The actions of the sympatho-adrenal system are central and peripheral, direct and indirect, with the release of noradrenaline from peripheral nerve ganglia and the release of both adrenaline and noradrenaline from the adrenal medulla. The rapid rise in plasma catecholamine concentration produces its effect via a- and p-adrenergic receptors. Cardiovascular changes occurring in the early response to injury result in the redistribution of blood from the skin and viscera (a) to the vital organs (02) and increased contractility of the heart (01).
Glycogenolysis, gluconeogenesis and lipolysis are the main metabolic changes occurring in direct response to stimulation of the sympatho-adrenal system. For example, plasma insulin concentrations are often acutely low after severe injuries despite a marked hyperglycaemia and this is a result of a suppres-sion of insulin secretion by adrenaline acting on pancreatic a-adrenergic receptors. In contrast, the secretion of glucagon is stimulated by raised catecholamine concentrations through a 0-adrenergic receptor mechanism. The peak hormonal response occurs within a few hours and usually declines rapidly.
The system eventually becomes hyperdynamic, with increased cardiac output in order to satisfy the demands of increased metabolism, changes in the thermoregulatory system and wound healing. The magnitude of the changes in metabolic rate varies depending on the injury. Treatment with aggressive fluid resuscitation and inotropic support may include additional catecholamines to maintain the body's response to injury. The induced hypermetabolic state peaks at 5-10 days after the injury at the height of inflammation, and returns to normal as wounds heal.
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