We undertook surgical bilateral lung volume reduction in 20 patients with severe chronic obstructive pulmonary disease to relieve thoracic distention and improve respiratory mechanics. The operation, done through median sternotomy, involves excision of 20% to 30% of the volume of each lung. The most affected portions are excised with the use of a linear stapling device fitted with strips of bovine pericardium attached to both the anvil and the cartridge to buttress the staple lines and eliminate air leakage through the staple holes. Preoperative and postoperative assessment of results has included grading of dyspnea and quality of life, exercise performance, and objective measurements of lung function by spirometry and plethysmography. There has been no early or late mortality and no requirement for immediate postoperative ventilatory assistance. Follow-up ranges from 1 to 15 months (mean 6.4 months). The mean forced expiratory volume in 1 second has improved by 82% and the reduction in total lung capacity, residual volume, and trapped gas has been highly significant. These changes have been associated with marked relief of dyspnea and improvement in exercise tolerance and quality of life. Although the follow-up period is short, these preliminary results suggest that bilateral surgical volume reduction may be of significant value for selected patients with severe chronic obstructive pulmonary disease.

Outcomes after lung transplantation are markedly inferior to those after other solid organ transplants. A better understanding of cellular and molecular mechanisms contributing to lung graft injury will be critical to improve outcomes. Advances in this field have been hampered by the lack of a mouse model of lung transplantation. Here, we report a mouse model of vascularized aerated single lung transplantation utilizing cuff techniques. We show that syngeneic grafts have normal histological appearance with minimal infiltration of T lymphocytes. Allogeneic grafts show acute cellular rejection with infiltration of T lymphocytes and recipient-type antigen presenting cells. Our data show that we have developed a physiological model of lung transplantation in the mouse, which provides ample opportunity for the study of nonimmune and immune mechanisms that contribute to lung allograft injury.

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