The morphology of smoke inhalation injury in sheep.

  title={The morphology of smoke inhalation injury in sheep.},
  author={Gene B. Hubbard and P C Langlinais and Takeshi Shimazu and Carlin Vance Okerberg and Arthur D. Mason and Basil A. Jr. Pruitt},
  journal={The Journal of trauma},
  volume={31 11},
Pulmonary injury resulting from inhalation of chemical and particulate products of incomplete combustion is one of the principal determinants of mortality following burn injury. In this study, the histopathology of inhalation injury was examined in sheep. Mild, moderate, or severe smoke injury was produced in anesthetized sheep by insufflation with various doses of ambient temperature smoke, generated by burning polyethylene, wood pulp, and nonwoven cellulose pads. A total of 64 sheep were… 

Effects of rolling inhibition on smoke inhalation injury.

Airway obstruction in sheep with burn and smoke inhalation injuries.

Results suggest that strategies to remove or decrease formation of upper airway obstructive material may reduce its deposition into small airways and parenchyma and may improve respiratory function in victims of smoke inhalation injury.

Inhalation injury and burn trauma: an experimental investigation of oxidative stress and histopathology

Evidence is provided that inhalation injury with and without burn decrease tissue antioxidant capacity and increase tissue peroxidative injury.

Smoke inhalation enhances early alveolar leukocyte responsiveness to endotoxin.

Smoke inhalation induces a massive influx of alveolar leukocytes that are primed for an early, enhanced LPS-activated cytokine response compared withAlveolarLeukocytes isolated after burn injury alone or normal controls.

A model of recovery from inhalation injury and cutaneous burn in ambulatory swine.


Evidence is provided that clearance of airway obstructive cast material is crucial in managing acute respiratory distress syndrome resulting from combined burn and smoke inhalation injury.

Protective effect of hydrogen sulfide in a murine model of acute lung injury induced by combined burn and smoke inhalation.

It is suggested that H2S exerts protective effects in acute lung injury, at least in part through the activation of anti-inflammatory and antioxidant pathways.

Pathophysiological Basis of Smoke Inhalation

The bronchial circulation contributes to edema formation in the lung that occurs after ALI caused by smoke inhalation injury, and this phenomenon has been confirmed by other investigators.


The study indicates that in uninjured sheep lung, endothelial (eNOS) is constitutively expressed in the endothelial cells associated with the airways and parenchyma, and in macrophages.



Experimental inhalation injury in the goat.

A model of inhalation injury has been produced in anesthetized goats through the use of a modified bee smoker, which produces necrotic tracheobronchitis and bronchiolitis with pseudomembrane and cast formation in association with mild multifocal atelectasis and Bronchopneumonia.

Animal model of human disease. Smoke inhalation injury in sheep

An animal model that permits the study of respiratory injury with or without concomitant cutaneous burns will facilitate development of effective therapy and lead to improvement in burn patient care.

The pathophysiology of smoke inhalation injury.

The presence of bacterial infection in dogs surviving beyond 24 hours appears pathogenically significant and no deterioration of lung function was seen with crystalloid overload imposed upon smoke inhalation.

The Pathophysiology of Smoke Inhalation Injury

The presence of bacterial infection in dogs surviving beyond 24 hours appears pathogenically significant and no deterioration of lung function was seen with crystalloid overload imposed upon smoke inhalation.

The pathophysiology of smoke inhalation injury in a sheep model.

The results of this study indicate that the pulmonary edema is the result of an increase in microvascular permeability, characterized by increases in lung lymph flow, lymph-to-plasma protein concentration ratio (L/P), and transvascular protein flux (Qlym X lung lymph protein concentration), while pulmonary vascular pressures remain constant.

Pathophysiology and management of the complications resulting from fire and the inhaled products of combustion: Review of the literature

Treatment includes administration of oxygen, use of bronchodilators, and when necessary, mechanical ventilation, and the long-term sequelae of smoke inhalation are unknown.

A dose-responsive model of smoke inhalation injury. Severity-related alteration in cardiopulmonary function.

The dose responsiveness of selected physiologic indices was studied in a sheep model of smoke inhalation injury and sigmoid or curved linear shape was suggested, reflecting the progressive deterioration.

The influence of inhalation injury and pneumonia on burn mortality.

It is indicated that inhalation injury and pneumonia have significant, independent, additive effects on burn mortality and that these effects vary with age and burn size in a predictable manner.

The effect of resuscitation on inhalation injury.

The lung microvascular permeability changes seen with smoke inhalation are made worse by inadequate fluid resuscitation, and the group with low-volume fluid resuscitate had a much higher lung-lymph flow and lymph-to-plasma protein concentration ratio and a lower cardiac output.

Pulmonary complications in burn patients.

Patients involved in a closed space fire and those who had a burn involving 50% or more of their surface area seem to be at the greatest risk of developing pulmonary complications.