The physiological alterations produced in animals by the endotoxins of Gram-negative bacteria include such diverse reactions as fever, leucopenia, hyperglycemia, and a series of vasomotor reactions terminating in a state similar to irreversible traumatic shock (1). The pathological effects of endotoxins suggest that the end result of their action is damage to the blood vessels, as exemplified by the hemorrhagic and necrotizing lesions of the local and generalized Shwartzman phenomena, but the mode of action of endotoxin remains unexplained. Studies of the latter reactions have indicated that they do not represent direct, destructive effects in blood vessels, but seem rather to involve a series of secondary events in which the animals' own mechanisms play a determining role in the production of tissue damage. For example, the hemorrhagic skin lesions of the local Shwartzman reaction develop as the result of occlusion of venules and capillaries by platelet-leucocyte thrombi, followed by dilatation of these vessels and rupture of their walls (2). The characteristic lesions of the generalized Shwaxtzman reaction are fibrinoid necrosis of the coronary arteries and bilateral renal cortical necrosis; these seem to be the result of the deposition of precipitated fibrinogen within the walls and lumen of blood vessels, leading to ischemic necrosis of the tissues which they supply (3)(4)(5).Although the numerous manifestations of endotoxin have been widely investigated, little is known about the pharmacological properties which cause these responses. It has been suggested that the systemic vasomotor effects in rabbits are similar to those of adrenalin (6), and that endotoxins may be toxic because of a direct action on autonomic centers or conduction pathways (7). Recent studies indicate that endotoxins have the property of greatly enhane-