Abstract
The effect of granulocyte depletion on the development of pulmonary edema after glass bead microembolization was examined. Anesthetized sheep were prepared with lung lymph fistulas. Studies were made in 3 groups: in group 1, 0.5 g/kg glass beads (200 .mu.m diameter) were injected i.v. to induce pulmonary embolization; in group 2, granulocytes were depleted with hydroxyurea treatment for 4 days prior to the study, and 0.5 g/kg glass beads were injected as in group 1; and in group 3, granulocytes were also depleted as in group 2, and 1.1 g/kg glass beads were injected i.v. to raise pulmonary arterial pressure to levels attained in group 1. In group 1, the increase in lung lymph flow (.ovrhdot.Qlym) was associated with no change in lymph-to-plasma protein concentration ratio (L/P) despite the decreased vascular surface area, indicating an increase in lung vascular permeability to proteins. The steady-state increases in .ovrhdot.Qlym and lymph protein clearance (.ovrhdot.Qlym .times. L/P) from base line in group 1 were greater than in group 2 (P < 0.05). There were greater increases in pulmonary arterial pressure and pulmonary vascular resistance in group 1 (P < 0.05). The increases in .ovrhdot.Qlym and protein clearance in group 3 were not sustained at the initial high levels but decreased (P < 0.05) to the levels attained in group 1 despite the greater degree of embolization in group 3. The increases in extravascular lung water content-to-bloodless dry lung weight ratios after embolization in both granulocyte-depleted groups were less than in group 1 (P < 0.05). The protective effect of granulocyte depletion may be due to smaller increments in pulmonary microvascular pressure and vascular permeability. Granulocyte sequestration and activation plays an active role in mediating the pulmonary edema after glass bead microembolization.

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