Pulmonary insufficiency remains a leading cause of mortality and morbidity in a burn patient. We have recently described the mechanism and treatment of the early transient lung injury immediately post-burn and during resuscitation. Our purpose now is to define the more severe and more complex lung dysfunction which occurs in the post-resuscitation period now inaccurately attributed solely to sepsis.
Our aims are to determine 1) whether arachidonic acid metabolites and other vasoactive factors are released from burn tissue in the post-resuscitation period, leading to hypoxia and pulmonary hypertension, 2) whether chemotactic factors and activators of neutrophil O2 radical release (chemiluminescence) are also absorbed, leading to lung permeability edema, 3) whether endotoxin in burn tissue accentuates the lung injury through the local production and release of these mediators of inflammation, and 4) the role of excision or manipulation of burn tissue in either correcting or amplifying the injury. The adult sheep with a 15-30% full thickness burn will be monitored for a ten day period. Lung lymph flow will be used to monitor fluid flux and protein permeability. Blood gases and lung compliance will also reflect function. Lung injury will be quantitated with measurements of lung water as well as biochemical alterations in lung tissue, specifically O2 radical-induced lipid peroxidation. Mediator release will be measured in burn lymph and plasma. Our long term objective is to not only obtain new general information on burn-induced lung injury but also to be able to answer specific clinically important questions such as the optimum and worst times to excise burn tissue relative to time post-burn and degree of inflammation or infection. Physiological, immunological and biochemical methods by three established investigators will be used.
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