Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0623, United States.
Respir Physiol Neurobiol. 2012 Mar 15;180(2-3):331-41. doi: 10.1016/j.resp.2011.12.013. Epub 2011 Dec 31.
Rapid intravenous saline infusion, a model meant to replicate the initial changes leading to pulmonary interstitial edema, increases pulmonary arterial pressure in humans. We hypothesized that this would alter lung perfusion distribution. Six healthy subjects (29 ± 6 years) underwent magnetic resonance imaging to quantify perfusion using arterial spin labeling. Regional proton density was measured using a fast-gradient echo sequence, allowing blood delivered to the slice to be normalized for density and quantified in mL/min/g. Contributions from flow in large conduit vessels were minimized using a flow cutoff value (blood delivered > 35% maximum in mL/min/cm(3)) in order to obtain an estimate of blood delivered to the capillary bed (perfusion). Images were acquired supine at baseline, after infusion of 20 mL/kg saline, and after a short upright recovery period for a single sagittal slice in the right lung during breath-holds at functional residual capacity. Thoracic fluid content measured by impedance cardiography was elevated post-infusion by up to 13% (p<0.0001). Forced expiratory volume in 1s was reduced by 5.1% post-20 mL/kg (p=0.007). Infusion increased perfusion in nondependent lung by up to 16% (6.4 ± 1.6 mL/min/g baseline, 7.3 ± 1.8 post, 7.4 ± 1.7 recovery, p=0.03). Including conduit vessels, blood delivered in dependent lung was unchanged post-infusion; however, was increased at recovery (9.4 ± 2.7 mL/min/g baseline, 9.7 ± 2.0 post, 11.3 ± 2.2 recovery, p=0.01). After accounting for changes in conduit vessels, there were no significant changes in perfusion in dependent lung following infusion (7.8 ± 1.9 mL/min/g baseline, 7.9 ± 2.0 post, 8.5 ± 2.1 recovery, p=0.36). There were no significant changes in lung density. These data suggest that saline infusion increased perfusion to nondependent lung, consistent with an increase in intravascular pressures. Dependent lung may have been "protected" from increases in perfusion following infusion due to gravitational compression of the pulmonary vasculature.
快速静脉盐水输注,一种旨在复制导致肺间质水肿的初始变化的模型,会增加人体肺动脉压。我们假设这会改变肺灌注分布。六名健康受试者(29 ± 6 岁)接受磁共振成像,使用动脉自旋标记法量化灌注。使用快速梯度回波序列测量局部质子密度,允许对切片中输送的血液进行密度归一化,并以 mL/min/g 进行量化。使用血流截止值(mL/min/cm³ 中输送的血液> 35%最大)来最小化来自大导管血管的血流贡献,以便获得输送到毛细血管床的血液(灌注)的估计值。仰卧位采集图像,在输注 20 mL/kg 盐水后,以及在功能残气量下进行单次右肺矢状切片的短暂直立恢复期间进行呼吸暂停后采集图像。通过阻抗心动描记法测量的胸腔液含量在输注后升高多达 13%(p<0.0001)。20 mL/kg 后 1 秒用力呼气量减少 5.1%(p=0.007)。输注使非依赖肺的灌注增加多达 16%(基线时 6.4 ± 1.6 mL/min/g,输注后 7.3 ± 1.8,恢复时 7.4 ± 1.7,p=0.03)。包括导管血管在内,输注后依赖肺的血液输送没有变化;然而,在恢复时增加(基线时 9.4 ± 2.7 mL/min/g,输注后 9.7 ± 2.0,恢复时 11.3 ± 2.2,p=0.01)。在考虑导管血管变化后,输注后依赖肺的灌注没有明显变化(基线时 7.8 ± 1.9 mL/min/g,输注后 7.9 ± 2.0,恢复时 8.5 ± 2.1,p=0.36)。肺密度没有明显变化。这些数据表明,盐水输注增加了非依赖肺的灌注,这与血管内压的增加一致。由于肺血管的重力压缩,输注后依赖肺可能“免受”灌注增加的影响。