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pubmed:abstractText |
Thrombin activation is an important underlying pathomechanism for septic organ failure. The selective thrombin inhibitor, hirudin, reduces the endotoxin-induced fibrinogen consumption and thus the formation of fibrin monomer, as well as the pulmonary vasoconstriction in pigs at plasma concentrations of 70 to 100 nmol/l. PMN cell activation with subsequent release of digestive proteases is in part responsible for the loss of fluid and protein from the vascular compartment during septic shock. Administration of the inhibitor of PMN elastase, cathepsin G and mast cell chymase, eglin C, reduces the loss of intravascular protein during the first 4 hours of endotoxin shock at plasma concentrations in the range of 2 mumol/l.
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