Redistribution of pulmonary blood flow impacts thermodilution-based extravascular lung water measurements in a model of acute lung injury.
Redistribution of pulmonary blood flow impacts thermodilution-based extravascular lung water measurements in a model of acute lung injury.
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DOI：
10.1097/aln.0b013e3181bc99cf
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发表时间：
2009-11
期刊：
影响因子：
8.8
通讯作者：
Simon BA
中科院分区：
文献类型：
--
作者：
Easley RB;Mulreany DG;Lancaster CT;Custer JW;Fernandez-Bustamante A;Colantuoni E;Simon BA
经胸热稀释研究表明，脓毒症和急性肺损伤期间水肿和水淹的进展导致血管外肺水（EVLW）测量增加。我们假设肺血流的重新分布可能导致继发于热沉默组织灌注增加的明显EVLW增加，而不是肺水肿增加。麻醉、机械通气的犬使用PiCCO®（德国慕尼黑的浦雷医疗公司）导管，通过重复盐水灌洗进行肺损伤。记录血液动力学和呼吸生理数据。肺损伤稳定后，给予内毒素灭活缺氧肺血管收缩。计算机断层成像定量体内肺体积、总组织（液）和空气含量以及血流的区域分布。灌洗损伤引起气道压力增加和动脉血氧含量降低，血流动力学影响最小。损伤后EVLW和分流分数升高，内毒素处理后明显升高。计算机断层扫描测量量化了内毒素诱导的肺血流增加到通气不良的区域，而肺组织总体积没有变化。内毒素给药后EVLW和分流分数的突然增加与缺氧肺血管收缩失活和先前热沉默的已经淹没的肺区域灌注增加是一致的。计算机断层扫描研究进一步证明了体内局部血流（但不包括肺水）的改变，并解释了分流分数和EVLW的这些改变。
Studies using transthoracic thermodilution have demonstrated increased extravascular lung water (EVLW) measurements attributed to progression of edema and flooding during sepsis and acute lung injury. We hypothesize that redistribution of pulmonary blood flow can cause increased apparent EVLW secondary to increased perfusion of thermally silent tissue, not increased lung edema. Anesthetized, mechanically ventilated canines were instrumented with PiCCO® (Pulsion Medical, Munich, Germany) catheters and underwent lung injury by repetitive saline lavage. Hemodynamic and respiratory physiologic data were recorded. After stabilized lung injury, endotoxin was administered to inactivate hypoxic pulmonary vasoconstriction. Computerized tomographic imaging was performed to quantify in vivo lung volume, total tissue (fluid) and air content, and regional distribution of blood flow. Lavage injury caused an increase in airway pressures and decreased arterial oxygen content with minimal hemodynamic effects. EVLW and shunt fraction increased after injury and then markedly following endotoxin administration. Computerized tomographic measurements quantified an endotoxin-induced increase in pulmonary blood flow to poorly aerated regions with no change in total lung tissue volume. The abrupt increase in EVLW and shunt fraction after endotoxin administration is consistent with inactivation of hypoxic pulmonary vasoconstriction and increased perfusion to already flooded lung regions that were previously thermally silent. Computerized tomographic studies further demonstrate in vivo alterations in regional blood flow (but not lung water) and account for these alterations in shunt fraction and EVLW.