O-028 Microvascular Tone In The Preterm Neonate: Gasotransmitter Interactions May Be The Key
Background and aimsHydrogen sulphide (H2S) can be produced by one of two enzymes: CSE or CBS. H2S is associated with transitional microvascular tone dysregulation in the preterm infant. We have animal model evidence that increases in H2S associated with microvascular dysregulation are driven by CSE-...
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Veröffentlicht in: | Archives of disease in childhood 2014-10, Vol.99 (Suppl 2), p.A32-A32 |
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description | Background and aimsHydrogen sulphide (H2S) can be produced by one of two enzymes: CSE or CBS. H2S is associated with transitional microvascular tone dysregulation in the preterm infant. We have animal model evidence that increases in H2S associated with microvascular dysregulation are driven by CSE-dependent mechanisms. Nitric oxide (NO) and carbon monoxide (CO) also play a role in the transitional circulation of preterm neonates. The aim of this study was to characterise the interrelationships of all 3 gasotransmitters using structural equation modelling analysis.Methods90 preterm neonates were studied at 24h postnatal age. Microvascular studies were performed by laser Doppler. Arterial COHb levels (a measure of CO) were determined through co-oximetry. NO was measured as total nitrate and nitrite in urine. H2S was measured as urinary thiosulphate by liquid chromatography.ResultsWe observed a positive relationship between NO and H2S (p = 0.008, r = 0.28) and an inverse relationship between CO and H2S (p = 0.01, r = –0.33). No relationship was observed between NO and CO (p = 0.18, r = 0.18). Structural equation modelling was used to examine the combination of these effects on microvascular blood flow. The model with the best fit (χ2 = 1.11) is presented.Abstract O-028 Figure 1ConclusionsNO production positively related to H2S production. Previous studies report that NO inhibits H2S production via the enzyme CBS but induces CSE expression. These results suggest that in the preterm newborn, CSE expression is significantly modulated by NO. The relationship between NO and CSE/H2S may thus be critical to the deleterious higher microvascular blood flow. |
doi_str_mv | 10.1136/archdischild-2014-307384.97 |
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H2S is associated with transitional microvascular tone dysregulation in the preterm infant. We have animal model evidence that increases in H2S associated with microvascular dysregulation are driven by CSE-dependent mechanisms. Nitric oxide (NO) and carbon monoxide (CO) also play a role in the transitional circulation of preterm neonates. The aim of this study was to characterise the interrelationships of all 3 gasotransmitters using structural equation modelling analysis.Methods90 preterm neonates were studied at 24h postnatal age. Microvascular studies were performed by laser Doppler. Arterial COHb levels (a measure of CO) were determined through co-oximetry. NO was measured as total nitrate and nitrite in urine. H2S was measured as urinary thiosulphate by liquid chromatography.ResultsWe observed a positive relationship between NO and H2S (p = 0.008, r = 0.28) and an inverse relationship between CO and H2S (p = 0.01, r = –0.33). No relationship was observed between NO and CO (p = 0.18, r = 0.18). Structural equation modelling was used to examine the combination of these effects on microvascular blood flow. The model with the best fit (χ2 = 1.11) is presented.Abstract O-028 Figure 1ConclusionsNO production positively related to H2S production. Previous studies report that NO inhibits H2S production via the enzyme CBS but induces CSE expression. These results suggest that in the preterm newborn, CSE expression is significantly modulated by NO. The relationship between NO and CSE/H2S may thus be critical to the deleterious higher microvascular blood flow.</description><identifier>ISSN: 0003-9888</identifier><identifier>EISSN: 1468-2044</identifier><identifier>DOI: 10.1136/archdischild-2014-307384.97</identifier><language>eng</language><publisher>London: BMJ Publishing Group LTD</publisher><subject>Animal models ; Blood flow ; Carbon monoxide ; Hydrogen sulfide ; Liquid chromatography ; Medical research ; Microvasculature ; Neonates ; Newborn babies ; Nitric oxide ; Oxygen saturation ; Urine</subject><ispartof>Archives of disease in childhood, 2014-10, Vol.99 (Suppl 2), p.A32-A32</ispartof><rights>2014 2014, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3197,27929,27930</link.rule.ids></links><search><creatorcontrib>Dyson, R</creatorcontrib><creatorcontrib>Palliser, H</creatorcontrib><creatorcontrib>Latter, J</creatorcontrib><creatorcontrib>Chwatko, G</creatorcontrib><creatorcontrib>Glowacki, R</creatorcontrib><creatorcontrib>Wright, I</creatorcontrib><title>O-028 Microvascular Tone In The Preterm Neonate: Gasotransmitter Interactions May Be The Key</title><title>Archives of disease in childhood</title><description>Background and aimsHydrogen sulphide (H2S) can be produced by one of two enzymes: CSE or CBS. H2S is associated with transitional microvascular tone dysregulation in the preterm infant. We have animal model evidence that increases in H2S associated with microvascular dysregulation are driven by CSE-dependent mechanisms. Nitric oxide (NO) and carbon monoxide (CO) also play a role in the transitional circulation of preterm neonates. The aim of this study was to characterise the interrelationships of all 3 gasotransmitters using structural equation modelling analysis.Methods90 preterm neonates were studied at 24h postnatal age. Microvascular studies were performed by laser Doppler. Arterial COHb levels (a measure of CO) were determined through co-oximetry. NO was measured as total nitrate and nitrite in urine. H2S was measured as urinary thiosulphate by liquid chromatography.ResultsWe observed a positive relationship between NO and H2S (p = 0.008, r = 0.28) and an inverse relationship between CO and H2S (p = 0.01, r = –0.33). No relationship was observed between NO and CO (p = 0.18, r = 0.18). Structural equation modelling was used to examine the combination of these effects on microvascular blood flow. The model with the best fit (χ2 = 1.11) is presented.Abstract O-028 Figure 1ConclusionsNO production positively related to H2S production. Previous studies report that NO inhibits H2S production via the enzyme CBS but induces CSE expression. These results suggest that in the preterm newborn, CSE expression is significantly modulated by NO. The relationship between NO and CSE/H2S may thus be critical to the deleterious higher microvascular blood flow.</description><subject>Animal models</subject><subject>Blood flow</subject><subject>Carbon monoxide</subject><subject>Hydrogen sulfide</subject><subject>Liquid chromatography</subject><subject>Medical research</subject><subject>Microvasculature</subject><subject>Neonates</subject><subject>Newborn babies</subject><subject>Nitric oxide</subject><subject>Oxygen saturation</subject><subject>Urine</subject><issn>0003-9888</issn><issn>1468-2044</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpNkM1OwzAMxyMEEmPwDpF27kjitE3gBBOMiY1xGFeikLpap60dSYu0GxdelCchYxy42Jb999ePkAFnQ84hu7TeLYsquGW1LhLBuEyA5aDkUOdHpMdlpmJWymPSY4xBopVSp-QshBVjXCgFPfI6T5hQ359fs8r55sMG162tp4umRjqp6WKJ9Nlji35Dn7CpbYtXdGxD03pbh03VxkrURWtdWzV1oDO7o7f42_iIu3NyUtp1wIs_3ycv93eL0UMynY8no5tp4jhAnoAVGlIB-CbTIncx4nmJFrHICm6ljHezLNUKUi0dpFYLcE5aYNyVGUoBfTI4zN365r3D0JpV0_k6rjSCQ2zOdAZRdX1QxVdD8Fiara821u8MZ2YP1PwHavZAzQGo0Tn8AMVLbOg</recordid><startdate>201410</startdate><enddate>201410</enddate><creator>Dyson, R</creator><creator>Palliser, H</creator><creator>Latter, J</creator><creator>Chwatko, G</creator><creator>Glowacki, R</creator><creator>Wright, I</creator><general>BMJ Publishing Group LTD</general><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88B</scope><scope>88E</scope><scope>88I</scope><scope>8A4</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>CJNVE</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0P</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEDU</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>201410</creationdate><title>O-028 Microvascular Tone In The Preterm Neonate: Gasotransmitter Interactions May Be The Key</title><author>Dyson, R ; Palliser, H ; Latter, J ; Chwatko, G ; Glowacki, R ; Wright, I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1337-3a293523eb45d7c52317feaeed6d1a44888065983594c35a923cc4a301cf6e423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animal models</topic><topic>Blood flow</topic><topic>Carbon monoxide</topic><topic>Hydrogen sulfide</topic><topic>Liquid chromatography</topic><topic>Medical research</topic><topic>Microvasculature</topic><topic>Neonates</topic><topic>Newborn babies</topic><topic>Nitric oxide</topic><topic>Oxygen saturation</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dyson, R</creatorcontrib><creatorcontrib>Palliser, H</creatorcontrib><creatorcontrib>Latter, J</creatorcontrib><creatorcontrib>Chwatko, G</creatorcontrib><creatorcontrib>Glowacki, R</creatorcontrib><creatorcontrib>Wright, I</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Education Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>Education Periodicals</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Social Science Premium Collection</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Education Collection</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>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Education Database</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Education</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 Basic</collection><jtitle>Archives of disease in childhood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dyson, R</au><au>Palliser, H</au><au>Latter, J</au><au>Chwatko, G</au><au>Glowacki, R</au><au>Wright, I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>O-028 Microvascular Tone In The Preterm Neonate: Gasotransmitter Interactions May Be The Key</atitle><jtitle>Archives of disease in childhood</jtitle><date>2014-10</date><risdate>2014</risdate><volume>99</volume><issue>Suppl 2</issue><spage>A32</spage><epage>A32</epage><pages>A32-A32</pages><issn>0003-9888</issn><eissn>1468-2044</eissn><abstract>Background and aimsHydrogen sulphide (H2S) can be produced by one of two enzymes: CSE or CBS. H2S is associated with transitional microvascular tone dysregulation in the preterm infant. We have animal model evidence that increases in H2S associated with microvascular dysregulation are driven by CSE-dependent mechanisms. Nitric oxide (NO) and carbon monoxide (CO) also play a role in the transitional circulation of preterm neonates. The aim of this study was to characterise the interrelationships of all 3 gasotransmitters using structural equation modelling analysis.Methods90 preterm neonates were studied at 24h postnatal age. Microvascular studies were performed by laser Doppler. Arterial COHb levels (a measure of CO) were determined through co-oximetry. NO was measured as total nitrate and nitrite in urine. H2S was measured as urinary thiosulphate by liquid chromatography.ResultsWe observed a positive relationship between NO and H2S (p = 0.008, r = 0.28) and an inverse relationship between CO and H2S (p = 0.01, r = –0.33). No relationship was observed between NO and CO (p = 0.18, r = 0.18). Structural equation modelling was used to examine the combination of these effects on microvascular blood flow. The model with the best fit (χ2 = 1.11) is presented.Abstract O-028 Figure 1ConclusionsNO production positively related to H2S production. Previous studies report that NO inhibits H2S production via the enzyme CBS but induces CSE expression. These results suggest that in the preterm newborn, CSE expression is significantly modulated by NO. The relationship between NO and CSE/H2S may thus be critical to the deleterious higher microvascular blood flow.</abstract><cop>London</cop><pub>BMJ Publishing Group LTD</pub><doi>10.1136/archdischild-2014-307384.97</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animal models Blood flow Carbon monoxide Hydrogen sulfide Liquid chromatography Medical research Microvasculature Neonates Newborn babies Nitric oxide Oxygen saturation Urine |
title | O-028 Microvascular Tone In The Preterm Neonate: Gasotransmitter Interactions May Be The Key |
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