Bates Melissa L, Farrell Emily T, Drezdon Alyssa, Jacobson Joseph E, Perlman Scott B, Eldridge Marlowe W
Department of Pediatrics, Critical Care Division and the John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States of America.
Department of Pediatrics, Critical Care Division and the John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States of America; Michigan State University College of Human Medicine, East Lansing, Michigan, United States of America.
PLoS One. 2014 Jul 11;9(7):e101146. doi: 10.1371/journal.pone.0101146. eCollection 2014.
Intrapulmonary arteriovenous anastomoses (IPAVs) are large diameter connections that allow blood to bypass the lung capillaries and may provide a route for right-to-left embolus transmission. These anastomoses are recruited by exercise and catecholamines and hypoxia. Yet, whether IPAVs are recruited via direct, oxygen sensitive regulatory mechanisms or indirect effects secondary to redistribution pulmonary blood flow is unknown. Here, we hypothesized that the addition of exercise to hypoxic gas breathing, which increases cardiac output, would augment IPAVs recruitment in healthy humans. To test this hypothesis, we measured the transpulmonary passage of 99mTc-macroaggregated albumin particles (99mTc-MAA) in seven healthy volunteers, at rest and with exercise at 85% of volitional max, with normoxic (FIO2 = 0.21) and hypoxic (FIO2 = 0.10) gas breathing. We found increased 99mTc-MAA passage in both exercise conditions and resting hypoxia. However, contrary to our hypothesis, we found the greatest 99mTc-MAA passage with resting hypoxia. As an additional, secondary endpoint, we also noted that the transpulmonary passage of 99mTc-MAA was well-correlated with the alveolar-arterial oxygen difference (A-aDO2) during exercise. While increased cardiac output has been proposed as an important modulator of IPAVs recruitment, we provide evidence that the modulation of blood flow through these pathways is more complex and that increasing cardiac output does not necessarily increase IPAVs recruitment. As we discuss, our data suggest that the resistance downstream of IPAVs is an important determinant of their perfusion.
肺内动静脉吻合支（IPAVs）是大直径的连接通道，可使血液绕过肺毛细血管，可能为右向左的栓子传播提供途径。这些吻合支在运动、儿茶酚胺和低氧状态下会被激活。然而，IPAVs是通过直接的、对氧敏感的调节机制被激活，还是继发于肺血流重新分布的间接效应，目前尚不清楚。在此，我们假设在低氧气体呼吸时增加运动（这会增加心输出量），会增强健康人IPAVs的激活。为了验证这一假设，我们在7名健康志愿者休息时以及以最大自主运动强度的85%进行运动时，分别在常氧（FIO2 = 0.21）和低氧（FIO2 = 0.10）气体呼吸条件下，测量了99mTc-大聚合白蛋白颗粒（99mTc-MAA）的经肺通过情况。我们发现，在运动状态和静息低氧状态下，99mTc-MAA的通过量均增加。然而，与我们的假设相反，我们发现静息低氧时99mTc-MAA的通过量最大。作为一个额外的次要终点，我们还注意到，运动期间99mTc-MAA的经肺通过量与肺泡-动脉氧分压差（A-aDO2）密切相关。虽然心输出量增加被认为是IPAVs激活的一个重要调节因素，但我们提供的证据表明，通过这些途径的血流调节更为复杂，增加心输出量不一定会增加IPAVs的激活。正如我们所讨论的，我们的数据表明，IPAVs下游的阻力是其灌注的一个重要决定因素。
