One of the detrimental complications of burns is the onset of acute lung injury (ALI). In patients with extensive cutaneous burns in which the burned area exceeds 30% of the total body surface area, capillary hyperpermeability occurs not only at the injured site but also in regions distant from the initial insult [1, 2]. The vascular hyperpermeability leads to a large amount of fluid flux from the circulating plasma to the interstitial spaces. This lung edema formation is even more severe when the thermal injury is associated with smoke inhalation eventually leading to acute respiratory distress syndrome (ARDS) . Previously, we designed an ovine model of combined burn and smoke inhalation injury and described the patho-physiology of ALI . The ALI in combined burn and smoke inhalation injury is characterized by severe deterioration of pulmonary gas exchange (decrease in PaO2/FiO2, and increase in pulmonary shunt fraction), pulmonary microvascular leakage with subsequent formation of interstitial edema which is evidenced by increased pulmonary transvascular fluid flux (increased lung lymph flow), increased lung water content (lung wet-to-dry weight ratio), and increased pulmonary vascular permeability to both fluid and protein. These pathological changes are associated with severe pulmonary hypertension, massive airway obstruction by obstructive cast material, and increased ventilatory (peak and pause airway) pressures. In previous studies, we have also evaluated factors that play a crucial role in patho-genesis of ALI. There are several pathogenic factors, which affect the pulmonary function.
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