Therapeutic effects of the combination of two proteinase inhibitors in endotoxin shock of the pig.

Abstract

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.

• Authors: M Siebeck, H Hoffmann, J Weipert, M Spannagl
• Journal: Progress in clinical and biological research (Prog Clin Biol Res) Vol. 308 Pg. 937-43 ( 1989) ISSN: 0361-7742 [Print] United States
• PMID: 2780741 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Blood Proteins
• Fibrin Fibrinogen Degradation Products
• Protease Inhibitors
• Proteins
• Recombinant Proteins
• Serpins
• eglin proteinase inhibitors
• fibrinmonomer
• Fibrinogen
• Pancreatic Elastase
• Thrombin

Topics

• Animals
• Blood Proteins (metabolism)
• Body Water (physiology)
• Fibrin Fibrinogen Degradation Products (metabolism)
• Fibrinogen (metabolism)
• Hirudin Therapy
• Lung (blood supply, physiopathology)
• Pancreatic Elastase (antagonists & inhibitors)
• Protease Inhibitors (therapeutic use)
• Proteins (therapeutic use)
• Recombinant Proteins
• Serpins
• Shock, Septic (drug therapy, physiopathology)
• Swine
• Swine, Miniature
• Thrombin (antagonists & inhibitors)
• Vascular Resistance