Effects of inhaled nitric oxide at rest and during exercise in idiopathic pulmonary fibrosis
Effects of inhaled nitric oxide at rest and during exercise in idiopathic pulmonary fibrosis
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DOI：
10.1152/japplphysiol.01104.2010
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发表时间：
2011-03-01
影响因子：
3.3
通讯作者：
Barbera, Joan A.
中科院分区：
文献类型：
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作者：
Blanco, Isabel;Ribas, Jesus;Barbera, Joan A.
Blanco I, Ribas J, Xaubet A, Gomez FP, Roca J, Rodriguez-Roisin R, Barbera JA。静息和运动时吸入一氧化氮对特发性肺纤维化的影响。中国生物医学工程学报（英文版），2011；首次发表于2010年12月23日；doi: 10.1152 / japplphysiol.01104.2010。特发性肺纤维化（IPF）患者在运动时通常会出现低氧血症和肺动脉高压。内皮衍生的血管舒张剂在多大程度上改变了这些变化尚不清楚。该研究旨在研究运动是否会引起IPF患者血浆内皮源性信号介质水平的变化，并评估吸入一氧化氮（NO）在静止和运动时对肺血流动力学和气体交换的急性影响。我们评估了7例IPF患者（6男1女；57 +/- 11岁；强迫肺活量，预测60 +/- 13%；一氧化碳扩散量，预测52 +/- 10%）。在静息和次极限运动时测量内皮素、6-酮-前列腺素- f -1 α、血栓素B-2和硝酸盐的水平。肺血流动力学和气体交换，包括通气-灌注关系，在休息和亚极限运动时呼吸环境空气和40 ppm NO进行评估。运动时血栓素B-2的浓度升高（P = 0.046），而其他介质的水平没有变化。6-酮前列腺素- f -1 α的变化与平均肺动脉压的变化相关（r = 0.94; P < 0.005）。吸入NO降低了静息时（-4.6 +/- 2.1 mmHg）和运动时（-11.7 +/- 7.1 mmHg）的平均肺动脉压（分别为P = 0.001和P = 0.004），在任何研究条件下均未改变动脉氧合或通气-灌注分布。运动期间肺泡至毛细血管的氧扩散限制导致了动脉PO2的降低，但一氧化氮并没有改变这一限制。我们得出结论，在IPF中，一些内皮来源的信号分子可能调节运动期间肺动脉高压的发展，并且吸入一氧化氮可以在不干扰气体交换的情况下降低肺血管阻力。
Blanco I, Ribas J, Xaubet A, Gomez FP, Roca J, Rodriguez-Roisin R, Barbera JA. Effects of inhaled nitric oxide at rest and during exercise in idiopathic pulmonary fibrosis. J Appl Physiol 110: 638-645, 2011. First published December 23, 2010; doi:10.1152/japplphysiol.01104.2010.-Patients with idiopathic pulmonary fibrosis (IPF) usually develop hypoxemia and pulmonary hypertension when exercising. To what extent endothelium-derived vasodilating agents modify these changes is unknown. The study was aimed to investigate in patients with IPF whether exercise induces changes in plasma levels of endothelium-derived signaling mediators, and to assess the acute effects of inhaled nitric oxide (NO) on pulmonary hemodynamics and gas exchange, at rest and during exercise. We evaluated seven patients with IPF (6 men/1 woman; 57 +/- 11 yr; forced vital capacity, 60 +/- 13% predicted; carbon monoxide diffusing capacity, 52 +/- 10% predicted). Levels of endothelin, 6-keto-prostaglandin-F-1 alpha, thromboxane B-2, and nitrates were measured at rest and during submaximal exercise. Pulmonary hemodynamics and gas exchange, including ventilation-perfusion relationships, were assessed breathing ambient air and 40 ppm NO, both at rest and during submaximal exercise. The concentration of thromboxane B-2 increased during exercise (P = 0.046), whereas levels of other mediators did not change. The change in 6-keto-prostaglandin-F-1 alpha correlated with that of mean pulmonary arterial pressure (r = 0.94; P < 0.005). Inhaled NO reduced mean pulmonary arterial pressure at rest (-4.6 +/- 2.1 mmHg) and during exercise (-11.7 +/- 7.1 mmHg) (P = 0.001 and P = 0.004, respectively), without altering arterial oxygenation or ventilation-perfusion distributions in any of the study conditions. Alveolar-to-capillary oxygen diffusion limitation, which accounted for the decrease of arterial PO2 during exercise, was not modified by NO administration. We conclude that, in IPF, some endothelium-derived signaling molecules may modulate the development of pulmonary hypertension during exercise, and that the administration of inhaled NO reduces pulmonary vascular resistance without disturbing gas exchange.