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Liver Perfusion And Hepatocellular Inflammatory Response In Sepsis
Sepsis is characterized by disturbances in liver perfusion and alterations in intrahepatic cellular functions and interactions. This provokes structural and functional liver damage as well as hepatocellular activation that is believed to perpetuate the immuno-inflammatory response. Changes in hepati...
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Published in: | Acta clinica belgica (English ed. Online) 1999-08, Vol.54 (4), p.201-206 |
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container_title | Acta clinica belgica (English ed. Online) |
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creator | Smets, D. Spapen, H. Diltoer, M. Nguyen, D.N. Hubloue, I. Huyghens, L. |
description | Sepsis is characterized by disturbances in liver perfusion and alterations in intrahepatic cellular functions and interactions. This provokes structural and functional liver damage as well as hepatocellular activation that is believed to perpetuate the immuno-inflammatory response. Changes in hepatic perfusion during sepsis are still poorly understood due to the heterogeneity of septic animal models and the difficult accessibility of the hepatic circulation in humans. Sinusoidal blood flow is severely compromised during sepsis due to a decline in perfused sinusoidal area in association with a decrease in sinusoidal flow velocity. Imbalances in the production of nitric oxide may account for these (micro) circulatory disorders.
Interactions between liver macrophages, activated endothelial cells and hepatocytes determine the intensity of inflammation and contribute to initial liver damage. Hepatocellular injury is then enhanced by attracted and invading neutrophils. The management of hepatic dysfunction during sepsis is largely supportive and based on prevention and vigorous resuscitation including early nutritional support and adequate oxygenation. Interestingly, experimental studies suggest that pharmacological interventions with significant hemodynamic effects, such as dobutamine and nitric oxide synthase inhibitors, may adversely affect the liver during the septic process. |
doi_str_mv | 10.1080/17843286.1999.11754232 |
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Interactions between liver macrophages, activated endothelial cells and hepatocytes determine the intensity of inflammation and contribute to initial liver damage. Hepatocellular injury is then enhanced by attracted and invading neutrophils. The management of hepatic dysfunction during sepsis is largely supportive and based on prevention and vigorous resuscitation including early nutritional support and adequate oxygenation. Interestingly, experimental studies suggest that pharmacological interventions with significant hemodynamic effects, such as dobutamine and nitric oxide synthase inhibitors, may adversely affect the liver during the septic process.</description><identifier>ISSN: 1784-3286</identifier><identifier>EISSN: 2295-3337</identifier><identifier>DOI: 10.1080/17843286.1999.11754232</identifier><identifier>PMID: 10544510</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>Animals ; Blood Flow Velocity - physiology ; Cell Communication ; Disease Models, Animal ; Endothelium, Vascular - pathology ; Endothelium, Vascular - physiopathology ; endotoxin ; Humans ; Liver ; Liver - immunology ; Liver - pathology ; Liver - physiopathology ; Liver Circulation - immunology ; Liver Circulation - physiology ; Macrophages - physiology ; Microcirculation - physiology ; Neutrophil Activation - physiology ; Neutrophil Infiltration - physiology ; nitric oxide ; Nitric Oxide - metabolism ; sepsis ; Systemic Inflammatory Response Syndrome - immunology ; Systemic Inflammatory Response Syndrome - physiopathology ; Vasodilator Agents - metabolism</subject><ispartof>Acta clinica belgica (English ed. Online), 1999-08, Vol.54 (4), p.201-206</ispartof><rights>Copyright © 1999 Acta Clinica Belgica 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-8c9b91a88d86eef2457779e98cedbcc08b7cc3da01ba4c05475a483e4b1161a33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10544510$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Smets, D.</creatorcontrib><creatorcontrib>Spapen, H.</creatorcontrib><creatorcontrib>Diltoer, M.</creatorcontrib><creatorcontrib>Nguyen, D.N.</creatorcontrib><creatorcontrib>Hubloue, I.</creatorcontrib><creatorcontrib>Huyghens, L.</creatorcontrib><title>Liver Perfusion And Hepatocellular Inflammatory Response In Sepsis</title><title>Acta clinica belgica (English ed. Online)</title><addtitle>Acta Clin Belg</addtitle><description>Sepsis is characterized by disturbances in liver perfusion and alterations in intrahepatic cellular functions and interactions. This provokes structural and functional liver damage as well as hepatocellular activation that is believed to perpetuate the immuno-inflammatory response. Changes in hepatic perfusion during sepsis are still poorly understood due to the heterogeneity of septic animal models and the difficult accessibility of the hepatic circulation in humans. Sinusoidal blood flow is severely compromised during sepsis due to a decline in perfused sinusoidal area in association with a decrease in sinusoidal flow velocity. Imbalances in the production of nitric oxide may account for these (micro) circulatory disorders.
Interactions between liver macrophages, activated endothelial cells and hepatocytes determine the intensity of inflammation and contribute to initial liver damage. Hepatocellular injury is then enhanced by attracted and invading neutrophils. The management of hepatic dysfunction during sepsis is largely supportive and based on prevention and vigorous resuscitation including early nutritional support and adequate oxygenation. Interestingly, experimental studies suggest that pharmacological interventions with significant hemodynamic effects, such as dobutamine and nitric oxide synthase inhibitors, may adversely affect the liver during the septic process.</description><subject>Animals</subject><subject>Blood Flow Velocity - physiology</subject><subject>Cell Communication</subject><subject>Disease Models, Animal</subject><subject>Endothelium, Vascular - pathology</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>endotoxin</subject><subject>Humans</subject><subject>Liver</subject><subject>Liver - immunology</subject><subject>Liver - pathology</subject><subject>Liver - physiopathology</subject><subject>Liver Circulation - immunology</subject><subject>Liver Circulation - physiology</subject><subject>Macrophages - physiology</subject><subject>Microcirculation - physiology</subject><subject>Neutrophil Activation - physiology</subject><subject>Neutrophil Infiltration - physiology</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>sepsis</subject><subject>Systemic Inflammatory Response Syndrome - immunology</subject><subject>Systemic Inflammatory Response Syndrome - physiopathology</subject><subject>Vasodilator Agents - metabolism</subject><issn>1784-3286</issn><issn>2295-3337</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNqFkE1Lw0AQhhdRbKn9CyUnb6n7lezusRa1hYLix3nZbCYQSbJxN1H6701IC96cy8DwzLzDg9CK4DXBEt8RITmjMl0TpdSaEJFwyugFmlOqkpgxJi7RfITikZqhZQifeCimeMroNZoRnHCeEDxH94fyG3z0Ar7oQ-maaNPk0Q5a0zkLVdVXxkf7pqhMXQ8jf4xeIbSuCTBMozdoQxlu0FVhqgDLU1-gj8eH9-0uPjw_7bebQ2yH3C6WVmWKGClzmQIUlCdCCAVKWsgza7HMhLUsN5hkhtvhQZEYLhnwjJCUGMYW6Ha623r31UPodF2G8UnTgOuDThWlQtF0ANMJtN6F4KHQrS9r44-aYD0K1GeBehSozwKHxdUpoc9qyP-sTboGYDMBZVM4X5sf56tcd-ZYOV9409gyaPZPyC9njX-N</recordid><startdate>19990801</startdate><enddate>19990801</enddate><creator>Smets, D.</creator><creator>Spapen, H.</creator><creator>Diltoer, M.</creator><creator>Nguyen, D.N.</creator><creator>Hubloue, I.</creator><creator>Huyghens, L.</creator><general>Taylor & Francis</general><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>19990801</creationdate><title>Liver Perfusion And Hepatocellular Inflammatory Response In Sepsis</title><author>Smets, D. ; Spapen, H. ; Diltoer, M. ; Nguyen, D.N. ; Hubloue, I. ; Huyghens, L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c394t-8c9b91a88d86eef2457779e98cedbcc08b7cc3da01ba4c05475a483e4b1161a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Blood Flow Velocity - physiology</topic><topic>Cell Communication</topic><topic>Disease Models, Animal</topic><topic>Endothelium, Vascular - pathology</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>endotoxin</topic><topic>Humans</topic><topic>Liver</topic><topic>Liver - immunology</topic><topic>Liver - pathology</topic><topic>Liver - physiopathology</topic><topic>Liver Circulation - immunology</topic><topic>Liver Circulation - physiology</topic><topic>Macrophages - physiology</topic><topic>Microcirculation - physiology</topic><topic>Neutrophil Activation - physiology</topic><topic>Neutrophil Infiltration - physiology</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>sepsis</topic><topic>Systemic Inflammatory Response Syndrome - immunology</topic><topic>Systemic Inflammatory Response Syndrome - physiopathology</topic><topic>Vasodilator Agents - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Smets, D.</creatorcontrib><creatorcontrib>Spapen, H.</creatorcontrib><creatorcontrib>Diltoer, M.</creatorcontrib><creatorcontrib>Nguyen, D.N.</creatorcontrib><creatorcontrib>Hubloue, I.</creatorcontrib><creatorcontrib>Huyghens, L.</creatorcontrib><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>Acta clinica belgica (English ed. Online)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Smets, D.</au><au>Spapen, H.</au><au>Diltoer, M.</au><au>Nguyen, D.N.</au><au>Hubloue, I.</au><au>Huyghens, L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Liver Perfusion And Hepatocellular Inflammatory Response In Sepsis</atitle><jtitle>Acta clinica belgica (English ed. Online)</jtitle><addtitle>Acta Clin Belg</addtitle><date>1999-08-01</date><risdate>1999</risdate><volume>54</volume><issue>4</issue><spage>201</spage><epage>206</epage><pages>201-206</pages><issn>1784-3286</issn><eissn>2295-3337</eissn><abstract>Sepsis is characterized by disturbances in liver perfusion and alterations in intrahepatic cellular functions and interactions. This provokes structural and functional liver damage as well as hepatocellular activation that is believed to perpetuate the immuno-inflammatory response. Changes in hepatic perfusion during sepsis are still poorly understood due to the heterogeneity of septic animal models and the difficult accessibility of the hepatic circulation in humans. Sinusoidal blood flow is severely compromised during sepsis due to a decline in perfused sinusoidal area in association with a decrease in sinusoidal flow velocity. Imbalances in the production of nitric oxide may account for these (micro) circulatory disorders.
Interactions between liver macrophages, activated endothelial cells and hepatocytes determine the intensity of inflammation and contribute to initial liver damage. Hepatocellular injury is then enhanced by attracted and invading neutrophils. The management of hepatic dysfunction during sepsis is largely supportive and based on prevention and vigorous resuscitation including early nutritional support and adequate oxygenation. Interestingly, experimental studies suggest that pharmacological interventions with significant hemodynamic effects, such as dobutamine and nitric oxide synthase inhibitors, may adversely affect the liver during the septic process.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>10544510</pmid><doi>10.1080/17843286.1999.11754232</doi><tpages>6</tpages></addata></record> |
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subjects | Animals Blood Flow Velocity - physiology Cell Communication Disease Models, Animal Endothelium, Vascular - pathology Endothelium, Vascular - physiopathology endotoxin Humans Liver Liver - immunology Liver - pathology Liver - physiopathology Liver Circulation - immunology Liver Circulation - physiology Macrophages - physiology Microcirculation - physiology Neutrophil Activation - physiology Neutrophil Infiltration - physiology nitric oxide Nitric Oxide - metabolism sepsis Systemic Inflammatory Response Syndrome - immunology Systemic Inflammatory Response Syndrome - physiopathology Vasodilator Agents - metabolism |
title | Liver Perfusion And Hepatocellular Inflammatory Response In Sepsis |
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