Cardiopulmonary Exercise Testing and Rehabilitation Laboratory, First Critical Care Medicine Department, Evgenidio Hospital, National and Kapodistrian University of Athens.
Respir Care. 2013 Dec;58(12):2134-41. doi: 10.4187/respcare.02113. Epub 2013 May 28.
Pulmonary microcirculation abnormalities are the main determinants of pulmonary arterial hypertension (PAH) pathophysiology. We hypothesized that PAH patients have peripheral tissue microcirculation alterations that might benefit from hyperoxic breathing. We evaluated peripheral muscle microcirculation with near-infrared spectroscopy, before and after hyperoxic breathing.
Eight PAH subjects, 8 healthy subjects (controls) matched for age, sex, and body mass index, and 16 subjects with chronic heart failure and matched for functional capacity with the PAH subjects underwent near-infrared spectroscopy. Tissue O(2) saturation, defined as the hemoglobin saturation (%) in the microvasculature compartments, was measured on the thenar muscle. Then the 3-min brachial artery occlusion technique was applied before, during, and after 15 min of breathing 100% O(2). We calculated the oxygen consumption rate (%/min), the reactive hyperemia time, and the time needed for tissue O(2) saturation to reach its baseline value after the release of the occlusion.
Compared to the controls, the PAH subjects had a significantly lower resting tissue O(2) saturation (65.8 ± 14.9% vs 82.1 ± 4.0%, P = .005), a trend toward a lower oxygen consumption rate (35.3 ± 9.1%/min vs 43.4 ± 19.7%/min, P = .60), and a significantly higher reactive hyperemia time (3.0 ± 0.6 min vs 2.0 ± 0.3 min, P < .001). The PAH subjects also had lower tissue O(2) saturation (P = .08), lower peripheral arterial oxygen saturation (P = .01), and higher reactive hyperemia time (P = .02) than the chronic heart failure subjects. After hyperoxic breathing, the PAH subjects had increased tissue O(2) saturation (65.8 ± 14.9% to 71.4 ± 14.5%, P = .01), decreased oxygen consumption rate (35.3 ± 9.1%/min to 25.1 ± 6.6%/min, P = .01), and further increased reactive hyperemia time (3.0 ± 0.6 min to 4.2 ± 0.7 min, P = .007).
The PAH subjects had substantial impairments of peripheral muscle microcirculation, decreased tissue O(2) saturation (possibly due to hypoxemia), slower reactive hyperemia time, (possibly due to endothelium dysfunction), and peripheral systemic vasoconstriction. Acute hyperoxic breathing improved resting tissue O(2) saturation (an expression of higher oxygen delivery) and decreased the oxygen consumption rate and reactive hyperemia time during reperfusion, possibly due to increased oxidative stress and evoked vasoconstriction.
肺微循环异常是肺动脉高压（PAH）病理生理学的主要决定因素。我们假设 PAH 患者存在外周组织微循环改变，这些改变可能受益于吸氧。我们使用近红外光谱技术评估了 PAH 患者在吸氧前后的外周肌肉微循环。
8 名 PAH 患者、8 名年龄、性别和体重指数匹配的健康对照者以及 16 名慢性心力衰竭患者接受了近红外光谱检查。组织氧饱和度定义为微脉管系统中血红蛋白饱和度（%），在手鱼际肌上进行测量。然后应用 3 分钟的肱动脉闭塞技术，在 15 分钟内 100%吸氧之前、期间和之后进行测量。我们计算了耗氧量（%/min）、反应性充血时间以及在释放闭塞后组织氧饱和度恢复到基线值所需的时间。
与对照组相比，PAH 患者的静息组织氧饱和度明显降低（65.8±14.9%比 82.1±4.0%，P=0.005），耗氧量呈下降趋势（35.3±9.1%/min 比 43.4±19.7%/min，P=0.60），反应性充血时间明显延长（3.0±0.6 分钟比 2.0±0.3 分钟，P<0.001）。PAH 患者的组织氧饱和度（P=0.08）、外周动脉血氧饱和度（P=0.01）和反应性充血时间（P=0.02）也低于慢性心力衰竭患者。吸氧后，PAH 患者的组织氧饱和度增加（65.8±14.9%比 71.4±14.5%，P=0.01），耗氧量降低（35.3±9.1%/min 比 25.1±6.6%/min，P=0.01），反应性充血时间进一步延长（3.0±0.6 分钟比 4.2±0.7 分钟，P=0.007）。
PAH 患者的外周肌肉微循环严重受损，组织氧饱和度降低（可能由于低氧血症），反应性充血时间延长（可能由于内皮功能障碍），外周系统性血管收缩。急性吸氧可改善静息组织氧饱和度（表达更高的氧输送）并降低再灌注期间的耗氧量和反应性充血时间，这可能是由于氧化应激增加和诱发的血管收缩所致。
