Clotting and Other Plasma Factors in Experimental Endotoxemia: Inhibition of Degradation by Exogenous Proteinase Inhibitors

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Abstract
Endotoxemia in dogs was induced by a slow intravenous infusion of E. coli endotoxin for 2 h. Thereby, a significant decrease was observed in the plasma levels of several clotting, fibrinolysis and complement factors. The changes were studied over an experimental period of 14 h and checked for statistical significance by three-way analysis of variance. Application of the broad-spectrum proteinase inhibitor aprotinin (Trasylol®) from bovine organs clearly lowered the endotoxin-induced decline of the plasma proteins studied. By intravenous application of a specific granulocytic proteinase inhibitor (Bow-man-Birk inhibitor from soybeans), the endotoxin-induced reduction of the plasma proteins was prevented in a similar manner. It can be concluded that at least some of the pathobiochemical mechanisms observed in clotting, fibrinolysis and complement systems during endotoxemia are not only caused by a severe consumption reaction but also by unspecific proteolytic degradation due to neutral granulocytic proteinases.