الفهرس 
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Abstract
Surgical trauma and postoperative pain evoke reproducible metabolic,
hormonal and hemodynamic responses (Buckingham, 1985). These
responses are characterized by hypermetabolism (Kinney, 1980), altered
carbohydrate metabolism (Imamura et aI., 1975 and Mizock, 1995), sodium
and water retention (Lequense et aI., 1985), increased lipolysis (Meguid,
1974) and protein catabolism (Oppenheim et aI., 1980). The magnitude of
thesechanges is essentially proportional to the extent of the injury (Chernow
etal., 1987).
Although, anaesthesia and surgery are considered as types of stress,
there is no agreement on their effects on the hormonal and metabolic
alteration of carbohydrate and lipid. Oyama et aI., (1973) and Traynor and
Hall (1981) have reviewed many of the endocrine effects of general
anaesthesia, however, the results were insignificantly compared with the
degree of response to surgical stimulation. They found that, ether,
cyclopropane, halothane and methoxyflurane increase adrenocortical
hormones, while ethrane causes depression of these hormones. On the other
hand, Oyama et al., (1973b) found no appreciable rise in plasma ACTH
level during operation carried out under spinal anaesthesia, but it increased
markedly when the influence of anaesthesia wore off. In addition, combined
thiopentone, nitrous oxide-oxygen and muscle relaxant has long been
recognized not to stimulate adrenocortical activity (Brunt and Ganong
1963).