Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state
Background/Aims: Ischemic preconditioning (IP) is known to protect hepatic tissue from ischemia–reperfusion injury. However, the mechanisms involved are not fully understood yet. Methods: Using intravital multifluorescence microscopy in the rat liver, we studied whether IP exerts its beneficial effe...
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| Veröffentlicht in: | Journal of hepatology 2003, Vol.38 (1), p.59-66 |
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| creator | Glanemann, Matthias Vollmar, Brigitte Nussler, Andreas K Schaefer, Thilo Neuhaus, Peter Menger, Michael D |
| description | Background/Aims: Ischemic preconditioning (IP) is known to protect hepatic tissue from ischemia–reperfusion injury. However, the mechanisms involved are not fully understood yet.
Methods: Using intravital multifluorescence microscopy in the rat liver, we studied whether IP exerts its beneficial effect by modulating postischemic Kupffer cell activation, leukocyte–endothelial cell interaction, microvascular no-reflow, mitochondrial redox state, and, thus, tissue oxygenation.
Results: Portal triad cross-clamping (45 min) followed by reperfusion induced Kupffer cell activation, microvascular leukocyte adherence, sinusoidal perfusion failure (no-reflow) and alteration of mitochondrial redox state (tissue hypoxia) (
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| doi_str_mv | 10.1016/S0168-8278(02)00327-6 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72886654</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0168827802003276</els_id><sourcerecordid>72886654</sourcerecordid><originalsourceid>FETCH-LOGICAL-c457t-b5695a4df4ed1073eb952610f26d5bf18e1cea97f76097967dbac10cdbddc4743</originalsourceid><addsrcrecordid>eNqFkc9u1DAQxi1ERZfCI4ByAcEhdOyN7eRUoYo_lSr1AJwtxx6zrpJ4sZ2KfQceuk6zosdebHn0m2_8zUfIGwqfKFBx_qMcbd0y2X4A9hFgy2QtnpENFQA1iIY-J5v_yCl5mdItFAq65gU5paxpgQu6If-uktnh6E21j2jCZH32YfLT7_IOGU1OlYthrHa417lQfsX1ecQ9RjenQtd-up3joeoPi0jCeKcXkSq4qgjHYHw087DW9GRLMQezK7Oi10MV0Ya_dco64yty4vSQ8PXxPiO_vn75efm9vr75dnX5-bo2DZe57rnouG6sa9BSkFvsO84EBceE5b2jLVKDupNOCuhkJ6TttaFgbG-taWSzPSPvV93i8c-MKaux-MJh0BOGOSnJ2lYIvoB8BYuLlCI6tY9-1PGgKKglBvUQg1p2rICphxiUKH1vjwPmfkT72HXcewHeHQGdjB5c1JPx6ZHjgnFgXeEuVg7LOu48RpWMx8mg9SWurGzwT3zlHnIBqXE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>72886654</pqid></control><display><type>article</type><title>Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Glanemann, Matthias ; Vollmar, Brigitte ; Nussler, Andreas K ; Schaefer, Thilo ; Neuhaus, Peter ; Menger, Michael D</creator><creatorcontrib>Glanemann, Matthias ; Vollmar, Brigitte ; Nussler, Andreas K ; Schaefer, Thilo ; Neuhaus, Peter ; Menger, Michael D</creatorcontrib><description><![CDATA[Background/Aims: Ischemic preconditioning (IP) is known to protect hepatic tissue from ischemia–reperfusion injury. However, the mechanisms involved are not fully understood yet.
Methods: Using intravital multifluorescence microscopy in the rat liver, we studied whether IP exerts its beneficial effect by modulating postischemic Kupffer cell activation, leukocyte–endothelial cell interaction, microvascular no-reflow, mitochondrial redox state, and, thus, tissue oxygenation.
Results: Portal triad cross-clamping (45 min) followed by reperfusion induced Kupffer cell activation, microvascular leukocyte adherence, sinusoidal perfusion failure (no-reflow) and alteration of mitochondrial redox state (tissue hypoxia) (
P<0.05). This resulted in liver dysfunction and parenchymal injury, as indicated by decreased bile flow and increased serum glutamate dehydrogenase (GLDH) levels (
P<0.05). IP (5 min ischemia and 30 min intermittent reperfusion) was capable to significantly reduce Kupffer cell activation (
P<0.05), which was associated with a slight attenuation of leukocyte adherence. Further, IP markedly ameliorated sinusoidal perfusion failure (
P<0.05), and, thereby, preserved adequate mitochondrial redox state (
P<0.05). As a consequence, IP prevented the decrease of bile flow (
P<0.05) and the increase in serum GLDH levels (
P<0.05).
Conclusions: IP may exert its beneficial effects on hepatic ischemia–reperfusion injury by preserving mitochondrial redox state, which is guaranteed by the prevention of reperfusion-associated Kupffer cell activation and sinusoidal perfusion failure.]]></description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/S0168-8278(02)00327-6</identifier><identifier>PMID: 12480561</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Cell Adhesion ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatic ischemia–reperfusion, Microcirculation ; Ischemic Preconditioning ; Ischemic tolerance ; Kupffer cell activation ; Kupffer Cells - physiology ; Leukocytes - physiology ; Leukocyte–endothelial cell interaction ; Liver - metabolism ; Liver - physiology ; Liver Circulation ; Male ; Medical sciences ; Microcirculation ; Mitochondria, Liver - metabolism ; Mitochondrial redox state ; No-reflow ; Oxidation-Reduction ; Oxygen - metabolism ; Phagocytosis ; Rats ; Rats, Wistar ; Reperfusion Injury - prevention & control ; Sinusoidal perfusion</subject><ispartof>Journal of hepatology, 2003, Vol.38 (1), p.59-66</ispartof><rights>2002 European Association for the Study of the Liver</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-b5695a4df4ed1073eb952610f26d5bf18e1cea97f76097967dbac10cdbddc4743</citedby><cites>FETCH-LOGICAL-c457t-b5695a4df4ed1073eb952610f26d5bf18e1cea97f76097967dbac10cdbddc4743</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168827802003276$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15625029$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12480561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Glanemann, Matthias</creatorcontrib><creatorcontrib>Vollmar, Brigitte</creatorcontrib><creatorcontrib>Nussler, Andreas K</creatorcontrib><creatorcontrib>Schaefer, Thilo</creatorcontrib><creatorcontrib>Neuhaus, Peter</creatorcontrib><creatorcontrib>Menger, Michael D</creatorcontrib><title>Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description><![CDATA[Background/Aims: Ischemic preconditioning (IP) is known to protect hepatic tissue from ischemia–reperfusion injury. However, the mechanisms involved are not fully understood yet.
Methods: Using intravital multifluorescence microscopy in the rat liver, we studied whether IP exerts its beneficial effect by modulating postischemic Kupffer cell activation, leukocyte–endothelial cell interaction, microvascular no-reflow, mitochondrial redox state, and, thus, tissue oxygenation.
Results: Portal triad cross-clamping (45 min) followed by reperfusion induced Kupffer cell activation, microvascular leukocyte adherence, sinusoidal perfusion failure (no-reflow) and alteration of mitochondrial redox state (tissue hypoxia) (
P<0.05). This resulted in liver dysfunction and parenchymal injury, as indicated by decreased bile flow and increased serum glutamate dehydrogenase (GLDH) levels (
P<0.05). IP (5 min ischemia and 30 min intermittent reperfusion) was capable to significantly reduce Kupffer cell activation (
P<0.05), which was associated with a slight attenuation of leukocyte adherence. Further, IP markedly ameliorated sinusoidal perfusion failure (
P<0.05), and, thereby, preserved adequate mitochondrial redox state (
P<0.05). As a consequence, IP prevented the decrease of bile flow (
P<0.05) and the increase in serum GLDH levels (
P<0.05).
Conclusions: IP may exert its beneficial effects on hepatic ischemia–reperfusion injury by preserving mitochondrial redox state, which is guaranteed by the prevention of reperfusion-associated Kupffer cell activation and sinusoidal perfusion failure.]]></description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Adhesion</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatic ischemia–reperfusion, Microcirculation</subject><subject>Ischemic Preconditioning</subject><subject>Ischemic tolerance</subject><subject>Kupffer cell activation</subject><subject>Kupffer Cells - physiology</subject><subject>Leukocytes - physiology</subject><subject>Leukocyte–endothelial cell interaction</subject><subject>Liver - metabolism</subject><subject>Liver - physiology</subject><subject>Liver Circulation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microcirculation</subject><subject>Mitochondria, Liver - metabolism</subject><subject>Mitochondrial redox state</subject><subject>No-reflow</subject><subject>Oxidation-Reduction</subject><subject>Oxygen - metabolism</subject><subject>Phagocytosis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Sinusoidal perfusion</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi1ERZfCI4ByAcEhdOyN7eRUoYo_lSr1AJwtxx6zrpJ4sZ2KfQceuk6zosdebHn0m2_8zUfIGwqfKFBx_qMcbd0y2X4A9hFgy2QtnpENFQA1iIY-J5v_yCl5mdItFAq65gU5paxpgQu6If-uktnh6E21j2jCZH32YfLT7_IOGU1OlYthrHa417lQfsX1ecQ9RjenQtd-up3joeoPi0jCeKcXkSq4qgjHYHw087DW9GRLMQezK7Oi10MV0Ya_dco64yty4vSQ8PXxPiO_vn75efm9vr75dnX5-bo2DZe57rnouG6sa9BSkFvsO84EBceE5b2jLVKDupNOCuhkJ6TttaFgbG-taWSzPSPvV93i8c-MKaux-MJh0BOGOSnJ2lYIvoB8BYuLlCI6tY9-1PGgKKglBvUQg1p2rICphxiUKH1vjwPmfkT72HXcewHeHQGdjB5c1JPx6ZHjgnFgXeEuVg7LOu48RpWMx8mg9SWurGzwT3zlHnIBqXE</recordid><startdate>2003</startdate><enddate>2003</enddate><creator>Glanemann, Matthias</creator><creator>Vollmar, Brigitte</creator><creator>Nussler, Andreas K</creator><creator>Schaefer, Thilo</creator><creator>Neuhaus, Peter</creator><creator>Menger, Michael D</creator><general>Elsevier B.V</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>2003</creationdate><title>Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state</title><author>Glanemann, Matthias ; Vollmar, Brigitte ; Nussler, Andreas K ; Schaefer, Thilo ; Neuhaus, Peter ; Menger, Michael D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-b5695a4df4ed1073eb952610f26d5bf18e1cea97f76097967dbac10cdbddc4743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Adhesion</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatic ischemia–reperfusion, Microcirculation</topic><topic>Ischemic Preconditioning</topic><topic>Ischemic tolerance</topic><topic>Kupffer cell activation</topic><topic>Kupffer Cells - physiology</topic><topic>Leukocytes - physiology</topic><topic>Leukocyte–endothelial cell interaction</topic><topic>Liver - metabolism</topic><topic>Liver - physiology</topic><topic>Liver Circulation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microcirculation</topic><topic>Mitochondria, Liver - metabolism</topic><topic>Mitochondrial redox state</topic><topic>No-reflow</topic><topic>Oxidation-Reduction</topic><topic>Oxygen - metabolism</topic><topic>Phagocytosis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Sinusoidal perfusion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Glanemann, Matthias</creatorcontrib><creatorcontrib>Vollmar, Brigitte</creatorcontrib><creatorcontrib>Nussler, Andreas K</creatorcontrib><creatorcontrib>Schaefer, Thilo</creatorcontrib><creatorcontrib>Neuhaus, Peter</creatorcontrib><creatorcontrib>Menger, Michael D</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>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Glanemann, Matthias</au><au>Vollmar, Brigitte</au><au>Nussler, Andreas K</au><au>Schaefer, Thilo</au><au>Neuhaus, Peter</au><au>Menger, Michael D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>2003</date><risdate>2003</risdate><volume>38</volume><issue>1</issue><spage>59</spage><epage>66</epage><pages>59-66</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract><![CDATA[Background/Aims: Ischemic preconditioning (IP) is known to protect hepatic tissue from ischemia–reperfusion injury. However, the mechanisms involved are not fully understood yet.
Methods: Using intravital multifluorescence microscopy in the rat liver, we studied whether IP exerts its beneficial effect by modulating postischemic Kupffer cell activation, leukocyte–endothelial cell interaction, microvascular no-reflow, mitochondrial redox state, and, thus, tissue oxygenation.
Results: Portal triad cross-clamping (45 min) followed by reperfusion induced Kupffer cell activation, microvascular leukocyte adherence, sinusoidal perfusion failure (no-reflow) and alteration of mitochondrial redox state (tissue hypoxia) (
P<0.05). This resulted in liver dysfunction and parenchymal injury, as indicated by decreased bile flow and increased serum glutamate dehydrogenase (GLDH) levels (
P<0.05). IP (5 min ischemia and 30 min intermittent reperfusion) was capable to significantly reduce Kupffer cell activation (
P<0.05), which was associated with a slight attenuation of leukocyte adherence. Further, IP markedly ameliorated sinusoidal perfusion failure (
P<0.05), and, thereby, preserved adequate mitochondrial redox state (
P<0.05). As a consequence, IP prevented the decrease of bile flow (
P<0.05) and the increase in serum GLDH levels (
P<0.05).
Conclusions: IP may exert its beneficial effects on hepatic ischemia–reperfusion injury by preserving mitochondrial redox state, which is guaranteed by the prevention of reperfusion-associated Kupffer cell activation and sinusoidal perfusion failure.]]></abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>12480561</pmid><doi>10.1016/S0168-8278(02)00327-6</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Cell Adhesion Gastroenterology. Liver. Pancreas. Abdomen Hepatic ischemia–reperfusion, Microcirculation Ischemic Preconditioning Ischemic tolerance Kupffer cell activation Kupffer Cells - physiology Leukocytes - physiology Leukocyte–endothelial cell interaction Liver - metabolism Liver - physiology Liver Circulation Male Medical sciences Microcirculation Mitochondria, Liver - metabolism Mitochondrial redox state No-reflow Oxidation-Reduction Oxygen - metabolism Phagocytosis Rats Rats, Wistar Reperfusion Injury - prevention & control Sinusoidal perfusion |
| title | Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state |
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