Dept. of Medicine, Univ. of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0931, USA.
J Appl Physiol (1985). 2010 Jan;108(1):53-9. doi: 10.1152/japplphysiol.00787.2009. Epub 2009 Nov 12.
Rapid infusion of intravenous saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized that infusion would disrupt pulmonary gas exchange by increasing ventilation/perfusion ((.)VA/(.)Q) inequality as opposed to a diffusive impairment in O2 exchange. Seven males (26 +/- 3 yr; FEV1: 110 +/- 16% predicted.) performed spirometry and had (.)VA/(.)Q mismatch measured using the multiple inert gas elimination technique, before and after 20 ml/kg iv of normal saline delivered in approximately 30 min. Infusion increased thoracic fluid content from transthoracic impedance by 12% (P < 0.0001) and left FVC unchanged but reduced expiratory flows (FEF(25-75) falling from 5.1 +/- 0.4 to 4.2 +/- 0.4 l/s, P < 0.05). However, (.)VA/(.)Q mismatch as measured by the log standard deviation of the ventilation (LogSD(.)V) and perfusion (LogSD(.)Q) distributions remained unchanged; LogSD(.)V: 0.40 +/- 0.03 pre, 0.38 +/- 0.04 post, NS; LogSD(.)Q: 0.38 +/- 0.03 pre, 0.37 +/- 0.03 post, NS. There was no significant change in arterial PO2 (99 +/- 2 pre, 99 +/- 3 mmHg post, NS) but arterial PCO2 was decreased (38.7 +/- 0.6 pre, 36.8 +/- 1.2 mmHg post, P < 0.05). Thus, infusion compressed small airways and caused a mild degree of hyperventilation. There was no evidence for a diffusive limitation to O2 exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at FIO2 = 0.125 (4.3 +/- 1.0 pre, 5.2 +/- 1.0 post, NS). After infusion, the fraction of perfusion going to areas with (.)VA/(.)Q < 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 +/- 0.06 (FIO2 = 0.21), 0.80 +/- 0.06 (FIO2 = 0.30), P < 0.05] with similar effects on ventilation in the face of unchanged (.)VA and (.)Q. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences.
快速静脉输注生理盐水，一种肺间质水肿模型，可改变肺灌注分布，增加肺毛细血管血容量，并增加人类支气管壁厚度。我们假设输注会通过增加通气/灌注（VA/Q）不匹配而不是通过氧交换的弥散障碍来破坏肺气体交换。七名男性（26 +/- 3 岁；FEV1：110 +/- 16%预测）在接受大约 30 分钟的静脉内生理盐水 20ml/kg 输注前后，进行了肺活量测定，并使用多惰性气体消除技术测量了 VA/Q 不匹配。输注通过经胸阻抗增加了 12%的胸腔液含量（P < 0.0001），左 FVC 不变，但降低了呼气流量（FEF（25-75）从 5.1 +/- 0.4 降至 4.2 +/- 0.4 l/s，P < 0.05）。然而，VA/Q 不匹配的测量，通过通气（LogSDV）和灌注（LogSDQ）分布的对数标准偏差，保持不变；LogSDV：0.40 +/- 0.03 预，0.38 +/- 0.04 后，NS；LogSDQ：0.38 +/- 0.03 预，0.37 +/- 0.03 后，NS。动脉 PO2 没有显著变化（99 +/- 2 预，99 +/- 3 mmHg 后，NS），但动脉 PCO2 降低（38.7 +/- 0.6 预，36.8 +/- 1.2 mmHg 后，P < 0.05）。因此，输注压缩了小气道并导致轻度过度通气。没有证据表明氧交换存在弥散限制，在 FIO2 = 0.125 时，测量的肺泡-动脉氧分压差异不受输注的影响（4.3 +/- 1.0 预，5.2 +/- 1.0 后，NS）。输注后，当受试者呼吸高氧气体混合物时，流向 VA/Q < 1 的灌注比例增加[0.72 +/- 0.06（FIO2 = 0.21），0.80 +/- 0.06（FIO2 = 0.30），P < 0.05]，同时对通气也有类似的影响，而 VA 和 Q 保持不变。这些结果表明，在空气呼吸期间，主动控制流向通气减少区域的血流，从而最小化气体交换的后果。
