Depressor Substances in Peritonitis

There is little experimental work to substantiate the clinical belief that death from peritonitis is due to vasomotor collapse incident to absorption of toxins from the peritoneum. Zinnser, Parker and Kuttner 1 and Branham 2 both demonstrated that Escherichia coli produced a soluble toxic substance. Steinberg and Ecker 3 and Steinberg 4 have emphasized the rôle of bacterial toxins in peritonitis. Steinberg and his co-workers 5 have demonstrated a slight blood pressure fall in early peritonitis. Scott and Wangensteen 6 have showed that the peritoneal exudates from uncomplicated experimental intestinal obstruction were innocuous.

It occurred to us that the vasomotor system of the host might be less sensitive than that of a normal animal to the toxic substances developed in the peritoneal cavity. Peritonitis was induced in 17 dogs by the method of Buchbinder, Heilman and Foster 7 which consists of leaving an open loop of ileum with intact blood supply free in the peritoneal cavity. An end to end or a lateral anastomosis is made around the loop to restore the continuity of the intestinal tract. Bile peritonitis was induced in 9 dogs by 3 methods: by the intraperitoneal injection of whole sterile dogs' bile, by the similar administration of a sterile bile salt solution and by ligature of the common bile duct followed by defundation of the gall bladder. Twenty-three specimens of peritoneal washings or of peritoneal exudates were obtained by aseptic lavage of animals with suppurative peritonitis some time prior to death. These fluids were then centrifuged at high speed until clear and the supernatant fluid injected intravenously into normal dogs under barbital or urethane anesthesia. In a few instances the supernatant fluid was passed through a Mandler filter of porosity corresponding to a Berkefeld-N filter.