Lowe C A, Shaffer T H
J Appl Physiol (1985). 1986 Jan;60(1):154-9. doi: 10.1152/jappl.1986.60.1.154.
Pulmonary vascular resistance was investigated in the fluorocarbon-filled lung in an in situ isolated lung preparation. Lungs were perfused at constant flow (100 ml X min-1 X kg-1) with whole blood from a donor cat. left atrial pressure was held constant at zero pressure. Measurements of pulmonary arterial pressure enabled calculation of pulmonary vascular resistance. Regional changes in pulmonary blood flow were determined by the microsphere technique. During quasi-static deflation over a range of 0-30 mmHg, dependent alveolar pressure was consistently greater for a volume of fluorocarbon than for gas, with each pressure-volume curve for the fluorocarbon-filled lung shifted to the right of the curve for the gas-filled lung. In turn, pulmonary vascular resistance was found to increase linearly as a function of increasing alveolar pressure, independent of the medium in the lung. Thus, for a given volume, pulmonary vascular resistance was consistently greater in the fluorocarbon-filled lung compared with the gas-filled lung. This increase in pulmonary vascular resistance was accompanied by a redistribution of pulmonary blood flow in which blood flow to the dependent region was decreased in the fluorocarbon-filled lung compared with the gas-filled lung. Conversely, the less-dependent regions of the lung received a relatively greater percentage of blood flow when filled with fluorocarbon compared with gas. These findings suggest that pulmonary vascular resistance is increased during liquid ventilation, largely as the result of mechanical interaction at the alveolar-vascular interface.
在原位分离肺制备中，对充满氟碳化合物的肺的肺血管阻力进行了研究。用供体猫的全血以恒定流量（100 ml×min⁻¹×kg⁻¹）灌注肺。左心房压力维持在零压力。通过测量肺动脉压力来计算肺血管阻力。采用微球技术测定肺血流的区域变化。在0 - 30 mmHg范围内的准静态放气过程中，对于一定体积的氟碳化合物，依赖肺泡压力始终高于气体，充满氟碳化合物的肺的每条压力 - 体积曲线都向充满气体的肺的曲线右侧偏移。相应地，发现肺血管阻力随肺泡压力升高呈线性增加，与肺内介质无关。因此，对于给定体积，充满氟碳化合物的肺的肺血管阻力始终高于充满气体的肺。肺血管阻力的这种增加伴随着肺血流的重新分布，与充满气体的肺相比，充满氟碳化合物的肺中流向依赖区域的血流减少。相反，与充满气体相比，充满氟碳化合物时肺的非依赖区域接受的血流百分比相对更大。这些发现表明，液体通气期间肺血管阻力增加，这主要是肺泡 - 血管界面机械相互作用的结果。
