Effects of local antifibrinolytic therapy for acute respiratory failure following DIC was investigated. Acute lung injury with DIC was evoked in rats by the intraperitoneal injection of 10mg/kg endotoxin. An intraperitoneal injection of endotoxin was followed by a rapid increase in plasminogen activator (PA) release from alveolar macrophages (AM) and corresponding increase in fibrinolytic activity in bronchoalveolar lavage (BAL) fluid. Ultrasonic nebulization of 500mg/kg tranexamic acid was performed 1 hour after injection of endotoxin. Ultrasonic nebulization of tranexamic acid prevented not only increase in fibrinolytic activity in BAL fluid, but widening of alveolar-arterial oxygen difference (AaDO2) and increase in protein BAL fluid. These results suggest increase in fibrinolytic activity in alveoli by AM may be one of the key phenomena in development of acute lung injury following DIC, and also suggest local antifibrinolytic therapy may be available for treatment of acute respiratory failure following DIC.
