Pulmonary microvascular leakage after microembolization and hemodilution.

This study examined the role of colloids versus crystalloids in pulmonary edema associated with the increased pulmonary microvascular permeability secondary to thrombin-induced pulmonary microembolism. Each of 23 healthy dogs received an intravenous injection of thrombin and a fibrinolysis inhibitor, which induced a microembolic state with increased (fivefold) pulmonary lymphatic flow and a lymph/plasma (L/P) protein ratio typical of a permeability change. Seven dogs received no treatment, eight received 15 ml/kg 10% dextran 40 (D40), and eight received 60 ml/kg Ringer's lactate solution (RL). Pulmonary water was measured serially by thermal conductivity and terminally by wet/dry weights. This preparation produced significant hemolysis; however, L/P ratios of hemoglobin approached unity in all groups. Initially there was hemoconcentration, which was reversed by RL and even more so by D40. Both D40 and RL temporarily raised the pulmonary artery and pulmonary artery wedge pressures to 15 mm Hg; D40 more than doubled the cardiac output of control or RL subjects--this was associated with a reduced pulmonary arteriolar resistance (P less than 0.05). In the early stage PaO2 was better maintained with D40 (P less than 0.02). Lymph flow increased and was comparable in all groups, as were lung water and lung weight, which tripled in all three groups. Results of this study indicated that in the presence of a pulmonary microvascular leak, colloids in doses that produced comparable microvascular pressures did not increase lung water and did not accumulate in the pulmonary interstitium. Colloids were superior to crystalloids in maintaining cardiac output, pulmonary vascular resistance, and oxygen tension in the early period after microembolism.U