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Bactericidal/permeability-increasing protein ameliorates hypercoagulability after hemorrhagic shock
1Department of Emergency Medicine, University of Tsukuba, Japan.
Thrombosis Research
|August 1, 1997
Summary
Bactericidal/permeability-increasing protein (BPI) reduces hypercoagulability and inflammatory responses following hemorrhagic shock. This suggests endotoxin plays a key role in the thrombotic complications of shock.
Area of Science:
- Biochemistry
- Immunology
- Physiology
Background:
- Massive hemorrhage induces plasminogen activator inhibitor-1 (PAI-1) and tissue factor (TF).
- Endotoxin is implicated in the hypercoagulable state post-hemorrhage.
Purpose of the Study:
- To investigate the effect of bactericidal/permeability-increasing protein (BPI) on PAI-1 and TF induction after hemorrhagic shock.
- To assess BPI's role in mitigating thrombotic responses following hemorrhagic shock.
Main Methods:
- Rats underwent hemorrhagic shock and resuscitation, with some receiving recombinant BPI (rBPI21).
- Plasma endotoxin, whole blood clotting time (WBCT), and PAI activity were measured.
- mRNA levels of TF, PAI-1, TNF-alpha, IL-1 beta, and IL-6 were analyzed in liver tissue.
Main Results:
- rBPI21 significantly reduced plasma endotoxin levels post-hemorrhage.
- BPI treatment attenuated the decrease in WBCT and the increase in PAI activity.
- rBPI21 treatment reduced the induction of TF, PAI-1, TNF-alpha, and IL-6 mRNA.
Conclusions:
- BPI ameliorates hypercoagulability and inflammatory gene expression after hemorrhagic shock.
- Endotoxin plays a significant role in the thrombogenic response to hemorrhagic shock.