Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor.
Open Access
- 1 June 1993
- journal article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 91 (6) , 2754-2760
- https://doi.org/10.1172/jci116516
Abstract
In septic shock, hypotension, disseminated intravascular coagulation, and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect of the C1-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock. Two groups were included: controls, which received Escherichia coli endotoxin, and a C1-INH group in which C1-INH was infused before E. coli endotoxin administration. In both groups, endotoxin produced hypodynamic shock; however, the decrease in the systolic index and the ventricular systolic work indexes were greater in controls than the C1-INH group. In controls, the arterial O2 partial pressure decreased by 30% and the alveolo-arterial O2 difference increased by 625%, these parameters remained unchanged in the C1-INH group. Hypoxemia was associated with increased intrapulmonary shunt, decreased blood coagulation contact factors, and decreased C3c. In contrast, C1-INH administration prevented endotoxin-induced hypoxemia, the increase in intrapulmonary shunt, and the decrease in blood coagulation contact factors. This study shows that, in dogs with endotoxic shock, pulmonary dysfunction is associated with an activation of the blood coagulation contact phase system. An inhibition of this system by C1-INH prevented the hypoxemia induced by endotoxic shock.Keywords
This publication has 43 references indexed in Scilit:
- Local abnormalities in coagulation and fibrinolytic pathways predispose to alveolar fibrin deposition in the adult respiratory distress syndrome.Journal of Clinical Investigation, 1989
- Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock.Journal of Clinical Investigation, 1986
- Cultured human endothelial cells generate tissue factor in response to endotoxin.Journal of Clinical Investigation, 1983
- The Risk Factors, Incidence, and Prognosis of ARDS following SepticemiaChest, 1983
- Cardiovascular alterations in the adult respiratory distress syndromeThe American Journal of Medicine, 1982
- Synthesis of Nitrate Reductase in ChlorellaPlant Physiology, 1980
- Gram-negative bacteremiaThe American Journal of Medicine, 1980
- KININ ACTIVATION IN BLOOD OF PATIENTS WITH SEPSIS1976
- Contribution of Kinins to Endotoxin Shock in Unanesthetized Rhesus MonkeysCirculation Research, 1968
- [HEPATIC AND SPLANCHNIC CIRCULATION].1965