ADRENOCORTICOTROPIN CORRELATES STRONGLY WITH ENDOTOXEMIA AFTER INTRAVENOUS BUT NOT AFTER INTRAPERITONEAL INOCULATIONS OF E. COLI Drew E. Carlson

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Abstract
To determine the influence of the site of infection on circulating endotoxin and hormonal release, male rats were prepared with arterial catheters and with either intravenous (i.v.) or intraperitoneal (i.p.) catheters under pentobarbital. Four days later, they were injected either i.v. or i.p. with Escherichia coli suspended in saline. Plasma was assayed for adrenocorticotropin (ACTH), corticosterone, and endotoxin activity. After ∼109 colony-forming units (CFU) of E. coli, plasma endotoxin in i.v. rats (496 ± 96 EU/mL) differed from that in i.p. rats (12.6 ± 3.6 EU/mL, p < .01). However, ACTH and corticosterone increased to the same extent in both groups. After ∼107 CFU, plasma endotoxin in i.v. rats (9.15 ± 2.09 EU/mL) was greater than in i.p. rats (2.56 ± .42 EU/mL, p < .05), and ACTH and corticosterone increased more at 1 h in i.v. rats than in i.p. rats (p < .01). Additional rats given ∼0.3 × 109 CFU i.p. had plasma endotoxin that did not differ from values measured after either ∼109 CFU i.p. or ∼107 CFU i.v. However, the ACTH responses in these three groups differed from one another (p < .01). ACTH was more strongly correlated to plasma endotoxin in i.v. rats (r = .915) 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 pathways that are independent of the circulation.

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