Positive pressure ventilation compresses pulmonary acinar microvessels but not their supply vessels

Abstract

Pulmonary alveolar septal capillaries receive their perfusion from a web of larger surrounding acinar vessels. Using 4 μm diam. Latex particles, we showed that positive pressure ventilation narrowed the acinar vessels as evidenced by venous 4 μm particle concentrations and perfusate flows <50% of particle concentrations in negative pressure ventilated lungs. We aimed to understand the effects of positive and negative pressure ventilation on flows of larger particles through the lung. Isolated, ventilated rat lungs (air, transpulmonary pressures of 15/5 cm H2O, 25 breaths/min) were perfused with a hetastarch solution at Ppulm art/PLA pressures of 10/0 cm H2O. Red latex 7 μm (2.5 mg, 4.8 × 106) or 15 μm (2.5 mg, 5.5 × 105) particles were infused into each lung during positive or negative pressure ventilation. An equal number of green particles was infused 20 min later. Flows through lungs infused with 7 μm and 15 μm particles were not different from flows through lungs infused with 4 μm particles (p = 0.811). Venous particle concentrations of 7 μm particles relative to infused particles were lower in positive pressure lungs (0.03 ± 0.03%) compared to negative pressure lungs (0.17 ± 0.12%) (p = 0.041). Venous particle concentrations of 15 μm particles were not different between positive (2.3 ± 1.9%) and negative (3.3 ± 1.8%) pressure ventilation (p = 0.406). Together with our previous study, we conclude that 4 μm and 7 μm particles both enter acinar vessels but that the 7 μm particles are too large to flow through those vessels. In contrast, we conclude that 15 μm particles bypass the acinar vessels, flowing instead through larger intrapulmonary vessels to enter the venous outflow. These findings suggest that intrapulmonary vessels are organized as a web that allows bypass of the acinar vessels by large particles and, that these bypass vessels are not compressed by positive pressure ventilation.