ABSTRACT
Tissue injury initiates a complex series of rapid homeostatic events.1'3. The host to prevent ongoing tissue damage and to activate the repair process initiates these events. Classically, inflammation has been recognized as the hallmark o f this re sponse. More recently, attention has been focused on defining these events at the cellular, metabolic and molecular level. The physiologic changes that develop after a traumatic insult occur irrespective o f the type o f injurious agent and result in a predictable increase in the level o f cortisol, catecholamines, insulin, glucagon, vaso pressin and growth factor.
