REVIEW OF THE LITERATURE

A surgical operation or any form of physical injury to a previously healthy person initiates a series of metabolic changes. Increased secretion of catabolic hormones, such as cortisol, glucagon and catecholamines, and the inhibition of anabolic hormones such as insulin and testosterone leads to substrate mobilization and, ultimately, to a catabolic state with negative nitrogen balance (KEHLET 1978). The current knowledge on stress in surgical patients as a neurophysiologic reflex response has recently been extensively reviewed by WILMORE & al, 1976. According to their view a wound directly or indirectly initiates the metabolic and physiologic changes which occur after injury. That the nervous afferent pathways transmit signals from the injured area to the central nervous system has been demonstrated in animals and in humans. Epidural analgesia is able to block the stress-induced substrate mobilization during surgery but may not be active in more severe forms of stress, viz. burns and sepsis, in which a releasing mechanism other than afferent neurogenic impulses may be operating. Thus, the possibility has not been eliminated that circulating factors, interacting with, or arising from, the area of injury influence the post-traumatic metabolic response. The role of such substances or wound toxins is yet not well established. Several reports describe a rapid rise in the plasma corticotropin (ACTH) (COOPER & NELSON 1962, OYAMA & TAKIGUCHI 1970, ICHIKAWA et al. 1971, NEWSOME & ROSE 1971), cortisol (OYAMA et al. 1968, OYAMA & TAKIGUCHI 1970 and SOWERS et al. 1977). growth hormone (GH) (ICHIKAWA et al. 1971, NEWSOME & ROSE 1971 and SOWERS et al. 1977) and prolactin (PRL) (NOEL et al. 1972, SOWERS et al. 1977 and SOULES et al. 1980) levels during surgery. The secretion of these hormones may be promoted by a number of such stressful stimuli as acute trauma (JOHNSTON 1972), physical stress and exercise (SCHALCH 1967), electroconvulsive shock therapy and insulin induced hypoglycemia (YALOW et al. 1 969). No changes in the concentrations of luteinizing hormone (LH) or follicle stimulating hormone (FSH) were observed in the first study performed on the gonadotropin secretion during surgery on men and women of all ages (CHARTERS et al. 1969). In men, LH rises during surgery (AONO et al. 1972, NAKASHIMA et al. 1975, OYAMA et al. 1977 and WANG et al. 1978), but the FSH level remains unchanged (AONO et al. 1972 and WANG et al. 1978). ADASHI et al. 1980 found no alterations in the circulating gonadotropins in female subjects during surgery. AONO et al. (1976) reported a 25% decrease in LH levels in women during halothane anesthesia. SOULES et a1 (1980) studied the hormonal fluctuations in women of reproductive age during and after surgery. They found an absolute intraoperative decrease in LH with subsequent postoperative rebound. Postoperatively, ovulation occured in all patients. Six out of nine patients had postoperative acyclic vaginal bleeding and the progesterone levels were significantly lower during the luteal phase than in the control group. The authors suggest that the declined progesterone levels may be due to an inhibition of ovarian steroidogenesis due to either a direct toxic effect of the anesthetic agents or to fluctuations in other hormones such as PRL.