TY - JOUR
T1 - Mechanisms of Adrenocortical Depression During Escherichia coli Shock
AU - Catalano, Richard D.
AU - Parameswaran, Venkateswaran
AU - Ramachandran, Janakiraman
AU - Trunkey, Donald D.
PY - 1984/2
Y1 - 1984/2
N2 - • 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).
AB - • 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).
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U2 - 10.1001/archsurg.1984.01390140011002
DO - 10.1001/archsurg.1984.01390140011002
M3 - Article
C2 - 6320764
AN - SCOPUS:0021322361
SN - 0004-0010
VL - 119
SP - 145
EP - 150
JO - Archives of Surgery
JF - Archives of Surgery
IS - 2
ER -