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pubmed-article:12462561pubmed:dateCreated2002-12-3lld:pubmed
pubmed-article:12462561pubmed:abstractTextPlatelets are suggested to participate in the pathogenesis of hepatic ischemia-reperfusion (I/R) injury. This study was designed to analyze platelet-endothelial cell interactions in the postischemic mouse liver in vivo and to define the role of endothelial versus platelet P-selectin for these interactions. Platelet-endothelial cell interactions were quantitatively analyzed using intravital fluorescence microscopy after lobar hepatic I/R in C57BL/6 wild-type and P-selectin-deficient mice after infusion of ex vivo rhodamine-6G-labeled wild-type and P-selectin-deficient platelets. Reperfusion injury and apoptosis were assessed by established methods. In wild-type animals, hepatic I/R caused significantly enhanced platelet-endothelial cell interactions in terminal arterioles and postsinusoidal venules as well as platelet stagnation in sinusoids. Concomitantly, transaminase and caspase-3 activities were elevated and sinusoidal perfusion was impaired. In contrast, platelet-endothelial cell interactions were nearly absent in arterioles and venules of mice lacking endothelial P-selectin, irrespective of the presence of P-selectin on infused platelets, but still significantly elevated in sinusoids. Simultaneously, sinusoidal perfusion failure was ameliorated, and transaminase- and caspase-3 activities were significantly reduced in P-selectin-deficient mice as compared with wild-type animals. The present intravital microscopic study provides, for the first time, quantitative analyses of platelet-endothelial cell interactions in the postischemic hepatic microcirculation. Our in vivo data show that endothelial P-selectin is critical for postischemic platelet-endothelial cell interactions within hepatic presinusoidal arterioles and postsinusoidal venules. P-selectin deficiency prevents microvascular injury and apoptosis after warm hepatic I/R.lld:pubmed
pubmed-article:12462561pubmed:languageenglld:pubmed
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pubmed-article:12462561pubmed:statusMEDLINElld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:BiberthalerPe...lld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:KrombachFritz...lld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:MessmerKonrad...lld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:TeupserDaniel...lld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:KhandogaAndre...lld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:EndersGeorgGlld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:AxmannStefanSlld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:HutterJoergJlld:pubmed
pubmed-article:12462561pubmed:authorpubmed-author:LuchtingBenja...lld:pubmed
pubmed-article:12462561pubmed:ownerNLMlld:pubmed
pubmed-article:12462561pubmed:authorsCompleteYlld:pubmed
pubmed-article:12462561pubmed:pagination529-35lld:pubmed
pubmed-article:12462561pubmed:dateRevised2007-11-15lld:pubmed
pubmed-article:12462561pubmed:articleTitleP-selectin mediates platelet-endothelial cell interactions and reperfusion injury in the mouse liver in vivo.lld:pubmed
pubmed-article:12462561pubmed:affiliationInstitute for Surgical Research, University of Munich, Germany.lld:pubmed
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