RESUMEN
BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.