Initiators and propagators of the metabolic response to injury

Abstract

Injury produces tissue hypoperfusion and subsequent reperfusion, afferent neural activity, and immune and vascular endothelial activation. These, in turn, set up a cascade of events coordinated by the central nervous system and at the level of individual tissues such as the liver, gut, and skeletal muscle. They are mediated by a complex array of neutrophil and macrophage products. The changes result in hypermetabolism, lypolysis, lysis of skeletal muscle and visceral protein, and expanded extracellular fluid with consequent organ failure.