ABSTRACT
Emphysema affects over 2 million Americans and is one of the most serious respiratory complications of cigarette smoking (1,2). The pathogenesis of this disease is complex, but an imbalance between pulmonary protease and antiprotease activity appears to be centrally involved (3,4). Protease-induced tissue destruction leads to the rupture of alveolar septa and the progressive enlargement of terminal airspaces: the pathological hallmark of emphysema (5,6). This tissue disruption directly reduces the surface area of the lung available for gas exchange and reduces inherent tissue elasticity. These anatomical and physiological changes lead over time to hyperinflation of the lungs, airflow obstruction, ventilation/perfusion mismatching, inadequate gas exchange, increased pulmonary vascular resistance, and right heart dysfunction (Fig. 1).
