Mechanisms of pulmonary microvascular dysfunction during severe burn injury.
Even in the absence of inhalational injury, acute lung injury is a common cause of morbidity and mortality for patients sustaining severe burns. Other than general supportive measures, there are few therapeutic options for improving survival in these critically ill patients. Numerous clinical and laboratory studies have implicated tumor necrosis factor (TNF)-a and neutrophils as important participants in the pathogenesis of burn-induced lung injury. There is, however, little information regarding the mechanism by which these and other pro-inflammatory mediators affect the movement of fluid and protein across the microvascular barrier into the interstitium of the lung. In addition to reviewing the evidence implicating TNF-a and neutrophils in the pathophysiology of burn-induced lung injury, this report summarizes current theories regarding potential mechanisms by which these mediators may alter microvascular barrier function to lead ultimately to the development of pulmonary edema.
Turnage
Richard H
RH
Department of Surgery, Louisiana State University Health Sciences Center, 1501 Kings Highway, P.O. Box 33932, Shreveport, Louisiana 71130-3932, USA.
Nwariaku
Fiemu
F
Murphy
Joseph
J
Schulman
Carl
C
Wright
Keith
K
Yin
Helen
H
D002056:Burns / Q000150:complications / Q000503:physiopathology*; D002199:Capillary Permeability / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators; D008171:Lung Diseases / Q000209:etiology / Q000503:physiopathology*; D009504:Neutrophils / Q000502:physiology*; D020545:Respiratory Mucosa / Q000098:blood supply / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha