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运动期间肺内分流对肺泡-动脉氧分压差的影响非常小。

The contribution of intrapulmonary shunts to the alveolar-to-arterial oxygen difference during exercise is very small.

作者信息

Vogiatzis Ioannis, Zakynthinos Spyros, Boushel Robert, Athanasopoulos Dimitris, Guenette Jordan A, Wagner Harrieth, Roussos Charis, Wagner Peter D

机构信息

Medical School of Athens University, Department of Critical Care and Pulmonary Services, Evangelismos Hospital, Athens, Greece.

出版信息

J Physiol. 2008 May 1;586(9):2381-91. doi: 10.1113/jphysiol.2007.150128. Epub 2008 Mar 13.

DOI:10.1113/jphysiol.2007.150128
PMID:18339692
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2479558/
Abstract

Exercise is well known to cause arterial PO2 to fall and the alveolar-arterial PO2 difference(Aa PO2 ) to increase. Until recently, the physiological basis for this was considered to be mostly ventilation/perfusion ((.)VA/(.)Q) inequality and alveolar-capillary diffusion limitation. Recently, arterio-venous shunting through dilated pulmonary blood vessels has been proposed to explain a significant part of the Aa PO2 during exercise. To test this hypothesis we determined venous admixture during 5 min of near-maximal, constant-load, exercise in hypoxia (in inspired O2 fraction, FIO2 , 0.13), normoxia (FIO2 , 0.21) and hyperoxia (FIO2 , 1.0) undertaken in balanced order on the same day in seven fit cyclists ((.)VO2max, 61.3 +/- 2.4 ml kg(-1) min(-1); mean +/- S.E.M.). Venous admixture reflects three causes of hypoxaemia combined: true shunt, diffusion limitation and ((.)VA/(.)Q) inequality. In hypoxia, venous admixture was 22.8 +/- 2.5% of the cardiac output; in normoxia it was 3.5 +/- 0.5%; in hyperoxia it was 0.5 +/- 0.2%. Since only true shunt accounts for venous admixture while breathing 100% O2, the present study suggests that shunt accounts for only a very small portion of the observed venous admixture, Aa PO2 and hypoxaemia during heavy exercise.

摘要

众所周知,运动可导致动脉血氧分压(PO2)下降,肺泡-动脉血氧分压差(Aa PO2)增大。直到最近,人们认为其生理基础主要是通气/血流比值((.)VA/(.)Q)失衡和肺泡-毛细血管扩散受限。最近,有人提出通过扩张的肺血管进行动静脉分流可解释运动期间Aa PO2增大的很大一部分原因。为验证这一假设,我们让7名健康的自行车运动员((.)VO2max为61.3±2.4 ml·kg-1·min-1;均值±标准误)在同一天按平衡顺序分别在低氧(吸入氧分数,FIO2,0.13)、常氧(FIO2,0.21)和高氧(FIO2,1.0)条件下进行5分钟接近最大强度的恒定负荷运动,并测定运动期间的静脉血掺杂情况。静脉血掺杂反映了导致低氧血症的三种因素的综合作用:真性分流、扩散受限和(.)VA/(.)Q失衡。在低氧条件下,静脉血掺杂占心输出量的22.8±2.5%;在常氧条件下为3.5±0.5%;在高氧条件下为0.5±0.2%。由于仅真性分流可解释呼吸100%氧气时的静脉血掺杂情况,因此本研究表明,在剧烈运动期间,分流仅占所观察到的静脉血掺杂、Aa PO2增大及低氧血症的非常小的一部分。

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