Alveolo-capillary diffusion of hyperpolarized 129Xe as a marker of pulmonary fibrosis.
Alveolo-capillary diffusion of hyperpolarized 129Xe as a marker of pulmonary fibrosis.
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超极化 129Xe 的肺泡毛细血管扩散作为肺纤维化的标志。
DOI：
10.1152/japplphysiol.00688.2014
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Hsia,ConnieCW
中科院分区：
文献类型：
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作者：
Hsia,ConnieCW
由于氧合血红蛋白解离曲线的非线性，通过扩散穿过肺泡-毛细血管组织-血浆屏障，然后与血红蛋白结合来定量肺的氧摄取能力并不简单。只有在低氧条件下，即肺泡毛细血管氧分压在解离曲线的线性部分内时，才可能采用侵入性方法直接评估肺氧弥散量（DLO 2）。相反，一氧化碳（CO）通常用作示踪气体，用于评估肺弥散量（DLCO），这是一种利用其更简单的血红蛋白结合动力学的非侵入性方法。与DL0 2一样，DLCO对组织-血浆屏障和红细胞（RBC）内部的电导变化敏感。经典的Roughton-Forster模型（6）试图将DLCO分解为两个连续的步骤-穿过组织-血浆屏障的扩散，以及向红细胞（RBC）内部的联合扩散加上与血红蛋白的反应-通过测量两个肺泡O2张力下的DLCO。后来，一氧化氮弥散量（DLNO）被用作另一种测量方法（1）。由于其对血红蛋白的极高结合亲和力，RBC内的NO电导大大超过了穿过组织-血浆屏障的电导，使得DLNO成为比DLCO更敏感的屏障电导指标。尽管它们的物理性质和反应动力学存在差异，但DLCO和DLNO都与DL0 2经验相关。在Roughton-Forster模型的背景下，CO和NO是否足以从RBC组分中分离组织血浆仍然存在争议，特别是在病理条件下。另一种评估肺的O2转移能力的方法，仅适用于死后固定肺，是估计肺泡结构可以支持的最大O2通量，其中关键决定因素使用体视学技术测量（表面积、调和平均屏障厚度、毛细血管血容量和毛细血管血细胞比容）（4）。由于基础O2流量的最大流量的一小部分，基于结构的估计扩散能力远远超过生理测量得到的休息，但差异减少时，与生理测量得到的峰值运动。弥散量的生理测量随肺容量、血流量和血红蛋白浓度而变化，易受通气-灌注和灌注-弥散异质性引起的误差的影响，并且不产生解剖信息。由于制备的非生理条件、采样变异性和忽略生理不均匀性，基于结构的估计会产生误差。
QUANTIFYING the lung’s capacity for O2 uptake by diffusion across the alveolo-capillary tissue-plasma barrier followed by binding to hemoglobin is not straightforward, owing to the nonlinearity of the oxyhemoglobin dissociation curve. Direct assessment of lung diffusing capacity for O2 (DLO2) is possible only by employing invasive methods under hypoxic conditions, ie, when alveolar capillary partial pressure of O2 is within the linear portion of the dissociation curve. Instead, carbon monoxide (CO) is commonly used as a tracer gas for assessing lung diffusing capacity (DLCO), a noninvasive approach that takes advantage of its simpler hemoglobin binding kinetics. Like DLO2, DLCO is sensitive to changes in the conductance both of the tissue-plasma barrier and inside the red blood cells (RBCs). The classic Roughton-Forster model (6) attempts to decompose DLCO into two serial steps—diffusion across tissue-plasma barrier, and the combined diffusion into the red blood cell (RBC) interior plus reaction with hemoglobin—by measuring DLCO at two alveolar O2 tensions. Later, diffusing capacity for nitric oxide (DLNO) was employed as another measure (1). Because of its extremely high binding affinity for hemoglobin, NO conductance within RBCs greatly exceeds that across the tissue-plasma barrier, making DLNO a more sensitive indicator of barrier conductance than DLCO. Despite the differences in their physical properties and reaction kinetics, both DLCO and DLNO empirically correlate with DLO2. It remains debated whether CO and NO in the context of the Roughton-Forster model sufficiently resolve the tissueplasma from the RBC components, especially in pathological conditions.Another approach to assess the lung’s capacity for O2 transfer, suitable only at postmortem in fixed lungs, is to estimate the maximum O2 flux that could be supported by alveolar structure, whereby the key determinants (surface area, harmonic mean barrier thickness, capillary blood volume, and capillary hematocrit) are measured using stereological techniques (4). Because basal O2 flux amounts to only a fraction of maximum flux, the structure-based estimates of diffusing capacity far exceeds physiological measurements obtained at rest, but the differences diminish when compared with physiological measurements obtained at peak exercise. The physiological measurements of diffusing capacity vary with lung volume, blood flow, and hemoglobin concentration, are subject to errors caused by ventilation-perfusion and perfusion-diffusion heterogeneity, and yield no anatomical information. The structure-based estimates are subject to errors due to the nonphysiological conditions of preparation, sampling variability, and the neglect of physiological inhomogeneity.