Abstract
GRAM-NEGATIVE bacteria produce endotoxin and cause intravascular coagulation, shock and ultimate death of an estimated 25% of patients with bloodstream infections1,2. The number of blood platelets in such patients decreases3. In animal experiments, endotoxin aggregates platelets, induces release of vasoactive amines and adenine nucleotides, and unmasks the phospholipid procoagulant (platelet factor 3, PF3), which accelerates blood clotting4. To determine the mechanism of endotoxin action in man we studied the endotoxin interaction with human platelets. Here we describe experiments which demonstrate that the endotoxin-sensitive component (receptor) is present on the membrane of human platelets. Two types of changes resulting from endotoxin interaction with this receptor have been noted: selective release of 5-hydroxytryptamine (5-HT) and unmasking of platelet phospholipid (PF3).
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HAWIGER, J., HAWIGER, A. & TIMMONS, S. Endotoxin-sensitive membrane component of human platelets. Nature 256, 125–127 (1975). https://doi.org/10.1038/256125a0
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DOI: https://doi.org/10.1038/256125a0
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