IT IS well known that the administration of Escherichia coli endotoxin in dogs leads to hemorrhagic intestinal necrosis1; this lesion occurs with such regularity that it has come to be the pathologic hallmark of this syndrome. Since this lesion is almost never seen in patients with gram-negative septicemia and shock, doubt has been cast upon the validity of interpreting the results of therapeutic regimens used in the laboratory in terms of these patients. For this reason, numerous studies have been undertaken in our laboratory in an attempt to further clarify the pathophysiology of this lesion.
Recent reports have shown that by the administration of hydrocortisone, chlorpromazine, phenoxybenzamine (Dibenzyline),2 and hyperbaric oxygen3 improvement in survival in animals exposed to E coli endotoxin can be achieved. It is interesting that this improvement in survival is associated with protection from the intestinal lesion. The question of whether this improved survival