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Ann Thorac Surg 1996;61:1435-1440
© 1996 The Society of Thoracic Surgeons


Original Articles: General Thoracic

Pulmonary Endothelial Permeability Changes After Major Lung Resection

David A. Waller, FRCS, Pauline Keavey, MSc, Lynne Woodfine, BSc, John H. Dark, FRCS

Regional Cardiothoracic Centre, Freeman Hospital, Newcastle-upon-Tyne, United Kingdom

Background. Increased pulmonary endothelial permeability has been proposed as a cause of postpneumonectomy pulmonary edema. This study investigated changes in pulmonary endothelial permeability after major lung resection.

Methods. Lung scintigraphy was performed in 21 men (median age, 66 years; range, 34 to 73 years) after pneumonectomy (10 patients) or lobectomy (11 patients). Pulmonary endothelial permeability was measured by the net pulmonary accumulation of intravenous technetium-99m--labeled albumin, calculated as a ratio of lung:heart radioactivity counts. Pulmonary hemodynamics were monitored continuously by a pulmonary artery catheter, and serum levels of inflammatory cytokines were assayed.

Results. The lung:heart radioactivity ratio increased significantly in the initial 8 hours after pneumonectomy but not after lobectomy (p < 0.01). Mean pulmonary artery pressure and pulmonary vascular resistance both increased significantly during pneumonectomy (p < 0.05). The intraoperative increase in mean pulmonary artery pressure was inversely related to preoperative mean pulmonary artery pressure (r = -0.47; p = 0.02). The postoperative change in lung:heart radioactivity ratio was related to the perioperative increase in pulmonary vascular resistance (r = 0.54; p = 0.02) but not to the increase in mean pulmonary artery pressure (r = 0.14; p > 0.05). Serum interleukin-8 and neutrophil elastase levels were elevated in all patients preoperatively. The postoperative change in lung:heart radioactivity ratio was related to preoperative elastase levels (r = 0.61; p = 0.02).

Conclusions. Pulmonary endothelial permeability appears to be increased after pneumonectomy. Preoperative neutrophil activation and the adaptation of the remaining pulmonary vasculature may be etiologic factors.




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