The neuroendocrine stress response after painful trauma is characterized by an increased secretion of catabolic hormones (ACTH, cortisol, glucagon, catecholamines) and a decreased secretion of anabolic hormones (insulin, testosterone, growth hormone). This results in hypermetabolism and release of substrates (glucose, amino acids, fat) from peripheral stores (muscle, fat tissue, liver). Hyperglycemia, increased protein breakdown, and a negative nitrogen balance are the consequences. In addition, the release of aldosterone and vasopressin is enhanced and results in sodium and water retention. Nociceptive impulses from the injured area contribute significantly to the initiation and maintainance of these effects, since regional anesthesia can potently reduce the stress response ( Keh.le.t.,,1...9.9.3). Other factors such as cell breakdown products or inflammatory mediators also play a role. Stress-induced activation of the hypothalamopituitary axis may cause suppression of immune functions and promote impaired wound healing and sepsis. Finally, the neuroendocrine stress response can cause molecular changes; for example, it can induce expression of heat shock proteins in the adrenal cortex, aorta, and vena cava ( ,Ke.hle.t,18.104.22.168).
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