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Published ahead of print on July 17, 2003, doi:10.1164/rccm.200207-690OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 1068-1074, (2003)
© 2003 American Thoracic Society

Airway Distension Promotes Leukocyte Recruitment in Rat Tracheal Circulation

Lina H. K. Lim and Elizabeth M. Wagner

Department of Medicine, Johns Hopkins University, Baltimore, Maryland

Correspondence and requests for reprints should be addressed to Elizabeth M. Wagner, Ph.D., Division of Pulmonary and Critical Care Medicine, Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224. E-mail: wagnerem{at}jhmi.edu

Mechanical distortion of blood vessels is known to activate endothelial cells. Whether airway distension likewise activates the vascular endothelium within the airway wall is unknown. Using intravital microscopy in the rat trachea, we investigated if airway distention with the application of positive end-expiratory pressure (PEEP) caused leukocyte recruitment to the airway. Tracheal postcapillary venules were visualized and leukocyte kinetics monitored in anesthetized, mechanically ventilated rats (80 breaths/minute, 6 ml/kg VT, 1 cm H2O PEEP). Leukocyte rolling velocity (Vwbc) and the number of adherent cells were not altered with normal ventilation over the course of 2 hours. Ventilation with sustained PEEP (8 cm H2O) for 1 hour reduced Vwbc and increased adhesion, reaching a maximum at 1 hour of PEEP. Intermittent (2x and 5x) 8 cm H2O PEEP also induced a similar reduction in Vwbc, accompanied by an increase in adhesion. However, leukocyte recruitment after airway distension is localized to the airways because increased PEEP did not induce leukocyte recruitment in the mesenteric microcirculation or when PEEP was applied to the lung distal to the site of measurement. Pretreatment with endothelin receptor and selectin inhibitors blocked the effects of distension on leukocyte recruitment, suggesting their involvement in the proinflammatory response.

Key Words: airway distension • endothelial activation, intravital microscopy • mechanical stress, positive end-expiratory pressure




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