Relationship of Impaired Insulin Secretion during Surgical Stress to Anesthesia andCatecholamine Release*

Abstract

Impaired insulin secretion has been observed during surgical stress in man. To determine the relationship between insulin secretion during anesthesia and surgical stress and plasma levels of norepinephrine (NE) and epinephrine (Epi), studies were performed in 16 patients before and during elective minor surgical procedures. In 8 patients studied during halothane inhalation anesthesia before operation, the acute insulin response (AIR) to glucose (5 g, IV) fell to 51 +/- 3% of the preanesthesia AIR (mean +/- SEM; P < 0.001). This inhibition of AIR appeared unrelated to increased adrenergic activity, since during anesthesia alone, plasma NE did not change significantly and plasma Epi fell from 94 +/- 11 to 34 +/- 10 pg/ml (P < 0.01). During the postoperative recovery period in these patients, after discontinuation of the anesthesia, the AIR to glucose was 50 +/- 5% of the preanesthesia baseline response (P < 0.001). At this time, both plasma NE and Epi were increased compared to preanesthesia levels [NE: 240 +/- 40 (preanesthesia) vs. 340 +/- 43 (postoperative); Epi: 219 +/- 43 (preanesthesia) vs. 94 +/- 11 (postoperative); both P < 0.05]. In eight patients undergoing similar operations during low spinal anesthesia, no inhibition of the AIR to glucose occurred, and plasma NE and Epi did not increase significantly during or after the operation. During the recovery period, there was a relationship between plasma Epi and the degree of inhibition of the AIR to glucose (r = 0.70; n = 11; P < 0.05). Thus, inhibition of insulin secretion during surgical stress may be mediated both by direct effect of the anesthesia used and by activation of the sympathetic nervous system.

Early impairment of insulin secretion in rats after surgical trauma

“…An early temporary reduction in plasma insulin (0.5 h) was seen in both groups of rats. Suppression of plasma insulin early after induction of anaesthesia has been observed previously in surgical patients (15,16) and has been suggested to be due to anaesthesia alone and not related to the surgical trauma (29).…”

Management of Diabetes Mellitus in Surgical Patients

“…The invariant features of the metabolic stress response include release of the catabolic hormones epinephrine, norepinephrine, cortisol, glucagons, and growth hormone [11][12][13][14][15][16] and inhibition of insulin secretion and action. [17][18][19] Anti-Insulin Effects of Surgical Stress In addition to insulin resistance induced by circulating stress hormones, surgical stress has a deleterious effect on pancreatic ␤-cell function. Plasma insulin levels fall, and insulin secretory responses to glucose become impaired during surgery.…”

“…Plasma insulin levels fall, and insulin secretory responses to glucose become impaired during surgery. [17][18][19] The mechanism of the impaired ␤-cell responsiveness during surgery is unclear, and the defect is poorly correlated with ambient intraoperative catecholamine levels. Postoperatively, however, there is a close inverse correlation between plasma epinephrine and insulin secretion.…”

“…Postoperatively, however, there is a close inverse correlation between plasma epinephrine and insulin secretion. 17 These anti-insulin effects of the metabolic stress response essentially reverse the physiological anabolic and anti-catabolic actions of insulin. The important anabolic actions of insulin that may be reversed or attenuated during the stress of surgery include: 1) stimulation of glucose uptake and glycogen storage, 2) stimulation of amino acid uptake and protein synthesis by skeletal muscle, 3) stimulation of fatty acid synthesis in the liver and storage in adipocytes, and 4) renal sodium reabsorption and intravascular volume preservation.…”

Effects of Midazolam and Nitrous Oxide on Endocrine and Metabolic Measurements in Children

“…Norepinephrine and epinephrine are rapidly released by the sympathetic adrenomedullary system, and the HPA axis is activated more slowly [12]. The hyperglycemic response is mediated mainly by catecholamines and cortisol, and partly by growth hormone [13] and the suppression of insulin secretion induced by the activation of the sympathetic nervous system [14,15]. …”