INHIBITION OF ADRENAL STEROIDOGENESIS BY THE ANESTHETIC ETOMIDATE
INHIBITION OF ADRENAL STEROIDOGENESIS BY THE ANESTHETIC ETOMIDATE
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DOI:
10.1056/nejm198405313102202
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发表时间:
1984-01-01
影响因子:
158.5
通讯作者:
FELDMAN, D
中科院分区:
文献类型:
--
作者:
WAGNER, RL;WHITE, PF;FELDMAN, D
The use of the i.v. anesthetic etomidate for prolonged sedation was associated with low levels of plasma cortisol and increased mortality. The cortisol and aldosterone responses to ACTH stimulation were measured in 5 patients receiving etomidate, and the direct effects of etomidate on enzymes in the rate steroidogenic pathway were studied. One patient who was receiving a 20-h infusion of etomidate (1.3-1.5 mg/kg body wt per h) had marked adrenocortical suppression that was still evident 4 days after etomidate was discontinued. Four surgical patients receiving etomidate during their operations all had adrenal suppression 4 h after the operation; mean increases in cortisol and aldosterone after ACTH stimulation were only 1.8 .+-. 0.5 .mu.g/dl and 0.5 .+-. 1.1 ng/dl, respectively. In rat adrenal cells, etomidate produced a concentration-dependent blockade of the 2 mitochondrial cytochrome P-450-dependent enzymes, cholesterol-side-chain cleavage enzyme and 11.beta.-hydroxylase, without evident inhibition of the microsomal enzymes in the glucocorticoid pathway. Physicians should be aware that etomidate inhibits adrenal steroidogenesis, and they should consider treating selected patients with corticosteroids if etomidate is used.