Moderate hypothermia blunts the inflammatory response and reduces organ injury after acute haemorrhage

Background: Reduced body temperature is a common companion to trauma/haemorrhage. Several clinical studies have identified hypothermia as an independent risk variable predisposing to increased morbidity and mortality. At the same time it is known that most enzymatic reactions are downregulated at te...

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Veröffentlicht in:Acta anaesthesiologica Scandinavica 2001-09, Vol.45 (8), p.994-1001
Hauptverfasser: Gundersen, Y., Vaagenes, P., Pharo, A., Valø, E. T., Opstad, P. K.
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container_end_page 1001
container_issue 8
container_start_page 994
container_title Acta anaesthesiologica Scandinavica
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creator Gundersen, Y.
Vaagenes, P.
Pharo, A.
Valø, E. T.
Opstad, P. K.
description Background: Reduced body temperature is a common companion to trauma/haemorrhage. Several clinical studies have identified hypothermia as an independent risk variable predisposing to increased morbidity and mortality. At the same time it is known that most enzymatic reactions are downregulated at temperatures below 37°C. Theoretically this should restrain the inflammatory response and protect the host from remote organ injury. The study was performed to test this hypothesis. Methods: Twenty‐six male Sprague Dawley rats were used for the experiments. Volume controlled haemorrhagic shock was induced by withdrawal of 2.5 ml blood/100 g body weight over 10 min. Half of the animals (n=13) were then cooled to 32.5–33°C, the other half (n=13) were kept normothermic (37.5±0.5°C). Seventy‐five minutes after initiation of bleeding, two‐thirds of the blood was retransfused. Thereafter the rats were observed for 2 h. Key substances of systemic inflammation were determined (plasma values of TNF‐α, IL‐6, IL‐10, and corticosterone; reactive oxygen species in peritoneal phagocytes), plasma markers of organ function and integrity (AST, ALT, αGST, creatinine, urea), and survival. Results: Hypothermia reduced the release of IL‐6 (P
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T. ; Opstad, P. K.</creator><creatorcontrib>Gundersen, Y. ; Vaagenes, P. ; Pharo, A. ; Valø, E. T. ; Opstad, P. K.</creatorcontrib><description>Background: Reduced body temperature is a common companion to trauma/haemorrhage. Several clinical studies have identified hypothermia as an independent risk variable predisposing to increased morbidity and mortality. At the same time it is known that most enzymatic reactions are downregulated at temperatures below 37°C. Theoretically this should restrain the inflammatory response and protect the host from remote organ injury. The study was performed to test this hypothesis. Methods: Twenty‐six male Sprague Dawley rats were used for the experiments. Volume controlled haemorrhagic shock was induced by withdrawal of 2.5 ml blood/100 g body weight over 10 min. Half of the animals (n=13) were then cooled to 32.5–33°C, the other half (n=13) were kept normothermic (37.5±0.5°C). Seventy‐five minutes after initiation of bleeding, two‐thirds of the blood was retransfused. Thereafter the rats were observed for 2 h. Key substances of systemic inflammation were determined (plasma values of TNF‐α, IL‐6, IL‐10, and corticosterone; reactive oxygen species in peritoneal phagocytes), plasma markers of organ function and integrity (AST, ALT, αGST, creatinine, urea), and survival. Results: Hypothermia reduced the release of IL‐6 (P&lt;0.01). The reductions of plasma levels of TNFα (P=0.07) and IL‐10 (P=0.09) were less clear‐cut. The release of reactive oxygen species diminished (P&lt;0.01). Organ injury was ameliorated, as reflected by decreased levels of AST (P&lt;0.01), αGST (P&lt;0.01), and creatinine (P&lt;0.01). Both groups experienced an almost identical increase of plasma corticosterone. None of the hypothermic rats died, compared to two normothermic. Conclusion: Moderate hypothermia had an organ protective effect in this model of controlled haemorrhagic shock. This coincided with a significant reduction of the proximal cytokine IL‐6 and reactive oxygen species, which conceivably influenced the outcome.</description><identifier>ISSN: 0001-5172</identifier><identifier>EISSN: 1399-6576</identifier><identifier>DOI: 10.1034/j.1399-6576.2001.450812.x</identifier><identifier>PMID: 11576051</identifier><identifier>CODEN: AANEAB</identifier><language>eng</language><publisher>Copenhagen: Munksgaard International Publishers</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; cytokines ; Emergency and intensive cardiocirculatory care. Cardiogenic shock. 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T.</creatorcontrib><creatorcontrib>Opstad, P. K.</creatorcontrib><title>Moderate hypothermia blunts the inflammatory response and reduces organ injury after acute haemorrhage</title><title>Acta anaesthesiologica Scandinavica</title><addtitle>Acta Anaesthesiol Scand</addtitle><description>Background: Reduced body temperature is a common companion to trauma/haemorrhage. Several clinical studies have identified hypothermia as an independent risk variable predisposing to increased morbidity and mortality. At the same time it is known that most enzymatic reactions are downregulated at temperatures below 37°C. Theoretically this should restrain the inflammatory response and protect the host from remote organ injury. The study was performed to test this hypothesis. Methods: Twenty‐six male Sprague Dawley rats were used for the experiments. Volume controlled haemorrhagic shock was induced by withdrawal of 2.5 ml blood/100 g body weight over 10 min. Half of the animals (n=13) were then cooled to 32.5–33°C, the other half (n=13) were kept normothermic (37.5±0.5°C). Seventy‐five minutes after initiation of bleeding, two‐thirds of the blood was retransfused. Thereafter the rats were observed for 2 h. Key substances of systemic inflammation were determined (plasma values of TNF‐α, IL‐6, IL‐10, and corticosterone; reactive oxygen species in peritoneal phagocytes), plasma markers of organ function and integrity (AST, ALT, αGST, creatinine, urea), and survival. Results: Hypothermia reduced the release of IL‐6 (P&lt;0.01). The reductions of plasma levels of TNFα (P=0.07) and IL‐10 (P=0.09) were less clear‐cut. The release of reactive oxygen species diminished (P&lt;0.01). Organ injury was ameliorated, as reflected by decreased levels of AST (P&lt;0.01), αGST (P&lt;0.01), and creatinine (P&lt;0.01). Both groups experienced an almost identical increase of plasma corticosterone. None of the hypothermic rats died, compared to two normothermic. Conclusion: Moderate hypothermia had an organ protective effect in this model of controlled haemorrhagic shock. This coincided with a significant reduction of the proximal cytokine IL‐6 and reactive oxygen species, which conceivably influenced the outcome.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>cytokines</subject><subject>Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care</subject><subject>Hemodynamics</subject><subject>hemorrhagic shock</subject><subject>Hypothalamo-Hypophyseal System - physiology</subject><subject>Hypothermia</subject><subject>Hypothermia, Induced</subject><subject>Inflammation - prevention &amp; control</subject><subject>Intensive care medicine</subject><subject>Interleukin-10 - blood</subject><subject>Interleukin-6 - blood</subject><subject>Luminescent Measurements</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pituitary-Adrenal System - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>reactive oxygen species</subject><subject>Shock, Hemorrhagic - complications</subject><subject>Shock, Hemorrhagic - immunology</subject><subject>systemic inflammation</subject><subject>Tumor Necrosis Factor-alpha - analysis</subject><issn>0001-5172</issn><issn>1399-6576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMFu1DAURS1ERYfCL6AgIXYJdhzb8Y5pBQXUgqAgltaL89LJkMRTOxEzf4-jjFqWXdlP79xj6xLymtGMUV6822aMa51KoWSWU8qyQtCS5dn-CVndb56SFY27VDCVn5LnIWzjyAutn5FTxiJABVuR5trV6GHEZHPYuXGDvm8hqbppGEMSx6Qdmg76HkbnD4nHsHNDwASGOg71ZDEkzt_CELntFAloRvQJ2Gk2AvbO-w3c4gty0kAX8OXxPCO_Pn74efEpvfp2-flifZXagqs8ZaWGipey1sCLympdKQpSWc1y2gjKQEtaChRMK1CyySsJZVUiV7qKwZrxM_J28e68u5swjKZvg8WugwHdFIyKolIqEUG9gNa7EDw2ZufbHvzBMGrmks3WzFWauUozl2yWks0-Zl8dH5mqHuuH5LHVCLw5AhAsdI2HwbbhPy7PRTFj7xfsb9vh4fEfMOv1zXKPinRRtGHE_b0C_B8jFVfC_P56ab6fn-viy48bo_g_aZCozw</recordid><startdate>200109</startdate><enddate>200109</enddate><creator>Gundersen, Y.</creator><creator>Vaagenes, P.</creator><creator>Pharo, A.</creator><creator>Valø, E. 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Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>cytokines</topic><topic>Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care</topic><topic>Hemodynamics</topic><topic>hemorrhagic shock</topic><topic>Hypothalamo-Hypophyseal System - physiology</topic><topic>Hypothermia</topic><topic>Hypothermia, Induced</topic><topic>Inflammation - prevention &amp; control</topic><topic>Intensive care medicine</topic><topic>Interleukin-10 - blood</topic><topic>Interleukin-6 - blood</topic><topic>Luminescent Measurements</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pituitary-Adrenal System - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>reactive oxygen species</topic><topic>Shock, Hemorrhagic - complications</topic><topic>Shock, Hemorrhagic - immunology</topic><topic>systemic inflammation</topic><topic>Tumor Necrosis Factor-alpha - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gundersen, Y.</creatorcontrib><creatorcontrib>Vaagenes, P.</creatorcontrib><creatorcontrib>Pharo, A.</creatorcontrib><creatorcontrib>Valø, E. T.</creatorcontrib><creatorcontrib>Opstad, P. K.</creatorcontrib><collection>Istex</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>Acta anaesthesiologica Scandinavica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gundersen, Y.</au><au>Vaagenes, P.</au><au>Pharo, A.</au><au>Valø, E. T.</au><au>Opstad, P. K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Moderate hypothermia blunts the inflammatory response and reduces organ injury after acute haemorrhage</atitle><jtitle>Acta anaesthesiologica Scandinavica</jtitle><addtitle>Acta Anaesthesiol Scand</addtitle><date>2001-09</date><risdate>2001</risdate><volume>45</volume><issue>8</issue><spage>994</spage><epage>1001</epage><pages>994-1001</pages><issn>0001-5172</issn><eissn>1399-6576</eissn><coden>AANEAB</coden><abstract>Background: Reduced body temperature is a common companion to trauma/haemorrhage. Several clinical studies have identified hypothermia as an independent risk variable predisposing to increased morbidity and mortality. At the same time it is known that most enzymatic reactions are downregulated at temperatures below 37°C. Theoretically this should restrain the inflammatory response and protect the host from remote organ injury. The study was performed to test this hypothesis. Methods: Twenty‐six male Sprague Dawley rats were used for the experiments. Volume controlled haemorrhagic shock was induced by withdrawal of 2.5 ml blood/100 g body weight over 10 min. Half of the animals (n=13) were then cooled to 32.5–33°C, the other half (n=13) were kept normothermic (37.5±0.5°C). Seventy‐five minutes after initiation of bleeding, two‐thirds of the blood was retransfused. Thereafter the rats were observed for 2 h. Key substances of systemic inflammation were determined (plasma values of TNF‐α, IL‐6, IL‐10, and corticosterone; reactive oxygen species in peritoneal phagocytes), plasma markers of organ function and integrity (AST, ALT, αGST, creatinine, urea), and survival. Results: Hypothermia reduced the release of IL‐6 (P&lt;0.01). The reductions of plasma levels of TNFα (P=0.07) and IL‐10 (P=0.09) were less clear‐cut. The release of reactive oxygen species diminished (P&lt;0.01). Organ injury was ameliorated, as reflected by decreased levels of AST (P&lt;0.01), αGST (P&lt;0.01), and creatinine (P&lt;0.01). Both groups experienced an almost identical increase of plasma corticosterone. None of the hypothermic rats died, compared to two normothermic. Conclusion: Moderate hypothermia had an organ protective effect in this model of controlled haemorrhagic shock. This coincided with a significant reduction of the proximal cytokine IL‐6 and reactive oxygen species, which conceivably influenced the outcome.</abstract><cop>Copenhagen</cop><pub>Munksgaard International Publishers</pub><pmid>11576051</pmid><doi>10.1034/j.1399-6576.2001.450812.x</doi><tpages>8</tpages></addata></record>
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subjects Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
cytokines
Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care
Hemodynamics
hemorrhagic shock
Hypothalamo-Hypophyseal System - physiology
Hypothermia
Hypothermia, Induced
Inflammation - prevention & control
Intensive care medicine
Interleukin-10 - blood
Interleukin-6 - blood
Luminescent Measurements
Male
Medical sciences
Pituitary-Adrenal System - physiology
Rats
Rats, Sprague-Dawley
reactive oxygen species
Shock, Hemorrhagic - complications
Shock, Hemorrhagic - immunology
systemic inflammation
Tumor Necrosis Factor-alpha - analysis
title Moderate hypothermia blunts the inflammatory response and reduces organ injury after acute haemorrhage
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