M. R. Brandt

The blocking effect of epidural analgesia on the adrenocortical and hyperglycemic responses to surgery.

The adrenocortical and hyperglycemic responses to hysterectomy were studied in five groups of patients receiving: general anesthesia (group I), general anesthesia + epidural analgesia extending from Th10‐S4–5 (group II), general anesthesia + epidural analgesia extending from Th8‐S4–5 (group III), general anesthesia + epidural analgesia extending from Th4–6‐S5 (group IV) and epidural analgesia extending from Th4‐S5 without general anesthesia (group V).

PREVENTION OF POSTOPERATIVE LYMPHOPENIA AND GRANULOCYTOSIS BY EPIDURAL ANALGESIA

Blood leucocyte-counts, cortisol, and glucose were measured in twelve healthy premenopausal women undergoing elective abdominal hysterectomy during either general anaesthesia (six women) or epidural analgesia (T4 to S5) (six women). Surgery during general anaesthesia caused significant lymphopenia 6 and 9 h after skin incision and significantly increased granulocyte-counts 6, 9, and 24 h after skin incision. Epidural analgesia prevented lymphopenia and reduced granulocytosis to about 40% of that seen in the group receiving general anaesthesia. The normal increase in plasma glucose and cortisol during and after surgery was abolished by epidural analgesia. These results indicate that neurogenic stimuli from the surgical area, probably through their influence on adrenal hormones (cortisol and adrenaline), are the main mediators of postoperative lymphopenia and are partly responsible for postoperative granulocytosis. Inhibition of the endocrine-metabolic response to surgery may prevent postoperative immunodepression.

Effect of epidural analgesia on the glycoregulatory endocrine response to surgery.

Plasma concentrations of glucose, insulin, glucagon, cortisol, growth hormone and prolactin were measured repeatedly in ten females undergoing abdominal hysterectomy during general anesthesia. In addition to general anesthesia five of the patients had continuous epidural analgesia effective for the 26 post‐operative hours. Plasma glucose was elevated during surgery and postoperatively, but not in patients having epidural analgesia. Insulin was low and unchanged in both groups. Glucagon was unchanged and similar in both groups. Cortisol was lower during surgery in the epidural group, but not postoperatively. Growth hormone increased during surgery in four of five patients receiving general anaesthesia alone, but not changes were observed in the epidural group. Prolactin was greatly elevated in all patients immediately after induction of anesthesia and then fell rapidly during surgery, similarly in both groups. It is concluded that epidural analgesia can inhibit the hyperglycaemic response to surgical stress, but this effect cannot be uniformly correlated to changes in peripheral plasma levels of insulin, glucagon, cortisol, growth hormone or prolactin.

Influence of Morphine Anaesthesia on the Endocrine‐Metabolic Response to Open‐Heart Surgery

Twelve patients scheduled for aortic valve replacement during extracorporal circulation were randomly allocated to either morphine anaesthesia or fluroxene anaesthesia. Morphine in a total dose of 4 mg/kg was administered bcforc skin incision. At the start of extracorporal circulation all patients received 25 g glucose intravascularly. The endocrine‐metabolic response to surgery, as expressed by changes in plasma ACTH, cortisol, insulin, growth hormone, cyclic adenosine ‐3′, ‐5′‐monophosphate (cyclic AMP), glucose, free fatty acids, blood b‐hydroxy‐butyrate and cumulative nitrogen balance was measured before and during anaesthesia and surgery, and on the first five post‐operative days.

Influence of Epidural Analgesia on Postoperative Changes in Various Serum Enzyme Patterns and Serum Bilirubin

Postoperative changes in serum bilirubin, various serum enzymes (alanine‐amino transferase (ALAT), alkaline phosphatase (AP), lactate‐dehydrogenase (LDH), and creatine‐phosphokinase (CPK)), plasma glucose and cortisol were studied in 20 healthy, premenopausal women undergoing elective abdominal hysterectomy under either general anaesthesia with halothane or epidural analgesia (T4‐S5). Surgery under general anaesthesia was followed by increased levels of bilirubin, LDH, CPK, glucose and cortisol, whereas AP and ALAT were unaffected by surgery. Epidural analgesia inhibited increases in LDH, CPK, glucose and cortisol (P< 0.05), but not the increase in bilirubin. The results indicate that afferent neurogenic stimuli from the surgical area are important in mediating the postoperative changes in LDH and CPK, whereas factors other than neurogenic stimuli or adrenal hormones are responsible for the postoperative changes in bilirubin.

The Postanesthetic Antiemetic Effect of Premedication with Dehydrobenzperidol Before Ether Anesthesia

A study was performed to evaluate the antiemetic effects after ether anesthesia when dehydrobenzperidol (DHB) and pentobarbital were used for premedication and to compare these effects with halothane anesthesia when pentobarbital was used as premedication. Eighty‐four patients undergoing minor surgical operations were randomly divided into three groups. The patients received ether and either DHB 0.2 mg/kg or pentobarbital 2 mg/kg for premedication, or halothane and pentobarbital 2 mg/kg for premedication. The complaints of nausea and vomiting were recorded 24 h after anesthesia. We found that DHB compared to pentobarbital had a greater antiemetic effect after ether anesthesia, but the difference was not significant (P > 0.05). However, if only persistent nausea and vomiting were considered, the difference was significant (P < 0.05). The incidence of nauseal/vomiting after ether anesthesia with DHB as premedication was a little higher compared to halothane anesthesia with pentobarbital as premedication, but the difference was not significant (P > 0.05). However, if only persistent nausea/vomiting was considered, the incidence of complaints was equal in the two groups.