Plasma cortisol and glucose concentrations were measured repeatedly from before the induction of anaesthesia until 9 h after skin incision in 36 patients undergoing abdominal hysterectomy. Twelve patients received general anaesthesia (halothane), and systemic opiates for postoperative pain; a further 12 patients underwent continuous extradural analgesia with a local anaesthetic agent (bupivacaine) and in the remaining 12 patients general anaesthesia (halothane) plus extradural morphine (4mg before skin incision and an additional 4mg at skin closure) were used. Patients receiving extradural morphine or bupivacaine were free of pain. The physiological cortisol and glucose response to surgery was blocked by the extradural analgesia with bupivacaine. Extradural morphine did not modify the initial increase in plasma cortisol and glucose concentrations during surgery, but suppressed the hyperglycaemic and cortisol response following surgery when compared with the general anaesthesia group receiving systemic opiates. However, cortisol and glucose concentrations were greater after operation in patients receiving extradural morphine compared with extradural bupivacaine, suggesting that the endocrine metabolic response to surgery is predominantly released by neurogenic stimuli other than pain stimuli involving opiate receptor-dependent nociceptive pathways.
Plasma cortisol and glucose were measured in 36 patients undergoing abdominal hysterectomy under either general anaesthesia (Group I), epidural analgesia (T4-S5) effective before surgery (Group II) or general anaesthesia plus epidural analgesia (T4-S5) effective from 30 min after initiation of surgery. The results confirmed that epidural analgesia effective before skin incision (Group II) prevented the normal per-and postoperative increase in plasma cortisol and glucose. Patients receiving posttraumatic epidural analgesia (Group III) showed the normal initial increase in plasma cortisol and glucose, but initiation of epidural analgesia immediately broke the stress-response and prevented any further increase in plasma cortisol and glucose. However, although posttraumatic neurogenic blockade inhibited a major part of the stress-response, resting endocrine-metabolic activity was not reestablished, suggesting that once released the endocrine-metabolic response to trauma leads to persistent changes even if further afferent stimuli from the traumatized area are prevented.
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