The Role of Fibrin in the Genesis of Pulmonary Edema after Embolization in Dogs

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We determined the degree of pulmonary edema at various times postembolization in mechanically ventilated dogs in which pulmonary emboli were induced with 0.7 g/kg glass beads (100 ion in diameter). All dogs received '"I-fibrinogen prior to embolization. The extravascular lung water contents-were determined at 1 or 2 hours postembolization. The increases in pulmonary arterial pressure (Pp.) and vascular resistance (PVR) were similar in both groups. Lung ""I acxtivity per g bloodless dry lung increased (P < 0.01) at 1 hour postembolization and decreased (P < 0.05) at 2 hours postembolization which suggested a time-dependent decrease in fibrin localization. Extravascular lung water/bloodless dry lung weight ratio of 3.10 ± 0.30 in control dogs was increased (P < 0.05) to 6.05 ± 0.82 1 hour postembolization and was decreased (P < 0.05) to 4.17± 0.38 at 2 hours postembolization. The possibility that the decrease in lung water at 2 hours postembolization was due to decreased fibrin in the lung at this time was studied in another group of dogs by infusing tranexamic acid to inhibit fibrinolysis after embolization. At 2 hours postembolization, a greater fibrin accumulation (P< 0.05) in the tranexamic acid-treated group was associated with an extravascular lung water/bloodless dry lung weight ratio of 6.33 ± 1.02, which was greater (P < 0.05) than the value in the untreated group at 2 hours postembolization. Therefore, the reduction in lung water at 2 hours postembolization was not due to decreases in Pp. or PVR. Because inhibition of fibrinolysis prevented the time-dependent decrease in pulmonary edema following microembolization, the decrease in extravascular lung water content may be due to clearance of fibrin from the lungs and subsequent dissipation of humoral factors which promote fluid accumulation. Ore Res 45:120-125, 1979

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