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Richard D. Catalano, MD; Venkateswaran Parameswaran, PhD; Janakiraman Ramachandran, PhD; Donald D. Trunkey, MD

Arch Surg. 1984;119(2):145-150.

Abstract
• The response of the adrenal cortex to corticotropin during sepsis is variable. We have previously demonstrated a significant decrease of corticosterone production by rat adrenocortical cells in response to corticotropin stimulation after incubation with septic shock plasma (SP) as compared with control plasma (CP). We have studied the mechanisms of this depression. The following defects were demonstrated. (1) Cells bound less radioiodinated corticotropin analog after SP treatment (2.9±0.4 femtomoles/50 µg DNA) than after CP treatment (6.4±0.3 fmole/50 µg DNA). (2) Cyclic adenosine monophosphate (cAMP) production was less after SP treatment (59.3 ± 4 pmole per 10⁵ cells per two hours) compared with CP treatment (110.3±11.3 pmole per 10⁵ cells per two hours). (3) Exogenously added dibutyryl cAMP was unable to correct the defect in corticosterone production after SP treatment (4.96±0.7 µg/24 hr) as compared with CP treatment (6.99±0.5 µg/24 hr). Our studies suggest this defect is located in the synthesis of pregnenolone from cholesterol. These mechanisms may be responsible for the low cortisol levels previously observed in humans during septic shock.

(Arch Surg 1984;119:145-150).

Author Affiliations
From the Hormone Research Laboratory, University of California, San Francisco (Drs Catalano, Parameswaran, and Ramachandran); and the Trauma Center, San Francisco General Hospital (Drs Catalano and Trunkey).

Footnotes
Accepted for publication Aug 23, 1983.

Read before the Third Annual Meeting of the Surgical Infection Society, Fort Lauderdale, Fla, May 9, 1983.

Reprint requests to Department of Surgery, Ward 3A, San Francisco General Hospital, 1001 Potrero Ave, San Francisco, CA 94110 (Dr Trunkey).

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