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G Muller-Berghaus and T Eckhardt
This study examines the role of neutrophils (PMN) in the pathogenesis of
endotoxin-induced microclot formation. It is intended to clarify whether
granulocytes are involved in endotoxin-induced activation of intravascular
coagulation (generation of soluble fibrin) and/or in endotoxin-induced
precipitation of soluble fibrin. Precipitation of soluble fibrin was
achieved by injection of endotoxin into ancrod- infused rabbits with
circulating soluble fibrin (first model). Activation of intravascular
coagulation was elicited by two intravenous injections of endotoxin into
rabbits (second model). Seventy-two and ninety-six hours after injection of
nitrogen mustard, leukopenic rabbits had PMN counts between 0 and 50 cells
per mul. Neutropenia did not prevent the occurrence of glomerular
microclots after infusion of ancrod and injection of endotoxin (first
model). Neutropenia influenced neither the decrease in mean fibrinogen
concentrations nor the drop in mean platelet counts after ancrod and
endotoxin administration. In contrast to the first model, neutropenia
prevented the occurrence of glomerular microclots and of circulating
soluble fibrin after two injections of endotoxin (second model). It did
not, however, protect rabbits from the decrease in mean platelet counts
after endotoxin administration. These data indicate that granulocytes are
involved in endotoxin-induced activation of intravascular coagulation and
the production of soluble fibrin but are not essential to endotoxin-induced
precipitation of soluble fibrin.
This article has been cited by other articles:
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| Copyright © 1975 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
