We have attempted to reproduce in animal experiments a group of pathological findings which we have observed to be associated with shock. In order to simulate the compensatory vasomotor reactions occurring in shock, we have utilized the intraperitoneal injection of adrenalin hydrochloride in dogs, cats, rabbits and guinea pigs. That the effect of adrenalin hydrochloride when injected by this route is of long duration has been shown by the prolonged hyperglycemia which it produces.

Our experiments have resulted in the production of a lesion in the digestive tract which is identical in the gross with those which we observed in our human material. The histological changes, however, have been found to differ from those encountered in the latter. These differences have been noted to occur only in the dog and cat, where the initial changes take place in the mucosa, and the alterations in the submucosa appear secondary to these. In the rabbit and guinea pig the histogenesis of the lesions is identical with that observed in man, the lesions first manifesting themselves in changes in the submucosa, congestion, edema and hernorrhage. Only later are similar changes seen in the mucosa, progressing finally to necrosis and ulceration.

The cause of the histological differences has been found in the presence of arteriovenous anastomoses which occur in the submucosa in the case of the dog and cat and in the mucosa in the case of the rabbit, guinea pig and man.

We have pointed out that variations in blood flow through the intestinal wall may result from the short circuiting of the blood through the arteriovenous anastomoses. This, associated with the vasoconstriction known to occur in shock, may if severe and prolonged, result in necrosis of the intestinal wall. We have experimentally reproduced the same lesion by the injection of adrenalin, which acts in a similar way.

The experimentally produced anatomical changes offer additional evidence in support of the clinical occurrence of a vasospasm which is of sufficient severity and duration to cause tissue necrosis.

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