Heat injury to cells in perfused systems.
Tissue injury in response to excessive heat results in a clinical burn. Burns cause a range of physiologic derangements, including denaturation of macromolecular structures, leakage of cell membranes, activation of cytokines, and cessation of blood flow, all leading to tissue death. The purpose of this paper is to examine the mechanisms and consequences of burn injury and to discuss potential therapies based on these mechanisms. Knowledge of the thermal properties of tissues can predict the time-temperature relationship necessary to cause a specified thermal insult. Changes in cell membrane biochemistry and the stabilization of proteins through the heat-shock response can enable biomacromolecules to withstand supraphysiological temperatures. Mechanisms of cellular repair allow recovery of cellular function after thermal insult. An understanding of the response of proteins, cellular organelles, and cells to heat provides the foundation for understanding the pathophysiology and treatment of burn injury. The physics, biochemistry, and cellular biology behind the host response to thermal injury in perfused systems are reviewed.
Division of Plastic Surgery, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. dorgill@partners.org
Dennis P
DP
Orgill
Stacy A
SA
Porter
Helena O
HO
Taylor
D002056:Burns / Q000473:pathology / Q000503:physiopathology; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D006358:Hot Temperature; D006801:Humans; D008954:Models, Biological