Differences in the ability to tolerate comparable degrees of shock-producing trauma are commonplace in clinical experience and animal experimentation. The phenomenon of tolerance to shock was not known to be related to any particular function until it was shown that an animal made resistant to a lethal dose of bacterial endotoxins would also survive an otherwise lethal exposure to hemorrhagic shock.1 We had already observed that similar prophylactic protection could also be provided by substantial suppression of the coliform flora in the intestine.2 From such data we concluded that a gram-negative bacterial factor is involved in the death from hemorrhagic shock that persists in spite of full replacement of the blood volume deficit. But, when prophylactic antiadrenergic agents and corticosteroid were also found to be equally protective, it was difficult to find a common factor among such apparently disparate agents that could explain the protection conferred. The likelihood