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一个世纪的运动生理学:运动期间和运动后的肺液平衡。

A century of exercise physiology: lung fluid balance during and following exercise.

机构信息

Dipartimento di Medicina e Chirurgia, Università Milano-Bicocca, Via Cadore 48, 20900, Monza, Italy.

出版信息

Eur J Appl Physiol. 2023 Jan;123(1):1-24. doi: 10.1007/s00421-022-05066-3. Epub 2022 Oct 20.

Abstract

PURPOSE

This review recalls the principles developed over a century to describe trans-capillary fluid exchanges concerning in particular the lung during exercise, a specific condition where dyspnea is a leading symptom, the question being whether this symptom simply relates to fatigue or also implies some degree of lung edema.

METHOD

Data from experimental models of lung edema are recalled aiming to: (1) describe how extravascular lung water is strictly controlled by "safety factors" in physiological conditions, (2) consider how waning of "safety factors" inevitably leads to development of lung edema, (3) correlate data from experimental models with data from exercising humans.

RESULTS

Exercise is a strong edemagenic condition as the increase in cardiac output leads to lung capillary recruitment, increase in capillary surface for fluid exchange and potential increase in capillary pressure. The physiological low microvascular permeability may be impaired by conditions causing damage to the interstitial matrix macromolecular assembly leading to alveolar edema and haemorrhage. These conditions include hypoxia, cyclic alveolar unfolding/folding during hyperventilation putting a tensile stress on septa, intensity and duration of exercise as well as inter-individual proneness to develop lung edema.

CONCLUSION

Data from exercising humans showed inter-individual differences in the dispersion of the lung ventilation/perfusion ratio and increase in oxygen alveolar-capillary gradient. More recent data in humans support the hypothesis that greater vasoconstriction, pulmonary hypertension and slower kinetics of alveolar-capillary O2 equilibration relate with greater proneness to develop lung edema due higher inborn microvascular permeability possibly reflecting the morpho-functional features of the air-blood barrier.

摘要

目的

本篇综述回顾了一个多世纪以来发展起来的原则,用于描述跨毛细血管液交换,特别是在运动期间的肺部液交换。在运动期间,呼吸困难是一个主要症状,问题是这种症状仅仅与疲劳有关,还是也意味着一定程度的肺水肿。

方法

回顾了肺水肿实验模型的数据,旨在:(1)描述在生理条件下,肺外血管水如何受到“安全因素”的严格控制;(2)考虑“安全因素”的减弱如何不可避免地导致肺水肿的发展;(3)将实验模型的数据与运动中的人类数据进行关联。

结果

运动是一种强烈的致水肿条件,因为心输出量的增加导致肺毛细血管募集、毛细血管表面积增加用于液交换以及毛细血管压力的潜在增加。生理低微血管通透性可能因导致间质基质大分子组装受损的条件而受损,导致肺泡水肿和出血。这些条件包括缺氧、过度通气时的周期性肺泡展开/折叠,这对隔片造成拉伸应力、运动的强度和持续时间以及个体发展肺水肿的倾向。

结论

运动中的人类数据显示出肺通气/灌注比的个体差异和氧气肺泡毛细血管梯度的增加。最近在人类中的数据支持了这样的假设,即更大的血管收缩、肺动脉高压和肺泡毛细血管 O2 平衡的更慢动力学与更大的发展肺水肿的倾向有关,这可能与更高的内在微血管通透性有关,可能反映了空气-血液屏障的形态功能特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/859d/9813172/d25f6330929e/421_2022_5066_Fig1_HTML.jpg

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