The Toxic Factors in Experimental Traumatic

The fundamental hemodynamic disturbances which characterize traumatic shock may be initiated by at least 3 different factors: gross hemorrhage or loss of plasma into a traumatized region, neurogenic and psychogenic elements, and the absorption of toxic materials from traumatized regions. Of these etiologic factors, the local loss of vascular fluid is generally conceded to be of greatest importance (3, 28, 31, 54), while the others can be at best but contributory. Since the original classical experiments of Cannon and Bayliss (1), the theory of traumatic toxemia has been furthered by two types of experimental evidence. In one, a state more or less resembling clinical shock is produced in animals by the parenteral administration of various extracts of normal or traumatized tissues or by the intraperitoneal implantation of tissue. In the other, attempts are made in various ways to control or limit local fluid loss and neurogenic factors in experimental traumatic shock and to demonstrate that an additional factor, presumably traumatic toxemia, is necessary to explain the results. This approach has been considered in another publication (55) and the present discussion will concern itself only with the first type of experiment. Many experiments have been reported in which extracts of various tissues were found to have definite vasodepressive or shock-producing properties (56 to 61). Certain techniques (62, 63) consist of introducing into the peritoneal cavity of dogs whole or pulped liver or muscle. Observed regularly were hemoconcentration, circulatory col-