低碳酸血症和通气过度作为运动后哮喘发病机制的相对作用。

Relative contributions of hypocarbia and hyperpnea as mechanisms in postexercise asthma.

作者信息

McFadden E R, Stearns D R, Ingram R H, Leith D E

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1977 Jan;42(1):22-7. doi: 10.1152/jappl.1977.42.1.22.

DOI:10.1152/jappl.1977.42.1.22

Abstract

The purpose of this investigation was to assess the relative contributions of hyperpnea and hypocapnia in the induction of postexercise asthma. To achieve these ends, eight young asthmatics were exercised on a treadmill while minute ventilations (VE) and end-tidal CO2 (PET CO2) tensions were continuously recorded. The subjects were then restudied using a partial rebreathing technique that allowed separation of minute and alveolar ventilations so that independent evaluations could be made of the relative effects of bulk airflow on pulmonary mechanics as well as a systematic study of hypocapnia in a dose-response fashion. Sustained hyperpnea with VEidentical to those recorded during exercise was totally without effect when the mean PET CO2 was isocapnic or lowered to approximately 30 Torr. Reduction in PETCO2 to 21.3 +/-0.9 Torr brought about significant changes in mechanics, but in every variable measured, exercise produced the greatest alterations and did so at PETCO2 values that had no effect when studied in a controlled fashion. Consequently, neither high VE per se, nor hypocapnia can be considered as the mechanisms underlying exercise induced asthma.

摘要

本研究的目的是评估深呼吸和低碳酸血症在运动诱发哮喘中的相对作用。为实现这些目标，让8名年轻哮喘患者在跑步机上运动，同时持续记录每分通气量（VE）和呼气末二氧化碳（PET CO2）分压。然后采用部分重复呼吸技术对受试者进行再次研究，该技术可分离每分通气量和肺泡通气量，从而能够独立评估总气流对肺力学的相对影响，并以剂量反应方式系统研究低碳酸血症。当平均PET CO2处于等碳酸状态或降至约30托时，与运动时记录的VE相同的持续性深呼吸完全无效。将PETCO2降至21.3±0.9托会引起力学上的显著变化，但在测量的每个变量中，运动产生的变化最大，且是在以受控方式研究时无影响的PETCO2值下产生的。因此，无论是高VE本身，还是低碳酸血症，都不能被视为运动诱发哮喘的潜在机制。