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The lung inflammatory response to thermal injury: relationship between physiologic and histologic changes
R H Demling1, C LaLonde, Y P Liu
1Longwood Area Trauma Center at Brigham and Women's Hospital, Boston, Mass 02115.
Surgery
|July 1, 1989
Summary
Severe burns trigger widespread inflammation and lung damage through oxidant release. Early wound removal can reduce lipid peroxidation, but neutrophil response persists, indicating early injury mechanisms.
Area of Science:
- Burn injury research
- Pulmonary physiology
- Inflammatory response
Background:
- Burn injuries cause significant systemic complications.
- Understanding the early mechanisms of burn-induced lung injury is crucial.
Purpose of the Study:
- To investigate the physiologic, biochemical, and histologic effects of a large burn on lung function.
- To determine the role of wound-derived oxidants in post-burn lung changes.
Main Methods:
- Induction of a 15% total-body-surface third-degree burn in adult sheep.
- Collection of lung tissue and plasma samples at 12 and 48 hours postburn.
- Assessment of lung compliance, lipid peroxidation, neutrophil sequestration, and inflammatory markers.
Main Results:
- Burns caused increased lung lipid peroxidation and neutrophil sequestration, with decreased lung compliance within 12 hours.
- Elevated plasma malondialdehyde and conjugated dienes indicated systemic oxidant release from burn tissue.
- Wound excision at 3 hours attenuated lipid peroxidation and compliance changes but not neutrophil sequestration.
Conclusions:
- Burn injury initiates local oxidant release, leading to systemic lipid peroxidation and lung inflammation.
- Early wound management can mitigate some systemic effects of burns.
- Neutrophil sequestration occurs early, likely via oxidant-initiated complement activation, independent of wound status.