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Within 30 to 60 seconds after endotoxin is in- jected into adult mongrel dogs there is a decline in systemic blood pressure, a rise in portal vein pressure, a reduction in the venous return of blood to the heart, and a decrease in renal blood flow (1, 2). Endotoxin shock is comparable in many ways to acute anaphylactic shock in the dog (3). Several observations have suggested that an immune mechanism causes the initial vas- cular changes. It was demonstrated that the action of endotoxin on blood vessels was medi- ated through a heat labile factor in plasma or serum (4, 5). Gilbert and Braude (6) in studies on Escherichia coli endotoxin shock in rabbits re- ported that doses of endotoxin greater than the LD50 caused a decline in the titer of complement and a decrease in the serum concentration of E. coli antibody. Spink and Potter (7) also ob- served a prompt decrease in plasma complement values in canine endotoxin shock.
Spink et al. (1964) studied this question.