The Initial Stage of Canine Endotoxin Shock as an Expression of Anaphylactic Shock: Studies on Complement Titers and Plasma Histamine Concentrations.

Within 30 to 60 seconds after endotoxin is injected 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 vascular changes. It was demonstrated that the action of endotoxin on blood vessels was mediated through a heat labile factor in plasma or serum (4, 5). Gilbert and Braude (6) in studies on Escherichia coli endotoxin shock in rabbits reported 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 observed a prompt decrease in plasma complement values in canine endotoxin shock. The immediate effect of endotoxin on smaller vessels suggested that a vasoactive substance or substances were also implicated. If an immune mechanism were involved, histamine could be one of the substances that was liberated by an antigenantibody mechanism, and studies do point to histamine as a factor causing the altered vascular activity (3, 8-10). This report concerns the study of complement titers, plasma histamine concentrations, and blood pressure changes in a series of dogs given a lethal