In vivo interaction of endotoxin and recombinant bactericidal/permeability-increasing protein (rBPI23): Hemodynamic effects in a human endotoxemia model

The cardiovascular derangement that results from the administration of endotoxin in healthy subjects is qualitatively similar to what is observed in patients in septic shock. The biological response to endotoxin is attributed in part to cytokine release. In experimental endotoxemia, recombinant bact...

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Bibliographic Details
Published in:The Journal of laboratory and clinical medicine 2002-10, Vol.140 (4), p.228-235
Main Authors: Jellema, Wilbert T., Veerman, D.Peter, de Winter, Robbert J., Wesseling, Karel H., van Deventer, Sander J.H., Hack, C.Erik, van Lieshout, Johannes J.
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure - drug effects
Cardiac Output - drug effects
Cardiology. Vascular system
Complement Activation - drug effects
Endotoxemia - etiology
Endotoxemia - physiopathology
Hemodynamics - drug effects
Hemodynamics - physiology
Humans
In Vitro Techniques
Lipopolysaccharides - administration & dosage
Lipopolysaccharides - toxicity
Male
Medical sciences
Membrane Proteins - administration & dosage
Membrane Proteins - pharmacology
Membrane Proteins - physiology
Miscellaneous
Recombinant Proteins - administration & dosage
Recombinant Proteins - pharmacology
Vasodilation - drug effects
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Summary:The cardiovascular derangement that results from the administration of endotoxin in healthy subjects is qualitatively similar to what is observed in patients in septic shock. The biological response to endotoxin is attributed in part to cytokine release. In experimental endotoxemia, recombinant bactericidal/permeability increasing protein (rBPI23) has shown a protective effect by binding endotoxin with the subsequent inhibition of the endotoxin-induced cytokine release and of neutrophil activation. In a controlled, blinded crossover study the early cardiovascular effects of rBPI23 were investigated in an experimental endotoxemia model in humans. The beat-to-beat changes in arterial pressure and cardiac output following infusion of endotoxin (40 EU/kg body weight) and rBPI23 (1 mg/kg) or placebo (human serum albumin, 0.2 mg/kg) were studied for 2 hours in 8 healthy male adults. Endotoxin or rBPI23 alone did not induce significant cardiovascular changes. Endotoxin following rBPI23 infusion elicited a fall in total peripheral resistance with its nadir after 4 minutes to 40% (range 16-53; P
ISSN:0022-2143
1532-6543
DOI:10.1067/mlc.2002.127170