Peripheral vascular failure caused by endotoxin in the dog has an initial stage of vasoconstriction. Preliminary studies in vitro demonstrated that the constriction was due to the interaction of endotoxin with a heat-labile serum or plasma factor and platelets, resulting in the liberation of histamine. Further studies on the intact dog support and extend this concept.

A standardized dose of Escherichia coli endotoxin produced fatal shock in control adult mongrel dogs within 28 hours. The characteristic pattern of changes included progressive hypotension, oliguria and anuria, hemoconcentration, and acidosis.

Normal dogs were protected against endotoxin by transfusions of blood in which the essential serum factor was depleted in one of two ways. First, plasma separated from the blood of normal animals was heated at 56°C for 30 minutes, and the infused reconstituted whole blood protected normal dogs. Protection was not afforded by unheated reconstituted blood. Second, blood from immune dogs obtained within 24 hours after a second lethal dose of endotoxin protected recipient dogs. However, protection was not demonstrated with blood collected 72 hours after a second injection of endotoxin.

The nature of the serum factor essential for endotoxin activity is not known. It is postulated that an enzyme or enzyme system is involved, and the possible role of complement is discussed.

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