What question did this study set out to answer?

To determine the biological mechanism by which bacterial endotoxin suppresses fibrinolysis and induces disseminated intravascular coagulation.

March 1, 1985Journal of Clinical InvestigationOpen Access

Generation in plasma of a fast-acting inhibitor of plasminogen activator in response to endotoxin stimulation.

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Authors

MCMario ColucciUniversity of Pavia JPJosé A. PáramoCross-Cutting Cardiology DCD CollenVascular / Pulmonary Vascular

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Implication

Experimental study demonstrates rapid elevation of plasminogen activator inhibitor following endotoxin exposure in rabbits and septic patients, suggesting a key mechanism in septic coagulopathy.

Key Points

To determine the biological mechanism by which bacterial endotoxin suppresses fibrinolysis and induces disseminated intravascular coagulation.
Injected Escherichia coli lipopolysaccharide into rabbits to monitor circulating plasminogen activator inhibitor levels and human t-PA complex formation via gel filtration.
Cultured human endothelial cells under endotoxin stimulation to track inhibitor secretion rates over time.
Measured plasma levels of the fast-acting inhibitor in 5 patients with septicemia and healthy controls, correlating inhibition against t-PA and urokinase.
Endotoxin injection in rabbits increased plasma inhibitor activity from 3.9 ± 0.7 to 41 ± 13.2 U/ml at 3 hours, clearing exogenous t-PA as an inactive 100,000-Da complex with a 7-minute half-life.
Cultured human endothelial cells exposed to endotoxin exhibited a 2- to 7-fold increase in the accumulation rate of inhibitor activity.
Patients with septicemia (N=5) showed elevated plasma inhibitor levels of 14.3 ± 15.5 U/ml compared to 1.3 ± 0.7 U/ml in controls, with a strong correlation between t-PA and urokinase inhibition (r = 0.98).

Cite This Study

Colucci et al. (1985) studied this question.

synapsesocial.com/papers/6a178a35aeefdf6d9c12abb8 https://doi.org/10.1172/jci111777

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Implication

Experimental study demonstrates rapid elevation of plasminogen activator inhibitor following endotoxin exposure in rabbits and septic patients, suggesting a key mechanism in septic coagulopathy.

Generation in plasma of a fast-acting inhibitor of plasminogen activator in response to endotoxin stimulation.

Discussion

Member takes

Implication

Key Points

Cite This Study

Generation in plasma of a fast-acting inhibitor of plasminogen activator in response to endotoxin stimulation.

Discussion

Member takes

Implication

Key Points

Cite This Study

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