It has been postulated that the development of irreversibility in shock initiated by trauma or hemorrhage is mediated primarily by a breakdown of bacterial defense mechanisms and an attendant vasculo-toxic sequela. The validity of this thesis rests in large part on experiments in dogs and rabbits (1, 2) in which pretreatment with antibiotics successfully circumvented the fatal consequences of a standardized episode of hemorrhagic shock. Further support has been derived from indirect evidence: a decreased tolerance to bacterial endotoxins (3), a fall in blood properdin levels (4), and an impaired capacity to clear bacteria from the bloodstream during the course of the shock reactions (5). The pathophysiologic alterations produced by bacterial endotoxins have been shown in recent experiments (6, 7) to be strikingly similar to the vascular manifestations of the shock syndromes produced by hemorrhage and trauma. Moreover, animals rendered tolerant to bacterial endotoxins by repeated exposure to these extracts were found to be resistant to both hemorrhagic and traumatic shock.Although the syndrome of traumatic or hemorrhagic shock in the rat is not accompanied by a systematic bacteriemia (8), as has been reported in the dog (9), the syndromes follow a similar course in both animals, as evidenced by observations of the peripheral circulation (10), by studies of tissue metabolism (11), and by histopathology (12). In order to gain more direct information concerning the influence of bacterial factors on the course of shock in the rat, experiments were undertaken with animals reared under bacteria-free conditions. It would seem a reasonable assumption that if the presence of bacteria in the tissues or blood of the shocked rat is of importance in determining the outcome, * These studies were aided