Effect of thermal injury on endotoxin-induced lung injury.
We studied the effects of a burn injury on the response of the lung to endotoxin. Seventeen unanesthetized sheep with lung lymph fistulas were studied. Eight were given Escherichia coli endotoxin (1.5 micrograms/kg) alone and nine were given the same dose 72 hours after a 25% total body surface burn injury. At this time after burn, all physiologic parameters were at baseline levels. A characteristic two-phase lung injury was seen after administration of endotoxin with an initial hypertension phase, characterized by pulmonary artery hypertension, and a second or permeability phase, characterized by an increase in protein-rich lymph flow. all eight animals that underwent only endotoxin administration survived, whereas four of the nine burned animals died during the permeability phase in pulmonary edema. Major physiologic differences between the groups were noted during the permeability phase, including a more severe hypoxia, pulmonary hypertension, and increased postburn lymph flow. Major biochemical changes included significant increases in lymph thromboxane, thromboxane B2, and beta-glucuronidase activity in the burn group. We conclude that the lung is more sensitive to endotoxin after burn,  probably as a result of an increased release of products of arachidonic acid metabolism and products of leukocyte activation caused by the body burn.
D000818:Animals; D002056:Burns / Q000150:complications*; D004731:Endotoxins / Q000009:adverse effects*; D004927:Escherichia coli Infections; D005402:Fistula / Q000150:complications; D005966:Glucuronidase / Q000032:analysis; D006976:Hypertension, Pulmonary / Q000209:etiology; D000860:Hypoxia / Q000209:etiology; D008171:Lung Diseases / Q000209:etiology*; D008196:Lymph / Q000032:analysis; D012756:Sheep; D013929:Thromboxane B2 / Q000032:analysis; D013931:Thromboxanes / Q000032:analysis
D004731:Endotoxins; D013931:Thromboxanes; D013929:Thromboxane B2; D005966:Glucuronidase