On the Role of Surface Tension in the Pathophysiology of Emphysema

Abstract

Pulmonary emphysema is a disease that is characterized, if not defined, by the destruction of lung parenchyma (1). This destruction is believed to result principally from the damaging effects of proteolytic enzymes and free radicals generated within the alveolar compartment in response to noxious stimuli. Other factors, including epithelial and endothelial cell apoptosis, incomplete lung remodeling in response to tissue injury, and mechanical forces, may also contribute (2, 3). Over many years, parenchymal destruction and incomplete healing result in loss of tissue collagen and elastin, enlargement of alveolar airspaces, and, ultimately, the classic physiologic characteristics of advanced emphysema: hyperinflation, loss of elastic recoil at a given lung volume, loss of surface area for gas exchange, and severe flow limitation. Because the major histologic difference between the normal lung and the emphysema lung is loss of lung parenchyma, it is logical to conclude that the physiology of emphysema is mechanically determined by loss of the tissue component of recoil. However, in the normal lung, recoil pressure decreases by 50 to 60% in the fluid-filled state, indicating that surface tension contributes substantially to lung recoil at any given pressure (4, 5). An obvious question is whether the same is true in the emphysema lung. Although emphysema is not primarily a disorder of surfactant, reflection on the critical role of surface tension in the normal lung indicates that an alteration in the physiologic effects of surface tension and the surfactant monolayer on overall lung recoil must occur in the emphysema lung. Otherwise one might naively expect that recoil pressure in emphysema could never decrease below one half to two thirds of normal. Why ask this question? Emphysema is irreversible destruction of lung tissue. Does it really matter whether surface tension contributes 30, 50, or 70% of recoil, or whether this percentage changes as disease progresses? For reasons outlined later, we believe the answer is a resounding “yes.” If surface tension does contribute significantly, surface-active agents designed to safely and favorably modulate surface tension might be used to increase recoil in emphysema.