The lung inflammatory response to thermal injury: relationship between physiologic and histologic changes.
We studied the effect of a body burn on lung physiologic, biochemical, and histologic changes in a 2-day postburn period. A 15% of total-body-surface third-degree burn was produced in 24 adult sheep with lung and burn lymph fistulas. Eight sheep were killed at 12 hours and eight at 48 hours. At 12 hours we noted increased lung tissue lipid peroxidation, lung congestion, and neutrophil sequestration, in addition to a 30% decrease in lung compliance. Lung permeability and water content were not increased. Increased release of lipid peroxides and prostanoids were noted from burn tissue, as evidenced by increased plasma levels of malondialdehyde and conjugated dienes that remained elevated for about 8 hours and were decreased with wound removal. The lung inflammatory response was still present at 48 hours, the cells being primarily neutrophils. Nevertheless, the lipid peroxidation process, as measured by lung tissue malondialdehyde, had resolved. There was no evidence of burn tissue infection, measured by quantitative culture, to explain the persistent increase in lung inflammatory cells. Excision and closure of the burn wound at 3 hours postburn in eight sheep attenuated the lipid peroxidation and compliance changes but did not decrease the neutrophil sequestration. We conclude that burn injury results in a local wound oxidant release that leads to lipid peroxidation, both in wounds and in lung, as well as lung inflammation. The lipid peroxidation process may be attenuated by removal of the wound. The neutrophil sequestration is not altered, however, indicating this response occurs very early after injury, probably as a result of oxidant-initiated complement activation.
Demling
R H
RH
Longwood Area Trauma Center at Brigham and Women's Hospital, Boston, Mass 02115.
LaLonde
C
C
Liu
Y P
YP
Zhu
D G
DG
D000818:Animals; D001794:Blood Pressure; D001798:Blood Proteins / Q000032:analysis; D002056:Burns / Q000503:physiopathology* / Q000601:surgery; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D011464:Epoprostenol / Q000032:analysis / Q000097:blood; D006439:Hemodynamics; D007249:Inflammation; D008168:Lung / Q000473:pathology / Q000503:physiopathology*; D008196:Lymph / Q000032:analysis; D008315:Malondialdehyde / Q000032:analysis / Q000097:blood; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D012016:Reference Values; D012756:Sheep; D013929:Thromboxane B2 / Q000032:analysis / Q000097:blood
D001798:Blood Proteins; D002245:Carbon Dioxide; D008315:Malondialdehyde; D013929:Thromboxane B2; D011464:Epoprostenol; D010100:Oxygen