title: [Pathophysiologic changes in patients with severe burns: role of hormones and chemical mediators].
abstract: The body's general response to serious thermal injury is characterized by increased vascular permeability immediately after injury and subsequent hypovolemic shock. Skeleto-muscular proteolysis, lipolysis, gluconeogenesis, increased metabolic rate, and a severe systemic inflammatory response induced by local infections or surgical procedures. The increased vascular permeability is mediated by histamine and numerous vasoactive substances, including serotonin, bradykinin, prostaglandins, leukotrienes, and platelet activating factor. Hyper-metabolism is mediated by hormones such as catecholamines, glucagon, and particularly cortisol. In addition, among the putative mediators of the metabolic response to injury, attention has recently been focused on cytokines and lipid mediators which are mainly produced by activated reticuloendothelial cells. Cytokines such as interleukin-1, interleukin-6 and tumor necrosis factor and cortisol responses are interrelated, since cytokines activate the hypothalamo-adrenal axis. The cytokine storm seen in burn patients may be associated with depression of the immune system and with susceptibility to infection. Thermal injury can also lead to activation of the renin-angiotensin-aldosterone system, increased ADH production, and production of atrial natriuretic polypeptide to maintain the circulatory volume. Burn wound infections or surgical procedures can produce and perpetuate a mediator-induced systemic inflammatory response that may lead to multiple organ failure. Serum levels of interleukin-6 are very sensitive to surgical stress, and may be a useful indicator of the general condition of severely burned patients.
authors.affiliation: Trauma and Critical Care Center, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Ikeda
authors.forename: K
authors.initials: K
authors.lastname: Kobayashi
mesh_terms: D002056:Burns / Q000503:physiopathology*; D002395:Catecholamines / Q000502:physiology; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*
chemical_list: D002395:Catecholamines; D016207:Cytokines; D018836:Inflammation Mediators