent or -independent cGMP-mediated pulmonary vasorelaxation.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood vessels and receptors</subject><subject>Calcimycin - pharmacology</subject><subject>Cyclic GMP - physiology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immune Sera</subject><subject>Lung - blood supply</subject><subject>Male</subject><subject>Muscle Relaxation - drug effects</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Neutropenia</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - physiology</subject><subject>Nitroprusside - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Vasomotor System - physiology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0022-4804</issn><issn>1095-8673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1LxDAQhoMouq5evQk9iLfWpEnT9Ch-g6t7UK8hTaYYaZs1aRf896Zs8eZpmHmfGYYHoTOCM4Ixv_oKHjJSVTzDpOR7aEFwVaSCl3QfLTDO85QJzI7QcQhfOPZVSQ_RoeCYF4Qt0Oq6H2ztzE-6AmPVACZ5gXHwbvNp2-QWNi0M1vXJ2kMAv4WQrMe2c73yP8mHCq5zg_PJ_djrCTtBB41qA5zOdYne7-_ebh7T59eHp5vr51RTLoZU1YzRvDaE5KahuGZ5U2pa4MJo0LkxFac1BRVHXBCt8qZouKasaJgmgjBBl-hyd3fj3fcIYZCdDRraVvXgxiDLsiqZ4DyC2Q7U3oVoqpEbb7v4vCRYTv7k5E9O_uTkLy6cz5fHugPzh8_CYn4x5ypo1TZe9dqGP4ziIqdVFTGxwyBa2FrwMmgLvY6OPehBGmf_--AXLv6NCQ</recordid><startdate>19960401</startdate><enddate>19960401</enddate><creator>Sheridan, Brett C.</creator><creator>McIntyre, Jr, Robert C.</creator><creator>Meldrum, Daniel R.</creator><creator>Cleveland, Jr, Joseph C.</creator><creator>Agrafojo, Jeanette</creator><creator>Eisenach, John H.</creator><creator>Harken, Alden H.</creator><creator>Fullerton, David A.</creator><general>Elsevier Inc</general><general>Elsevier</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></search><sort><creationdate>19960401</creationdate><title>Antibody-Mediated Neutrophil Depletion Preserves Pulmonary Vasomotor Function</title><author>Sheridan, Brett C. ; McIntyre, Jr, Robert C. ; Meldrum, Daniel R. ; Cleveland, Jr, Joseph C. ; Agrafojo, Jeanette ; Eisenach, John H. ; Harken, Alden H. ; Fullerton, David A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-ab4432bd112df30b42f7c3505dcec2dd963b3eac35681ca2f5f6c345f4c181483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood vessels and receptors</topic><topic>Calcimycin - pharmacology</topic><topic>Cyclic GMP - physiology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immune Sera</topic><topic>Lung - blood supply</topic><topic>Male</topic><topic>Muscle Relaxation - drug effects</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Neutropenia</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - physiology</topic><topic>Nitroprusside - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Vasomotor System - physiology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sheridan, Brett C.</creatorcontrib><creatorcontrib>McIntyre, Jr, Robert C.</creatorcontrib><creatorcontrib>Meldrum, Daniel R.</creatorcontrib><creatorcontrib>Cleveland, Jr, Joseph C.</creatorcontrib><creatorcontrib>Agrafojo, Jeanette</creatorcontrib><creatorcontrib>Eisenach, John H.</creatorcontrib><creatorcontrib>Harken, Alden H.</creatorcontrib><creatorcontrib>Fullerton, David A.</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><jtitle>The Journal of surgical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sheridan, Brett C.</au><au>McIntyre, Jr, Robert C.</au><au>Meldrum, Daniel R.</au><au>Cleveland, Jr, Joseph C.</au><au>Agrafojo, Jeanette</au><au>Eisenach, John H.</au><au>Harken, Alden H.</au><au>Fullerton, David A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antibody-Mediated Neutrophil Depletion Preserves Pulmonary Vasomotor Function</atitle><jtitle>The Journal of surgical research</jtitle><addtitle>J Surg Res</addtitle><date>1996-04-01</date><risdate>1996</risdate><volume>62</volume><issue>1</issue><spage>74</spage><epage>78</epage><pages>74-78</pages><issn>0022-4804</issn><eissn>1095-8673</eissn><coden>JSGRA2</coden><abstract>Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor-dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia (<75 neutrophils/μl) was induced with anti-neutrophil antibody serum 24 hr prior to lung harvest in five rats. Saline-injected rats were controls (n= 5). Dose–response curves to ACh, A23187, and SNP were generated in isolated pulmonary artery rings preconstricted with phenylepherine. Statistical comparison was performed using one-way ANOVA with post-hoc Bonferroni–Dunn, andP< 0.05 was accepted as significant. Relaxation to ACh, A23187, and SNP was complete in both control and neutropenic rats. Thus, antibody-mediated depletion does not impair endothelial-dependent or -independent cGMP-mediated pulmonary vasorelaxation.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8606514</pmid><doi>10.1006/jsre.1996.0176</doi><tpages>5</tpages></addata></record> |
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subjects | Acetylcholine - pharmacology Animals Biological and medical sciences Blood vessels and receptors Calcimycin - pharmacology Cyclic GMP - physiology Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Fundamental and applied biological sciences. Psychology Immune Sera Lung - blood supply Male Muscle Relaxation - drug effects Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Neutropenia Neutrophils - immunology Neutrophils - physiology Nitroprusside - pharmacology Rats Rats, Sprague-Dawley Vasomotor System - physiology Vertebrates: cardiovascular system |
title | Antibody-Mediated Neutrophil Depletion Preserves Pulmonary Vasomotor Function |
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