Background: Perfusion of intrapulmonary arteriovenous anastomoses (IPAVA) is increased during exercise and in hypoxia and is associated with variations in oxygen saturation (SPO2), resulting in blood bypassing the pulmonary microcirculation. Sildenafil is a pulmonary vasodilator that improves SPO2 and endurance performance in hypoxia. The purpose of this study was to determine if 50 mg sildenafil would reduce IPAVA perfusion (QIPAVA) and if the decrement in maximal exercise capacity (VO2max) in hypoxia is related to QIPAVA. We hypothesized that during progressive levels of hypoxia at rest (FIO2 = 0.21, 0.14, 0.12), sildenafil would increase SPO2 and reduce bubble score (estimate of QIPAVA) compared to placebo, and that the decrement in VO2max in hypoxia would be positively correlated with bubble score at rest in hypoxia. Materials and Methods: Fourteen endurance-trained men performed a graded maximal exercise test at sea level and at a simulated altitude of 3000 m, followed by two experimental visits where, after randomly ingesting sildenafil or placebo, they underwent agitated saline contrast echocardiography during progressive levels of hypoxia at rest. Results: All participants experienced a decrement in power output in hypoxia that ranged from 9% to 19% lower than sea level values. Compared to normoxia, bubble score increased significantly in hypoxia (p < 0.001) with no effect of sildenafil (p = 0.580). There was a negative correlation between SPO2 and bubble score (p < 0.001). The decrement in peak power output at VO2max in hypoxia was unrelated to IPAVA perfusion in resting hypoxia (p = 0.32). Several participants demonstrated QIPAVA greater than zero in room air, indicating that arterial hypoxemia may not be the sole mechanism for QIPAVA. Conclusion: These results indicate that the VO2max decrement caused by hypoxia is not related to QIPAVA and that sildenafil does not improve VO2max in hypoxia through modulation of QIPAVA.

中文翻译：

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肺内动静脉吻合术的灌注与低氧时的最大摄氧量无关，口服西地那非不会改变。

背景：运动中和缺氧时肺内动静脉吻合术（IPAVA）的灌注增加，并且与血氧饱和度（SPO2）的变化有关，导致血液绕过肺微循环。西地那非是一种肺血管扩张剂，可改善缺氧时的SPO2和耐力表现。这项研究的目的是确定50 mg西地那非是否会降低IPAVA灌注（QIPAVA），以及缺氧时最大运动能力（VO2max）的降低是否与QIPAVA有关。我们假设与安慰剂相比，在休息时进行性低氧（FIO2 = 0.21、0.14、0.12）时，西地那非会增加SPO2并降低气泡评分（QIPAVA的估计值），并且低氧时VO2max的减少与缺氧休息时的气泡评分。材料和方法：14名耐力训练的男性在海平面和模拟海拔3000 m上进行了最大程度的分级运动测试，随后进行了两次实验性访问，在随机摄入西地那非或安慰剂后，他们在休息时逐渐出现低氧水平时接受了搅拌盐水超声心动图检查。结果：所有参与者在缺氧状态下的功率输出均比海平面值降低了9％至19％。与正常氧相比，缺氧时气泡评分显着增加（p <0.001），而昔多芬无影响（p = 0.580）。SPO2与气泡评分之间呈负相关（p <0.001）。缺氧时最大摄氧量最大输出功率的减少与静息性缺氧时IPAVA灌注无关（p = 0.32）。一些参与者证明室内空气中的QIPAVA大于零，提示动脉血氧不足可能不是QIPAVA的唯一机制。结论：这些结果表明，低氧引起的VO2max降低与QIPAVA无关，而昔多芬非不能通过调节QIPAVA改善低氧条件下的VO2max。