BACKGROUND Studies suggest that acute decreases in lung hyperinflation at rest improves cardiac function and increases lung vascular perfusion from decompression of a compromised heart. In those studies, changes in resting oxygen uptake induced by medications, an alternative explanation for compensatory increased cardiac function, were not explored. METHODS This double-blind, multicenter, double-crossover study enrolled adults with chronic obstructive pulmonary disease, resting hyperinflation, and > 10% improvement in inspiratory capacity after 2 inhalations of budesonide/formoterol 160/4.5 μg. Metabolic, cardiac, and ventilatory function were measured 60 min pre-/post-dose at each visit. Primary endpoint was change in resting oxygen uptake for budesonide/formoterol versus placebo. RESULTS Fifty-one patients (median age: 63 years) received treatment. Compared with placebo, budesonide/formoterol significantly increased resting oxygen uptake (mean change from baseline: 1.25 vs 11.37 mL/min; P = 0.007) as well as tidal volume and minute ventilation. This occurred despite improvements in the inspiratory capacity, forced vital capacity, and expiratory volume in 1 s. No significant treatment differences were seen for oxygen saturation, respiratory rate, and resting dyspnea. There was a numerical increase in oxygen pulse (oxygen uptake/heart rate). Correlations between inspiratory capacity and oxygen pulse were weak. CONCLUSIONS Budesonide/formoterol treatment in resting hyperinflated patients with COPD results in significant deflation. The increase in oxygen uptake and minute ventilation at lower lung volumes, without changes in heart rate and with minimal improvement in oxygen pulse, suggests increased oxygen demand as a contributor to increased cardiac function. TRIAL REGISTRATION ClinicalTrials.gov identifier: NCT02533505.

中文翻译：

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布地奈德/福莫特罗在慢性阻塞性肺病中减少肺过度充气的代谢和心肺作用：一项随机，双交叉，安慰剂对照的多中心试验。

背景研究表明，静息时肺过度充气的急性减少会改善心脏功能，并因心脏受损而导致肺血管灌注增加。在那些研究中，没有探索药物引起的静息摄氧量的变化，这是代偿性心脏功能增加的另一种解释。方法这项双盲，多中心，双交叉的研究纳入了患有慢性阻塞性肺疾病，静息过度充气，并在两次吸入布地奈德/福莫特罗160 / 4.5μg后吸气能力提高> 10％的成年人。每次就诊前/后60分钟测量代谢，心脏和通气功能。主要终点是布地奈德/福莫特罗相对于安慰剂的静息摄氧量变化。结果51例患者（中位年龄：63岁）接受治疗。与安慰剂相比，布地奈德/福莫特罗显着增加了静息摄氧量（相对于基线的平均变化：1.25 vs. 11.37 mL / min； P = 0.007）以及潮气量和分钟通气量。尽管吸气能力，强制肺活量和呼气量在1 s内有所改善，但仍发生了这种情况。氧饱和度，呼吸频率和静息呼吸困难均未见明显的治疗差异。氧气脉冲（氧气摄取/心率）在数值上有所增加。吸气量与氧气脉冲之间的相关性较弱。结论布地奈德/福莫特罗在静息过度充气的COPD患者中导致明显的放气。在较低的肺容量下，摄氧量增加和分钟通气量增加，在没有心率变化且氧气脉搏改善最小的情况下，提示氧气需求增加是心脏功能增强的原因。试验注册ClinicalTrials.gov标识符：NCT02533505。