Demonstration of a Toxic Factor in the Blood of Rats Shocked by Burn.

In previous studies published from this laboratory (1) it was shown that 2 major factors are implicated in the production of burn shock in mice and rats; the one, fluid loss at the site of the thermal injury, and the other, stagnation of blood in atonic visceral capillaries. Capillary atony was demonstrated in burn shock whether thermal trauma was accompanied by much or little local fluid loss. In certain forms of thermal injury there is very little edema formation (2); yet the circulatory blood volume as represented by the bleeding volume is drastically reduced and the animal dies in shock (1). In this instance, local fluid loss is eliminated as the principal cause of the reduction in the bleeding volume, and the pooling of blood in the capillary bed is chiefly responsible for the decrease in the effective circulating volume. In burn shock the number and diameter of open capillaries were found to be considerably increased (1, 3), and the amount of blood retained in the viscera significantly augmented. Atony of the capillary blood vessels is a primary disturbance since it develops within 2 minutes after a severe burn. Following mild burns, capillary atony persists in surviving animals for less than 24 hours. In order to demonstrate capillary congestion, controlled observations -were made upon the hemoglobin content of visceral organs after exsanguinating the animal. There was little or no difference in the apparent degree of congestion in the burned and unburned animals when sacrificed by a method other than bleeding, but a striking difference was demonstrated after exsanguination. After bleeding, the organs of a normal unburned animal became pale and bloodless, whereas in burn shock the tissues remained dark and engorged. A toxic factor has been previously demonstrated in experiments in which injection of blood from burned rats into normal rats caused a significantly