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Abstract:
Endotoxin interacts rapidly with platelet membranes and, within minutes after experimental inoculation into animals, most is associated with the platelet fraction of the buffy coat. The endotoxin-platelet interaction contributes to inflammation by formation of aggregates and release of factors such as platelet factor 3, nucleotides, and serotonin. Also platelets may facilitate delivery of the toxin to the liver and spleen. Most visible endotoxin effects are seen on platelets from subprimate animals which have immune adherence receptor sites. The initial part of this reaction involves the lipid region of the molecule and is followed by assembly of alternative complement pathway components on the polysaccharide portion of the molecule. This latter interaction causes platelet lysis. The presence of antibody to the Opolysaccharide region of the toxin alters the rabbit platelet response, so that aggregation occurs more rapidly and reversibly. Primate platelets lack immune adherence receptor sites found in other animals. These platelets do interact with endotoxin and, through this process, can affect the inflammatory process. Host factors generated in response to endotoxin can significantly affect platelet function and survival. For example, responses of endothelial cells, leukocytes and macrophages during endotoxemia are responsible for increased levels of factors such as thromboxane, prostacyclin, hydrogen peroxide and other substances which can enhance or reduce platelet aggregation. Reprints.
| Limitations: |
 APPROVED FOR PUBLIC RELEASE |
| Pages: |
20 |
| Report Date: |
Jan-1985 |
| Report Number: |
A305202 |
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Keywords relating to this report:
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