Time course of pulmonary vascular response to microembolization

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Abstract
Time course of the pulmonary hemodynamic and gas exchange adjustments was determined following i.v. infusion of 100 .mu.m glass beads (0.7 g/kg). Three groups of anesthetized controlled ventilated dogs were studied for 1 h postembolization (PE): 1, sham; 2, beads; and 3, heparin (500 units/kg) 30 min before beads. In sham dogs, pulmonary blood flow (.ovrhdot.QL), pulmonary arterial pressure (Pa), left atrial pressure (LAP), pulmonary vascular resistance (PVR), blood gases, dead space (VD), venous admixture (.ovrhdot.Qs/.ovrhdot.Qt) and PAO2 - PaO2 gradient did not change. PVR increased in groups 2 and 3 five min PE, but to a greater (P < 0.01) extent in group 2. Increases in PVR were sustained in both cases. The greater increase in PVR in group 2 was associated with greater increase (P < 0.01) in Pa. LAP did not change in either group and changes in .ovrhdot.QL were similar. VD increased similarly in both groups 5 min PE and remained elevated. PaO2 decreased, and .ovrhdot.Qs/.ovrhdot.Qt and PAO2 - PaO2 increased to similar levels in both groups 5 min PE. The values were maintained at these levels in group III, while gas exchange deteriorated progressively in group 2. Intravascular coagulation as assessed by deposition of labeled fibrin occurred only in group 2. Pulmonary edema was also evident in group 2 (wet/dry lung wt of 4.61 .+-. 0.37), while the ratio of 3.51 .+-. 0.12 in group 3 was not different from sham dogs. Therefore, progressive pulmonary insufficiency did not occur following pulmonary microembolization in heparinized dogs. Humoral factors released during microembolization associated with intravascular coagulation may play a role in greater pulmonary vasoconstriction, development of pulmonary edema and progressive gas exchange impairment following pulmonary thromboembolization.