The influence of epidural neural blockade on postoperative insulin resistance was studied using the euglycaemic insulin clamp technique. Eighteen patients undergoing elective upper abdominal surgery of moderate severity were allocated to two groups: group G patients underwent operation under general anaesthesia, and postoperative pain was relieved by systemic administration of analgesia; and group E patients received epidural analgesia during surgery and epidural morphine postoperatively. In each patient the euglycaemic insulin clamp test was performed twice: several days before surgery and on postoperative day 1. Peroperative catecholamine and cortisol responses were also measured to investigate possible endocrine mechanisms of the insulin resistance. Glucose disposal (M) decreased in both groups on postoperative day 1 at plasma insulin concentrations ranging from 1.2 to 10.0 milliunits ml-1, resulting in the downward shift of dose-response curves. However, this downward shift was significantly smaller in group E than in group G patients. Urinary adrenaline excretion increased markedly on the day of operation in group G, but was significantly inhibited in group E. Urinary noradrenaline excretion increased mainly on postoperative day 1 in group G, but was significantly inhibited in group E. Plasma cortisol response was lower in group E than in group G during and shortly after operation, and was significantly inhibited in group E on postoperative day 1. These results indicate that insulin resistance after elective abdominal surgery is due to a postreceptor deficit in glucose utilization, as indicated by the downward shift of the dose-response curves. This disturbance in glucose metabolism was reduced by epidural analgesia, the results being associated with inhibited catecholamine and cortisol responses.
The splanchnic nerves are inevitably stimulated during upper abdominal surgery and this may produce various responses. To assess the role of splanchnic nerve stimulation on the endocrine-metabolic responses to abdominal surgery, intra-operative splanchnic nerve blockade was carried out in 12 patients undergoing elective gastrectomy under general anaesthesia and the results compared with those of patients undergoing gastrectomy under general anaesthesia or epidural analgesia alone. In the splanchnic blockade group, intra-operative increase in plasma cortisol, glucose, FFA (free fatty acids) and urinary adrenaline excretion were significantly less than that of the general anaesthesia group. This inhibitory effect of splanchnic blockade on these endocrine-metabolic responses was almost the same as, but slightly less remarkable than, that of high spinal epidural blockade. Urinary noradrenaline excretion reached the highest level on the first postoperative day in the general anaesthesia group. This noradrenaline response was significantly inhibited in the splanchnic group as well as in the epidural group. These results appeared to indicate that mechanical stimulation to the splanchnic nerve due to operative manipulation is largely responsible for the endocrine-metabolic responses in abdominal surgery. The results also suggested that, in addition to the splanchnic nerve stimulation, conscious pain perception is responsible for catecholamine release.
Blood concentrations of glucose, lactate, non-esterified fatty acids (NEFA) and insulin (IRI) were measured in two groups of ten patients undergoing elective gastrectomy under general anesthesia with halothane (Group G) or epidural analgesia extending from Th3-4 to L1-2 without halothane (Group E). The rise in blood glucose and the rise in NEFA in group E during operation were significantly less than in Group G. Blood lactate levels during operation were lower in group E than in group G although the difference was not statistically significant. The increase in IRI/glucose ratio on postoperative day 1 was significantly less in Group E than in Group G, suggesting that insulin sensitivity after surgery was higher in Group E. The postoperative course was uneventful in all subjects. These results suggest that the endocrine-metabolic response to major upper abdominal surgery can be inhibited by epidural analgesia.
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