One of the common hypotheses of the cause of death from peritonitis is that of vasomotor collapse incident to the absorption of toxins from the peritoneum. It has long been assumed that causative micro-organisms have been the source of the toxins, with the peritoneum acting merely as an absorptive membrane of a large surface area. As early as 1902 certain authors,¹ on the basis of experimental results, advocated preliminary nonspecific irritation of the peritoneum to prevent the absorption of toxins. They believed that peritoneal absorption was retarded by a fibrinous exudate. The physiology of the peritoneum is now better understood. This knowledge has been reviewed by Cunningham² and by Livingston.³ Steinberg⁴ clarified the situation with a clearcut series of experiments in which the diphtheria bacillus was used for intraperitoneal injection. While he found death to be due to the corresponding toxin, resistance was believed to be