Malik A B, van der Zee H, Neumann P H, Gertzberg N B
J Appl Physiol Respir Environ Exerc Physiol. 1980 Nov;49(5):834-40. doi: 10.1152/jappl.1980.49.5.834.
Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.
通过在2至3小时内输注179.2 - 659.4毫升/千克生理盐水，在犬身上诱导出不同程度的肺水肿，在此期间测定局部肺血流量。在基线期和输注后30分钟测量肺血流动力学和局部血流量。肺水肿程度通过最终血管外肺水与去血干肺重量比（W/D）来确定。在出现明显肺泡水肿的犬中（W/D为10.70±0.88，而对照组为3.10±0.30），血流转移至肺的上部或下垂区域。转移至上部区域与肺动脉压（Ppa）升高（P<0.05）相关，而转移至下垂肺区域与Ppa的显著变化无关。呼吸100%氧气并不能阻止这些转移，表明它们不是由于局部低氧性肺血管收缩所致。血流分布模式也与水肿的局部差异无关。与暴发性水肿期间的变化相反，中度肺水肿（W/D为6.03±0.69）后血流分布没有改变，这表明肺血流重新分布需要明显的肺泡灌洗。气道灌洗期间血流向上肺重新分布可能是由于Ppa升高，而在相同程度水肿期间下垂肺血流增加可能是由于表面活性降低继发肺泡血管“膨出”至气腔所致。
