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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). |