H.C. Bergman

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

Ineffectiveness of adrenocortical hormones, thiamine, ascorbic acid, nupercaine, and posttraumatic serum in shock due to scalding burns

Abstract Our results demonstrate that, under the conditions of these experiments, neither desoxycorticosterone acetate, adrenal cortical extract, thiamine, ascorbic acid, nupercaine, nor posttraumatic convalescent serum from burned rats possessed significant antiburn shock activity. Of the agents tested, all seemed definitely ineffective, with the possible exception of thiamine, which, although it did not decrease mortality, did somewhat increase the average survival. It will be seen that this beneficial effect was not consistent. Therefore, we conclude that, although thiamine may be slightly effective in burn shock, its activity is small as compared to the results obtained with a highly effective agent such as large volumes of saline solution or pretreatment with liver extract. 1 Examination of the results with all of the agents under investigation reveals that, in any single test, using twenty animals per group, apparently positive results are obtainable; but, when the tests are repeated, and the results are evaluated in composite form, it is evident that the so-called positive effects are due to variability of the method. Although we cannot state definitely that similar variations are encountered in evaluating antishock activity with other methods, it does appear possible that some of the conflicting results regarding various agents in shock may be explicable in terms of variability factors which were not taken into account. It is not intended to imply that our observations necessarily apply to other forms of shock, produced by other procedures, for there is now evidence that the cause and treatment of various types of shock may be fundamentally dissimilar. 28, 29

Further studies on the liver principle which is effective against burn shock

These experiments demonstrate that liver extract, which has significant antiburn shock activity, either when administered parenterally, as in previous work,1 or orally, as in the present study, is without comparable activity in the shock states which follow hind-leg ischemia or bacterial infection. It has been demonstrated that the mechanism of tourniquet shock in rats is complicated by several factors which are difficult to control. Before a final conclusion regarding the ineffectiveness of liver extract in this type of shock could be drawn, it would appear necessary that complicating factors be controlled. The negative results obtained with liver extract after acute exsanguination permit no conclusions to be drawn regarding liver activity in hemorrhagic shock. The fact that liver is effective in burn shock, but not in tourniquet or bacterial shock, is further evidence for the concept that there are different mechanisms responsible for various types of shock, although all may give rise to a similar terminal picture. It further indicates that therapeutic measures must be evaluated individually for each type of shock, and that results obtained with one type of shock cannot be justifiably transferred to other types of shock.