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急性哮喘发作时肺总量增加的机制。

The mechanism of increase in total lung capacity during acute asthma.

作者信息

Peress L, Sybrecht G, Macklem P T

出版信息

Am J Med. 1976 Aug;61(2):165-9. doi: 10.1016/0002-9343(76)90165-0.

Abstract

In order to investigate the mechanism underlying the increased total lung capacity (TLC) observed during an acute asthmatic attack, we measured respiratory mechanics in a specially trained, exercise-induced, asthmatic. During the acute attack his TLC (determined plethysmographically) increased from 7.8 to 9.2 liters. The static pressure-volume curve of the lung shifted to the left and expiratory compliance increased from 0.24 to 0.55 liter/cm H2O. There was a parallel shift of the static pressure-volume curve of the chest wall resulting in an increase in the outward recoil of this structure. The maximum inspiratory pressure-volume curve of the total respiratory system was shifted so that the inspiratory muscles were able to generate greater pressures at any given lung volume during the attack. The findings indicate that the increase in TLC during acute bronchospasm results from the combination of loss of lung recoil, increased outward recoil of the chest wall and increased strength of contraction of the inspiratory muscles.

摘要

为了研究急性哮喘发作期间观察到的肺总量(TLC)增加的潜在机制,我们对一名经过特殊训练、运动诱发哮喘的患者进行了呼吸力学测量。在急性发作期间,他的TLC(通过体积描记法测定)从7.8升增加到9.2升。肺的静态压力-容积曲线向左移动,呼气顺应性从0.24升/厘米水柱增加到0.55升/厘米水柱。胸壁的静态压力-容积曲线也发生了平行移动,导致该结构的向外回缩增加。整个呼吸系统的最大吸气压力-容积曲线发生了移动,使得吸气肌在发作期间的任何给定肺容积下都能够产生更大的压力。这些发现表明,急性支气管痉挛期间TLC的增加是由于肺回缩力丧失、胸壁向外回缩增加以及吸气肌收缩力量增强共同作用的结果。

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