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Antithrombin III (AT) and recombinant tissue plasminogen activator (R-TPA) used singly and in combination versus supportive care for treatment of endotoxin-induced disseminated intravascular coagulation (DIC) in the neonatal pig

DOI: 10.1186/1477-9560-4-7

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Abstract:

DIC was induced in twenty-seven neonatal pigs (7 to 14 days of age) by intravenous administration of E. coli endotoxin (800 μg/kg over 30 min). The piglets were divided into 4 groups on the basis of treatment protocol [A: supportive care alone; B: Antithrombin III (AT, 50 μg/kg bolus, 25 μg/kg per hr continuous infusion) and supportive care; C: Recombinant Tissue Plasminogen Activator (R-TPA, 25 μg/kg per hr continuous infusion) and supportive care; D: AT, R-TPA and supportive care] and monitored for 3 primary outcome parameters (survival time, macroscopic and microscopic organ involvement) and 4 secondary outcome parameters (hematocrit; platelet count; fibrinogen level; and antithrombin III level).Compared with supportive care alone, combination therapy with AT and R-TPA resulted in a significant improvement of survival time, hematocrit, AT level, macroscopic and microscopic organ involvement, p < 0.05. Compared with supportive care alone, R-TPA alone significantly reduced macroscopic organ involvement and AT alone increased AT levels.The findings suggest that combining AT, R-TPA and supportive care may prove more advantageous in treating the clinical manifestations of DIC in this neonatal pig model than either single modality or supportive care alone.DIC is a combination of enhanced thrombosis and decreased fibrinolysis. It is precipitated by some underlying disorder, e.g. sepsis, that results in production and release of proinflammatory cytokines. These activate the coagulation cascade, inhibit physiologic anticoagulant pathways, and depress fibrinolysis, resulting in enhanced fibrin formation and impaired fibrin removal [1].Initiated by either contact phase or tissue factor activation, the coagulation cascade is a set of reactions involving multiple coagulation factors and cofactors [2] that result in the generation of thrombin which acts on the fibrin polymer to produce a fibrin clot [3]. This process is subject to regulation by intrinsic inhibitors, e.g. AT an

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