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The Role of Complement in Endotoxin Shock and Disseminated Intravascular Coagulation: Experimental Observations in the Dog
Author(s) -
Garner R.,
Chater B. V.,
Brown D. L.
Publication year - 1974
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1974.tb00820.x
Subject(s) - disseminated intravascular coagulation , beagle , shock (circulatory) , platelet , coagulation , medicine , complement system , hemorrhagic shock , immunology , pathology , immune system
S ummary . The endotoxin shock response of Beagle dogs, characterized by profound hypotension and progressive fatal disseminated intravascular coagulation (DIC) was compared in anaesthetized normal dogs and in dogs previously decomplemented with purified cobra venom factor. The hypotension and the early thrombocytopenia were abolished in the decomplemented group, while the subsequent DIC was greatly ameliorated. Factor VII was apparently activated in decomplemented dogs but consumed in normal dogs. An observation as yet to be defined in relation to the shock syndrome was that dog platelets lost their collagen aggregation throughout the period of total decomplementation. It is suggested that complement activation is a major requirement for the full expression of fatally progressive DIC in endotoxin shock and that the activation of the coagulation system occurs, at least in part, via the extrinsic pathway.