Stress failure in pulmonary capillaries

Abstract

In the mammalian lung, alveolar gas and blood are separated by an extremely thin membrane, despite the fact that mechanical failure could be catastrophic for gas exchange. We raised the pulmonary capillary pressure in anesthetized rabbits until stress failure occurred. At capillary transmural pressures greater than or equal to 40 mmHg, disruption of the capillary endothelium and alveolar epithelium was seen in some locations. The three principal forces acting on the capillary wall were analyzed. 1) Circumferential wall tension caused by the transmural pressure. This is approximately 25 dyn/cm (25 mN/m) at failure where the radius of curvature of the capillary is 5 microns. This tension is small, being comparable with the tension in the alveolar wall associated with lung elastic recoil. 2) Surface tension of the alveolar lining layer. This contributes support to the capillaries that bulge into the alveolar spaces at these high pressures. When protein leakage into the alveolar spaces occurs because of stress failure, the increase in surface tension caused by surfactant inhibition could be a powerful force preventing further failure. 3) Tension of the tissue elements in the alveolar wall associated with lung inflation. This may be negligible at normal lung volumes but considerable at high volumes. Whereas circumferential wall tension is low, capillary wall stress at failure is very high at approximately 8 x 10(5) dyn/cm2 (8 x 10(4) N/m2) where the thickness is only 0.3 microns. This is approximately the same as the wall stress of the normal aorta, which is predominantly composed of collagen and elastin. The strength of the thin part of the capillary wall is probably attributable to the collagen IV of the basement membranes. The safety factor is apparently small when the capillary pressure is raised during heavy exercise. Stress failure causes increased permeability with protein leakage, or frank hemorrhage, and probably has a role in several types of lung disease.

Ventilation with high tidal volume induces inflammatory lung injury

“…They showed an increase in DLW and fractional 125 I-labeled albumin uptake by the lungs in the group ventilated at 45 cmH 2 O peak inspiratory pressure compared with those ventilated at 7 cmH 2 O, and ultrastructural alterations such as damage of type I cells, denuding of the epithelial basement membrane, interstitial and alveolar edema and hyaline membranes. West et al (24), using electron microscopy, demonstrated microvascular injury induced by high distending pressures. These authors detected a large number of endothelial and epithelial breaks, which they called stress fractures, at high lung volumes compared with low lung volumes.…”

Time to generate ventilator-induced lung injury among mammals with healthy lungs: a unifying hypothesis

“…Traditionally VILI has been considered to be strictly related, among other mechanisms [5][6][7][8], to the application of excessive airway pressure (barotrauma) [2,9,10] and excessive tidal volume (V T , volutrauma) [11]. More recently, two different parameters describing the mechanical insult associated with ventilation have been proposed as actual determinants of VILI: lung stress, defined as the pressure developing within the lung fibrous skeleton, which equals the applied transpulmonary pressure [12], and lung strain, defined as the ratio between the lung volume variation (due to both V T and positive end-expiratory pressure, PEEP) and the lung resting volume [13].…”

Hypoxia and β2-Agonists Regulate Cell Surface Expression of the Epithelial Sodium Channel in Native Alveolar Epithelial Cells

“…Rapid ascent to high altitude may induce in some subjects the development of pulmonary edema. Although the initial cause of alveolar flooding is likely related to altered hemodynamics or increased lung microvascular permeability (7,8), new data from human and animal studies support the concept that defective alveolar fluid clearance could have a pathogenic role in the development of high altitude pulmonary edema (HAPE) and could be a potential target for therapy. Sartori et al (9) recently reported that HAPE-sensitive subjects at low altitude have a decrease in nasal transepithelial potential difference compared with HAPE-insensitive subjects, suggesting that these subjects may have a genetically determined impairment of transepithelial sodium and liquid clearance in the lungs.…”