Structural and Functional Evidence for the Scaffolding Effect of Alveolar Blood Vessels

A contribution of pulmonary blood distension to alveolar opening was first proposed more than 100 years ago. To investigate the contribution of blood distension to lung mechanics, we studied control mice (normal perfusion), mice after exsanguination (absent perfusion) and mice after varying degrees of parenchymal resection (supra-normal perfusion). On inflation, mean tracheal pressures were higher in the bloodless mouse (4.0 ± 2.5 cm HO); however, there was minimal difference between conditions on deflation (0.7 ± 0.9 cm HO). To separate the peripheral and central mechanical effects of blood volume, multi-frequency lung impedance data was fitted to the constant-phase model. The presence or absence of blood had no effect on central airway resistance (p > .05). In contrast, measures of tissue damping (G), tissue elastance (H) and hysteresivity (η) demonstrated a significant increase in bloodless mice relative to control mice (p < .001). After varying amount of surgical resection and associated supra-normal perfusion of the remaining lung, there was an increase in G and H. Although the absolute difference in G and H increased with the amount of parenchymal resection, the proportional contribution of blood was identical in all conditions. The presence of blood in the pulmonary vasculature resulted in a constant 64 ± 5% reduction in tissue damping (G) and a 55 ± 4% reduction in tissue elastance (H). This nearly-constant contribution of blood to lung hysteresivity was only reduced by positive end-expiratory pressure (PEEP). To identify a distinct structural subset of vessels in the lung potentially contributing to these observations, vascular casting and scanning electron microscopy of the lung demonstrated morphologically distinct vascular rings at the alveolar opening. Our results suggest that intravascular blood distension, likely attributable to a subset of vessels in the alveolar entrance ring, contributes a measurable scaffolding effect to the functional recruitment of the peripheral lung.