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   <subfield code="a">Atherosclerosis aggravates ischemia/reperfusion injury in the gut and remote damage in the liver and the lung</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[René Schramm, Frank Appel, Manfred Reinacher, Hans-Joachim Schäfers, Benjamin Bierbach, Jan Slotta, Henrik Thorlacius, Michael Menger]</subfield>
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   <subfield code="a">Objective: We investigated whether mesenteric ischemia/reperfusion (I/R)-associated gut injury and remote liver and lung damage are affected by prevalent atherosclerosis. Methods: Mesenteric ischemia was induced in atherosclerotic ApoE-deficient (ApoE−/−) and control C57BL/6 mice by clamping the superior mesenteric artery for 30min. Mesenteric microcirculatory dysfunction and leukocytic inflammation were studied in the terminal ileum by intravital fluorescence microscopy (IVM). Histological analyses included quantitative assessment of parenchymal injury in the terminal ileum, liver and lung. Results: In the gut, IVM of the terminal ileum revealed aggravated postischemic microcirculatory dysfunction and absence of reactive hyperemia-induced vasodilation in atherosclerotic mice compared to controls. In addition, leukocyte-endothelial cell adhesive interactions, i.e. rolling and firm adhesion, were significantly increased in atherosclerotic animals. This was associated with enhanced mucosal tissue damage in ApoE−/− mice. Moreover, mesenteric I/R-provoked remote parenchymal injury in the liver was found to be significantly aggravated in atherosclerotic mice. This was accompanied by enhanced neutrophilic lung inflammation in ApoE−/− mice. Conclusion: Prevalent generalized atherosclerosis not only aggravates splanchnic microcirculatory dysfunction and leukocytic inflammation in response to mesenteric I/R, but also exacerbates mucosal tissue damage and remote injury in the liver and the lung.</subfield>
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   <subfield code="a">Springer Basel AG, 2011</subfield>
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   <subfield code="a">Atherosclerosis</subfield>
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   <subfield code="a">GI inflammation</subfield>
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   <subfield code="a">In vivo inflammation</subfield>
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   <subfield code="a">Intravital microscopy</subfield>
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   <subfield code="a">Schramm</subfield>
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   <subfield code="u">Clinic of Cardiac Surgery, Ludwig-Maximilians-University of Munich-Grosshadern, Marchioninistr.15, 81377, Munich, Germany</subfield>
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   <subfield code="a">Appel</subfield>
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   <subfield code="u">Institute for Clinical and Experimental Surgery, University of Saarland, Homburg, Germany</subfield>
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   <subfield code="a">Reinacher</subfield>
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   <subfield code="u">Institute for Veterinary Pathology, University of Giessen, Giessen, Germany</subfield>
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   <subfield code="a">Schäfers</subfield>
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   <subfield code="u">Department of Surgery, Lund University, Lund, Sweden</subfield>
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   <subfield code="t">Inflammation Research</subfield>
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