Smoke inhalation injury is recognized as a major killer of burn patients. Clinical analysis of the causes of death of 534 fire victims (with 311 autopsies) has demonstrated that about 60 percent of those victims died in less than 12 h following accidents, and the most common causes of those deaths were CO poisoning, respiratory tract involvement, and pulmonary parenchymal damage. Smoke inhalation produces lesions in both the upper and lower respiratory tract. The tracheobronchial and parenchymal lesions have been attributed to increase in pulmonary microvascular permeability. Decrease of oxygen content, increase of carbon monoxide (CO) and high levels of chemicals in smoke such as oxides of nitrogen, sulfur dioxide and aldehydes were reported and have been thought to be responsible for the abnormalities following smoke inhalation. Even though previous studies have provided a much better understanding of smoke inhalation, the nature of the injury has not yet been explored entirely. Therefore, in order to define the effects of inhaled smoke on pulmonary gas exchange as well as the tracheobronchial tree and lungs and to find mechanisms of the pathogenesis of CO poisoning and acute respiratory failure (ARF), the most common complications after smoke inhalation, we created a sheep smoke inhalation model with chronic lung lymph fistulas.
We also simultaneously monitored respiratory function, pulmonary mechanics, exchanges of fluid, protein and gases in lungs and observed morphologic alterations of the tracheobronchial tree and pulmonary parenchyma by transmission electron microscopy (ТЕМ), scanning electron microscopy (SEM) and freeze-etching technique. This article will present the sheep smoke inhalation injury model established, the HbCO dynamics, results of blood gas analysis, change of pulmonary compliance and pathologic findings in part and discussion of the mechanisms of complications following smoke inhalation.