The role of fibrin in the genesis of pulmonary edema after embolization in dogs.

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Abstract
The degree of pulmonary edema was determined at various times postembolization in mechanically ventilated dogs in which pulmonary emboli were induced with 0.7 g/kg glass beads (100 .mu.m in diameter). All dogs received 125I-fibrinogen prior to embolization. Extravascular lung H2O content was determined at 1 or 2 h postembolization. Increases in pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (PVR) were similar in both groups. Lung 125I activity per g bloodless dry lung increased (P < 0.01) at 1 h postembolization and decreased (P < 0.05) at 2 h postembolization, suggesting a time-dependent decrease in fibrin localization. Extravascular lung H2O/bloodless dry lung wt ratio of 3.10 .+-. 0.30 in control dogs was increased (P < 0.05) to 6.05 .+-. 0.82 at 1 h postembolization and was decreased (P < 0.05) to 4.17 .+-. 0.38 at 2 h postembolization. The possibility that the decrease in lung H2O at 2 h postembolization was due to decreased fibrin in the lung was studied in another group of dogs by infusing tranexamic acid to inhibit fibrinolysis after embolization. At 2 h postembolization, a greater fibrin accumulation (P < 0.05) in the tranexamic acid-treated group was associated with an extravascular lung H2O/bloodless dry lung wt ratio of 6.33 .+-. 1.02, which was greater (P < 0.05) than the value in the untreated group at 2 h postembolization. The reduction in lung H2O at 2 h postembolization was not due to decreases in Ppa or PVR. Because inhibition of fibrinolysis prevented the time-dependent decrease in pulmonary edema following microembolization, the decrease in extravascular lung H2O content may be due to clearance of fibrin from the lungs and subsequent dissipation of humoral factors which promote fluid acclumation.