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http://purl.uniprot.org/citations/19333141http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19333141http://www.w3.org/2000/01/rdf-schema#comment"In severely injured and hypoperfused trauma patients, endogenous acute coagulopathy (EAC) is associated with an increased morbidity and mortality. Recent human data correlate this coagulopathy with activation of the protein C pathway. To examine the mechanistic role of protein C in the development of EAC, we used a mouse model of trauma and hemorrhagic shock, characterized by the combination of tissue injury and severe metabolic acidosis. Mice were subjected to one of four treatment groups: 1) C, control; 2) T, trauma (laparotomy); 3) H, hemorrhage (MAP, 35 mmHg x 60 min); 4) TH, trauma + hemorrhage. After 60 min, blood was drawn for analysis. Compared with C mice, the TH mice had a significantly elevated activated partial thromboplastin time (23.3 vs. 34.5 s) and significantly increased levels of activated protein C (aPC; 2.30 vs. 13.58 ng/mL). In contrast, T and H mice did not develop an elevated activated partial thromboplastin time or increased aPC. Selective inhibition of the anticoagulant property of aPC prevented the coagulopathy seen in response to trauma/hemorrhage (23.5 vs. 38.6 s [inhibitory vs. control monoclonal antibody]) with no impact on survival during the shock period. However, complete blockade of both the anticoagulant and cytoprotective functions of aPC caused 100% mortality within 45 min of shock, with histopathology evidence of pulmonary thrombosis and perivascular hemorrhage. These results indicate that our unique mouse model of T/H shock mimics our previous observations in trauma patients and demonstrates that EAC is mediated by the activation of the protein C pathway. In addition, the cytoprotective effect of protein C activation seems to be necessary for survival of the initial shock injury."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.org/dc/terms/identifier"doi:10.1097/shk.0b013e3181a5a632"xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Xu J."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Chesebro B.B."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Cohen M.J."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Frith D."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Esmon C.T."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Pittet J.F."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Brohi K."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Carles M."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/author"Rahn P."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/name"Shock"xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/pages"659-665"xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/title"Increase in activated protein C mediates acute traumatic coagulopathy in mice."xsd:string
http://purl.uniprot.org/citations/19333141http://purl.uniprot.org/core/volume"32"xsd:string
http://purl.uniprot.org/citations/19333141http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19333141
http://purl.uniprot.org/citations/19333141http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19333141
http://purl.uniprot.org/uniprot/#_P33587-mappedCitation-19333141http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19333141
http://purl.uniprot.org/uniprot/P33587http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/19333141