Seeling W, Fehm H L
Reg Anaesth. 1984 Jan;7(1):11-4.
The basis of this investigation was the question of whether low plasma cortisol concentrations during epidural anaesthesia are caused by sympathetic denervation of the adrenals. In 6 otherwise healthy patients undergoing upper abdominal operation 15-20 ml 0.75% bupivacaine was given via epidural catheter which had been inserted thoracically. Ringer's lactate solution 1,000 ml was infused during the time of onset of anaesthesia. When segmental epidural anaesthesia had spread from T2/3 to T12/L1/2 0.01 U/kg of ACTH were given intravenously. 5, 10, 20, and 30 minutes thereafter plasma ACTH and cortisol concentrations were measured. The same experimental procedure was carried out in a control group without epidural anaesthesia. The patients in both groups were unpremedicated and unanaesthetized. Plasma ACTH levels rose from 100 pg/ml (basic values) to 500-600 pg/ml immediately after ACTH injection in both groups and then decreased logarithmically. The increase of plasma cortisol concentrations was significant 15 minutes after the ACTH peak and rose from 0.28-0.3 mumol/l (10-11 micrograms/dl) up to 0.7 mumol/l (25 micrograms/dl) in both groups. We can, therefore, rule out that thoracic epidural anaesthesia with 0.75% bupivacaine impairs ACTH stimulated cortisol secretion.