Effect of the administration of cortisone on the response of chicks to the endotoxin of Salmonella pullorum.

Previous investigations conducted in our laboratory have shown that the arginase system and, consequently, the Krebs ornithine cycle, is reactivated in baby chicks experimentally infected with Salmonella pullorum (Ross et al., 1956). A similar reactivation, as evidenced by an alteration in the nitrogen excretion pattern, was demonstrated in chicks treated with the endotoxin of S. pullorum (Dooley and Holtman, 1957). Under the conditions of both of these experiments, urea replaced uric acid as the major nitrogen excretion compound of the chicks. Urea synthesis represents the principal pathway of nitrogen excretion during the early stages of embryonic development, but in newly hatched chicks, this synthesis accounts for only a small amount of the total nitrogen excreted. In the developing embryo the production of urea parallels arginase activity (Needham et al., 1935). According to Moog (1952) the peak of arginase activity occurs on the third day of incubation. Then the activity declines rapidly and can not be detected in the 8-day-old embryo. In studies of the reaction of chick embryos to bacterial endotoxins, Smith and Thomas (1956) observed that the period of maximal susceptibility occurs on the 10th day of incubation. At 6 days, and at 16 days, the embryos appear to be completely insusceptible. The administration of cortisone was reported to protect 10-dayold embryos against the lethal effects of endotoxin. Since the period of maximal susceptibility to endotoxin occurs subsequent to the period of arginase activity in the developing embryo, it became of interest to us to study the possible relationship between susceptibility and arginase