ADRENOCORTICOTROPIN CORRELATES STRONGLY WITH ENDOTOXEMIA AFTER INTRAVENOUS BUT NOT AFTER INTRAPERITONEAL INOCULATIONS OF ESCHERICHIA-COLI

To determine the influence of the site of infection on circulating end otoxin and hormonal release, male rats were prepared with arterial cat heters and with either intravenous (i.v.) or intraperitoneal (i.p.) ca theters under pentobarbital. Four days later, they were injected eithe r i.v. or i.p. with Escherichia coli suspended in saline. Plasma was a ssayed for adrenocorticotropin (ACTH), corticosterone, and endotoxin a ctivity. After similar to 10(9) colony-forming units (CFU) of E. coli, plasma endotoxin in i.v, rats (496 +/- 96 EU/mL) differed from that i n i.p. rats (12.6 +/- 3.6 EU/mL, p < .01). However, ACTH and corticost erone increased to the same extent in both groups. After similar to 10 (7) CFU, plasma endotoxin in i.v. rats (9.15 +/- 2.09 EU/mL) was great er than in i.p. rats (2.56 +/- .42 EU/mL, p < .05), and ACTH and corti costerone increased more at 1 h in i.v. rats than in i.p. rats (p < .0 1). Additional rats given similar to 0.3 x 10(9) CFU i.p. had plasma e ndotoxin that did not differ from values measured after either similar to 10(9) CFU i.p. or similar to 10(7) CFU i.v. However, the ACTH resp onses in these three groups differed from one another (p < .01). ACTH was more strongly correlated to plasma endotoxin in i.v. rats (r = .91 5) than in i.p. rats (r = .528, p < .01 for difference from i.v. group ). The weak relationship between plasma endotoxin and ACTH after i.p. inoculations suggests that peritoneal infections activate important pa thways that are independent of the circulation.