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      Inhaled platelet-activating factor causes pulmonary neutrophil sequestration in normal humans.

      The American review of respiratory disease

      Administration, Inhalation, Adult, Blood Platelets, drug effects, physiology, Bronchial Provocation Tests, Erythrocytes, Humans, Indium Radioisotopes, diagnostic use, Lung, radionuclide imaging, Male, Neutrophils, Organometallic Compounds, Platelet Activating Factor, administration & dosage, pharmacology, Platelet Count, Technetium, Time Factors, Tropolone, analogs & derivatives

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          Abstract

          Inhaled platelet-activating factor (PAF) causes bronchoconstriction and transient peripheral neutropenia in humans. We studied eight normal subjects to investigate whether inhaled PAF caused pulmonary neutrophil sequestration. All subjects received autologous 99mTc-red cells as a blood pool marker, seven received 111In-neutrophils, and one received 111In-platelets. Six subjects inhaled 48 micrograms of PAF. There was immediate pulmonary sequestration of 111In-neutrophils, maximal (218% baseline) at 6 min (p less than 0.001), returning to normal by 3 h. There was no change in circulating platelet count or pulmonary 111In-platelet transit. Methacholine inhalation caused equivalent bronchoconstriction to PAF, but it had no effect on neutrophil count or pulmonary 111In-neutrophil activity. We have demonstrated pulmonary neutrophil, but not platelet, sequestration after PAF. This supports a role for PAF as an inflammatory mediator in humans. This may be a useful model for exploring pulmonary neutrophil kinetics and preinflammatory processes.

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          Journal
          1416388
          10.1164/ajrccm/146.4.1003

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