Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: a hypothesis
Cirrhosis is associated with the development of a hyperdynamic circulation, which is secondary to the presence of systemic vasodilatation. Several mechanisms have been postulated to be involved in the development of systemic vasodilatation, including increased synthesis of nitric oxide, hyperglucago...
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Veröffentlicht in: | Gut 2005-12, Vol.54 (12), p.1668-1671 |
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description | Cirrhosis is associated with the development of a hyperdynamic circulation, which is secondary to the presence of systemic vasodilatation. Several mechanisms have been postulated to be involved in the development of systemic vasodilatation, including increased synthesis of nitric oxide, hyperglucagonaemia, increased carbon monoxide synthesis, and activation of KATP channels in vascular smooth muscle cells in the systemic and splanchnic arterial circulation. Hydrogen sulphide (H2S) has recently been identified as a novel gaseous transmitter that induces vasodilatation through activation of KATP channels in vascular smooth muscle cells. In this brief review, we comment on what is known about H2S, vascular and neurological function, and postulate its role in the pathogenesis of the vascular abnormalities in cirrhosis. |
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Several mechanisms have been postulated to be involved in the development of systemic vasodilatation, including increased synthesis of nitric oxide, hyperglucagonaemia, increased carbon monoxide synthesis, and activation of KATP channels in vascular smooth muscle cells in the systemic and splanchnic arterial circulation. Hydrogen sulphide (H2S) has recently been identified as a novel gaseous transmitter that induces vasodilatation through activation of KATP channels in vascular smooth muscle cells. In this brief review, we comment on what is known about H2S, vascular and neurological function, and postulate its role in the pathogenesis of the vascular abnormalities in cirrhosis.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.2004.056556</identifier><identifier>PMID: 16174660</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Aqueous solutions ; Biological and medical sciences ; carbon monoxide ; Carbon Monoxide - metabolism ; cirrhosis ; Coronary vessels ; Enzymes ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene expression ; H2S ; Humans ; Hydrogen Sulfide - metabolism ; hydrogen sulphide ; hyperdynamic circulation ; Hypotheses ; Leading ; Liver Circulation ; Liver Cirrhosis - physiopathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; N-methyl-D-aspartate ; Nervous system ; Nitric oxide ; Nitric Oxide - metabolism ; NMDA ; Other diseases. 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Several mechanisms have been postulated to be involved in the development of systemic vasodilatation, including increased synthesis of nitric oxide, hyperglucagonaemia, increased carbon monoxide synthesis, and activation of KATP channels in vascular smooth muscle cells in the systemic and splanchnic arterial circulation. Hydrogen sulphide (H2S) has recently been identified as a novel gaseous transmitter that induces vasodilatation through activation of KATP channels in vascular smooth muscle cells. In this brief review, we comment on what is known about H2S, vascular and neurological function, and postulate its role in the pathogenesis of the vascular abnormalities in cirrhosis.</description><subject>Aqueous solutions</subject><subject>Biological and medical sciences</subject><subject>carbon monoxide</subject><subject>Carbon Monoxide - metabolism</subject><subject>cirrhosis</subject><subject>Coronary vessels</subject><subject>Enzymes</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene expression</subject><subject>H2S</subject><subject>Humans</subject><subject>Hydrogen Sulfide - metabolism</subject><subject>hydrogen sulphide</subject><subject>hyperdynamic circulation</subject><subject>Hypotheses</subject><subject>Leading</subject><subject>Liver Circulation</subject><subject>Liver Cirrhosis - physiopathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>N-methyl-D-aspartate</subject><subject>Nervous system</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>NMDA</subject><subject>Other diseases. Semiology</subject><subject>Physiology</subject><subject>Potassium Channels - physiology</subject><subject>Pulmonary arteries</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Studies</subject><subject>Veins & arteries</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc2P0zAQxS0EYrsLZ24oEoIDUrr-dswBCVXQRSyFA3DgYrmO07gkdrGTFf3vcZRqF7hwsTWa3zy9mQfAEwSXCBF-uRuHJYaQLiHjjPF7YIEor0qCq-o-WECIRMkElWfgPKU9hLCqJHoIzhBHgnIOF-Dj1bGOYWd9kcbu0LraFtrXxdDaoj0ebKyPXvfOFMZFM3Z6cMEXzk9lbENy6VWhJzDkgVw9Ag8a3SX7-PRfgK_v3n5ZXZXXn9bvV2-uyy3DeChFdkJ1xWAlORcUN5ISQwy3xCAoKJSNwKixpM6vlKZmWwIx5prUsNGCSXIBXs-6h3Hb29pYP0TdqUN0vY5HFbRTf3e8a9Uu3CgkBBUSZ4EXJ4EYfo42Dap3ydiu096GMSleCcnysTL47B9wH8bo83KTliQEUkIydTlTJoaUom1urSCopqBUDkpNQak5qDzx9M8N7vhTMhl4fgJ0MrprovbGpTtOYJ4vMRksZ86lwf667ev4Q3FBBFObbyu1Xn9gm-90oz5n_uXMb_v9f13-BhfTuB0</recordid><startdate>20051201</startdate><enddate>20051201</enddate><creator>Ebrahimkhani, M R</creator><creator>Mani, A R</creator><creator>Moore, K</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>Copyright 2005 by Gut</general><scope>BSCLL</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</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>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20051201</creationdate><title>Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: a hypothesis</title><author>Ebrahimkhani, M R ; Mani, A R ; Moore, K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b522t-70004a8508966742f943c3c6e3c107409f721fe3d21f99cd5b30226a3d0fa7593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aqueous solutions</topic><topic>Biological and medical sciences</topic><topic>carbon monoxide</topic><topic>Carbon Monoxide - metabolism</topic><topic>cirrhosis</topic><topic>Coronary vessels</topic><topic>Enzymes</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene expression</topic><topic>H2S</topic><topic>Humans</topic><topic>Hydrogen Sulfide - metabolism</topic><topic>hydrogen sulphide</topic><topic>hyperdynamic circulation</topic><topic>Hypotheses</topic><topic>Leading</topic><topic>Liver Circulation</topic><topic>Liver Cirrhosis - physiopathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>N-methyl-D-aspartate</topic><topic>Nervous system</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>NMDA</topic><topic>Other diseases. 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Several mechanisms have been postulated to be involved in the development of systemic vasodilatation, including increased synthesis of nitric oxide, hyperglucagonaemia, increased carbon monoxide synthesis, and activation of KATP channels in vascular smooth muscle cells in the systemic and splanchnic arterial circulation. Hydrogen sulphide (H2S) has recently been identified as a novel gaseous transmitter that induces vasodilatation through activation of KATP channels in vascular smooth muscle cells. In this brief review, we comment on what is known about H2S, vascular and neurological function, and postulate its role in the pathogenesis of the vascular abnormalities in cirrhosis.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>16174660</pmid><doi>10.1136/gut.2004.056556</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aqueous solutions Biological and medical sciences carbon monoxide Carbon Monoxide - metabolism cirrhosis Coronary vessels Enzymes Gastroenterology. Liver. Pancreas. Abdomen Gene expression H2S Humans Hydrogen Sulfide - metabolism hydrogen sulphide hyperdynamic circulation Hypotheses Leading Liver Circulation Liver Cirrhosis - physiopathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences N-methyl-D-aspartate Nervous system Nitric oxide Nitric Oxide - metabolism NMDA Other diseases. Semiology Physiology Potassium Channels - physiology Pulmonary arteries Rodents Smooth muscle Studies Veins & arteries |
title | Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: a hypothesis |
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