Stress-induced injury of pulmonary capillaries.

Abstract

The lung is particularly vulnerable to injury because the blood-gas barrier is so extremely thin. Furthermore, the mechanical stresses in the barrier become very high when capillary pressure is raised, or when the lung is inflated to a high volume. The strength of the blood-gas barrier on the thin side can be attributed to the type IV collagen in the basement membranes. Abnormally high stresses in the walls of the pulmonary capillaries result in ultrastructural changes including disruptions of both the alveolar epithelial and capillary endothelial layers. All Thoroughbred racehorses break their pulmonary capillaries when they gallop. Also, elite human athletes develop changes in the permeability of the blood-gas barrier at high levels of exercise. Pathological conditions resulting in stress failure include: 1) high-altitude pulmonary edema; 2) neurogenic pulmonary edema; 3) severe left ventricular failure; 4) mitral stenosis; and 5) overinflation of the lung. There is a spectrum of low permeability to high permeability edema as the capillary pressure is raised. Remodeling of pulmonary capillaries apparently occurs at high capillary pressures. It is likely that the extracellular matrix of the capillaries is continuously regulated in response to capillary wall stress.