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Plasma thrombin activatable fibrinolysis inhibitor and tissue factor pathway inhibitor changes following sepsis.

Authors: Ravindranath, TM  Goto, M  Iqbal, O  Florian-Kujawski, M  Hoppensteadt, D  Hammadeh, R  Sayeed, MM  Fareed, J 
Citation: Ravindranath TM, etal., Clin Appl Thromb Hemost. 2007 Oct;13(4):362-8.
Pubmed: (View Article at PubMed) PMID:17911187
DOI: Full-text: DOI:10.1177/1076029607305580

Sepsis-induced systemic inflammation results in coagulation abnormalities that may be different in gram-positive and gram-negative infections. We used ciprofloxacin to induce a predominantly gram-positive Enterococcus faecalis polymicrobial sepsis in rats. Ciprofloxacin-untreated rats exhibited a predominantly gram-negative polymicrobial sepsis. Rats were subjected to 30% body surface area burn (B), cecal ligation puncture (CLP) with a 22-gauge needle, and B + CLP. Ciprofloxacin-treated B + CLP rats showed a significant decrease in plasma thrombin activatable fibrinolysis inhibitor (TAFI) levels compared with sham rats. However, plasma tissue factor pathway inhibitor (TFPI) levels decreased significantly in B, CLP, and B + CLP groups compared with sham rats. The ciprofloxacin-untreated group showed a significant decrease in plasma TAFI levels in CLP and B + CLP and plasma TFPI levels decreased in all 3 groups compared with sham rats. Histological changes in the liver and kidney included vascular congestion and parenchyma bleed following B + CLP in ciprofloxacin-untreated rats. These results suggest that plasma TAFI and TFPI levels differ depending on the type of bacteria involved in the septic process.


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RGD Object Information
RGD ID: 2313646
Created: 2009-10-06
Species: All species
Last Modified: 2009-10-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.