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Mechanism of hypoxemia in acute lung injury evaluated by multidetector-row CT.

机译：多排行CT评估急性肺损伤中低氧血症的机制。

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RATIONALE AND OBJECTIVES: Hypoxic pulmonary vasoconstriction (HPV) is a homeostatic mechanism causing pulmonary arterial constriction in response to local hypoxia, redistributing blood flow to lung regions with better oxygenation and ventilation. We present the use of computed tomographic (CT) volume and perfusion imaging to show differences in the mechanisms of hypoxemia from alterations in blood flow distribution within different animal models of acute lung injury (ALI). MATERIALS AND METHODS: Three anesthetized, instrumented, and ventilated sheep were studied, two with induced ALI and one with native pneumonia. One subject was injured by using intravenous infusion of lipopolysaccharide (LPS), and the other, by repetitive saline lavage. Subjects were imaged using multidetector-row CT (MDCT) before and after injury. Lung volume scans were gated to the respiratory cycle. Contrast injection perfusion images were electrocardiogram gated. Computer-based image analysis quantified regional blood flow and total lung, air, and tissue volumes. RESULTS: Total lung air fraction was decreased in both ALI models. In lavage injury, there was a decrease in perfusion to dependent poorly aerated regions, with perfusion shifting to nondependent regions. Conversely, LPS injury greatly increased perfusion to dependent poorly aerated regions. In the subject with pneumonia, decreasing fraction of inspired oxygen redistributed blood flow into the injured regions. CONCLUSIONS: MDCT techniques can be used to investigate regional lung perfusion and lung volume distributions to explain physiological mechanisms in ALI. Our findings suggest that after lavage injury, blood flow is redistributed, consistent with preserved HPV and resulting in better oxygenation despite greater lung volume loss compared with LPS injury. In native pneumonia, HPV inactivation can be localized to the injured regions.
机译：理由和目的：缺氧性肺血管收缩（HPV）是一种稳态机制，可响应局部缺氧而引起肺动脉收缩，从而通过更好的氧合和通气将血流重新分配到肺区域。我们目前使用计算机断层扫描（CT）量和灌注成像来显示低氧血症机制的差异，这是由不同的急性肺损伤（ALI）动物模型中的血流分布变化引起的。材料与方法：研究了三只麻醉，器械和通气的绵羊，其中两只患有诱导性ALI，另一只患有天然肺炎。一名受试者因静脉内注射脂多糖（LPS）而受伤，另一名受试者因重复盐水冲洗而受伤。受伤前后使用多排行CT（MDCT）对受试者进行成像。肺部容积扫描控制在呼吸循环中。造影剂灌注图像是心电图门控的。基于计算机的图像分析可量化区域血流量以及总肺，空气和组织体积。结果：在两种ALI模型中总肺空气分数均降低。在灌洗损伤中，对依赖的充气不足区域的灌注减少，而灌注转移到非依赖的区域。相反，LPS损伤大大增加了对依赖的充气不足区域的灌注。在患有肺炎的受试者中，越来越少的吸入氧气将血液重新分配到受伤区域。结论：MDCT技术可用于调查局部肺灌注和肺体积分布，以解释ALI的生理机制。我们的发现表明，灌洗液损伤后，与LPS损伤相比，尽管肺体积损失更大，但血流重新分配，与HPV保持一致，并导致更好的氧合作用。在天然肺炎中，HPV失活可以局限于受损区域。

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