PURPOSE: To evaluate the effects of a monoclonal antibody against interleukin-8 (K2.2) on the microvascular fluid flux after combined injury by burn and smoke inhalation. METHODS: Fourteen sheep were prepared surgically by placing a lung lymph catheter and a flank lymph catheter to examine the microvascular fluid flux. After a recovery period, they were subjected to a combined injury of 40% third-degree burns on the flank and smoke inhalation. RESULTS: This combined injury induced a rapid increase in burned tissue lymph flow (b-Q(L)) and a delayed-onset increase in lung lymph flow (l-Q(L)). The initial increase in b-Q(L) was associated with an elevation of the lymph-to-plasma oncotic pressure ratio, which led to a predominant increase in the burned tissue permeability index (b-PI). Pretreatment with K2.2 had no effect on the permeability change seen in the burned tissue; however, the lung permeability changes were attenuated by pretreatment with K2.2. CONCLUSION: These findings indicate that the pathogenesis of the increase in microvascular fluid flux seen after the combined injury differs in burned tissue and the lung.
PURPOSE: To evaluate the effects of a monoclonal antibody against interleukin-8 (K2.2) on the microvascular fluid flux after combined injury by burn and smoke inhalation. METHODS: Fourteen sheep were prepared surgically by placing a lung lymph catheter and a flank lymph catheter to examine the microvascular fluid flux. After a recovery period, they were subjected to a combined injury of 40% third-degree burns on the flank and smoke inhalation. RESULTS: This combined injury induced a rapid increase in burned tissue lymph flow (b-Q(L)) and a delayed-onset increase in lung lymph flow (l-Q(L)). The initial increase in b-Q(L) was associated with an elevation of the lymph-to-plasma oncotic pressure ratio, which led to a predominant increase in the burned tissue permeability index (b-PI). Pretreatment with K2.2 had no effect on the permeability change seen in the burned tissue; however, the lung permeability changes were attenuated by pretreatment with K2.2. CONCLUSION: These findings indicate that the pathogenesis of the increase in microvascular fluid flux seen after the combined injury differs in burned tissue and the lung.
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