ENDOTOXEMIA-INDUCED LEUKOPENIA IN SHEEP - CORRELATION WITH LUNG VASCULAR-PERMEABILITY AND HYPOXEMIA BUT NOT WITH PULMONARY-HYPERTENSION

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Abstract
The effects of endotoxin on white blood cell (WBC) counts, hemodynamics and lung fluid and solute exchange were studied in 26 unanesthetized sheep. Seven sheep also received the same dose of Escherichia coli endotoxin in the presence of meclofenamate (5 mg/kg bolus plus 3 mg/kg/h). Endotoxemia caused an initial increase in pulmonary artery pressure (Ppa from 18 .+-. 1 SEM [standard error of the mean] to 59 .+-. 7 cm H2O). At 4 h after endotoxemia, lymph protein clearance (Clp = lymph flow times lymph/plasma protein concentration) increased to 255.6% .+-. 28 SEM of the pre-endotoxin control values; the alveolar to arterial O2 differences (.DELTA.AaPo2) increased from 12 .+-. 4 to 38 .+-. 3 mm Hg. The WBC counts dropped dramatically early in the endotoxin reaction (WBC counts = 29% .+-. 6 SEM of baseline at 1 h after endotoxin); the WBC counts did not correlate with the severity of the early pulmonary hypertension. The WBC counts rose more rapidly in some animals than in others, so that at 4 h after endotoxin, WBC counts ranged between 1111 and 12,134 cells/mm3. At this time, Clp (r = 0.53, P < 0.01) and .DELTA.AaPO2 (r = 0.83, P < 0.01) correlated with the WBC counts. Meclofenamate markedly attenuated the early pulmonary hypertension; it had no effect on the leukopenia caused by endotoxemia. Thus, pulmonary leukostasis does not contribute to the early pulmonary hypertension after endotoxemia, but leukocytes may be involved in the late increase in lung vascular permeability and hypoxemia.