Clotting and other plasma factors in experimental endotoxemia: inhibition of degradation by exogenous proteinase inhibitors.
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 (Bowman-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.
D000818:Animals; D001779:Blood Coagulation Factors / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism*; D002403:Cathepsins / Q000494:pharmacology; D004195:Disease Models, Animal; D004211:Disseminated Intravascular Coagulation / Q000097:blood / Q000378:metabolism*; D004285:Dogs; D010450:Endopeptidases / Q000494:pharmacology; D004731:Endotoxins / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D005260:Female; D008297:Male; D010196:Pancreatic Elastase / Q000494:pharmacology; D011480:Protease Inhibitors / Q000378:metabolism / Q000494:pharmacology; D014115:Toxemia / Q000139:chemically induced*
D001779:Blood Coagulation Factors; D001798:Blood Proteins; D004731:Endotoxins; D011480:Protease Inhibitors; D002403:Cathepsins; D010450:Endopeptidases; D010196:Pancreatic Elastase