Low tidal volume ventilation facilitates spontaneous increase in bronchoconstriction and air trapping that can be resolved by deep inspiration and bronchodilator.

IF 3.6 2区 医学 Q1 PHYSIOLOGY
Yuto Yasuda, Geoffrey N Maksym, Lu Wang, Pasquale Chitano, Chun Y Seow
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引用次数: 0

Abstract

Prolonged absence of deep inspiration (DI) increases airway resistance. The underlying mechanism is not entirely clear. We hypothesize that DI prohibition allows basal airway smooth muscle (ASM) tone to narrow and close airways over time, resulting in elevation of airway and lung resistance, as well as air trapping. We further hypothesize that DI or pharmacological bronchodilators can prevent or alleviate the resistance increase and air trapping. Physiological respiration was simulated in ex vivo sheep lungs. Lung resistance, elastance, and volume were measured using small tidal volume (120 mL), ventilation frequencies of 0.25 and 2 Hz, and transpulmonary pressure of 7.5 cmH2O in the presence and absence of DI and bronchodilators. A DI maneuver, involving rapid inflation to total lung capacity followed by deflation to zero transpulmonary pressure, was used to resolve air trapping. Lung resistance and elastance were recorded pre- and post-DI. The experiments were also conducted in the presence of the bronchodilator salbutamol to assess the role of ASM. Ventilation without DI increased lung resistance and elastance, as well as air trapping. DI effectively resolved air trapping, restoring resistance and elastance to their initial values. Salbutamol also alleviated the increase in lung resistance, elastance, and air trapping. DI prevented air trapping and reduced lung resistance and elastance in ex vivo sheep lungs during tidal ventilation, playing a similar role as a pharmacological bronchodilator.NEW & NOTEWORTHY We showed that air trapping is a consistent feature in ex vivo sheep lungs possessing spontaneous bronchoconstriction, when the lungs are ventilated with small tidal volume without intermittent deep inspirations. We further demonstrated that in the presence of salbutamol, air trapping does not occur. This explains the importance of deep inspirations in normal breathing and indicates that airway smooth muscle tone could result in air trapping in the absence of deep inspiration.

低潮气量通气促进支气管收缩和空气潴留的自发增加:通过深吸气和支气管扩张剂解决。
背景:长时间无深度吸气(DI)增加气道阻力。其潜在机制尚不完全清楚。我们假设,随着时间的推移,DI禁止允许基底气道平滑肌(ASM)张力变窄和关闭气道,导致气道和肺阻力升高,以及空气潴留。我们进一步假设DI或药理学支气管扩张剂可以预防或减轻阻力增加和空气潴留。方法:模拟绵羊离体肺的生理呼吸。采用小潮气量(120 ml)、0.25和2 Hz通气频率以及7.5 cmH2O经肺压在使用和不使用DI和支气管扩张剂的情况下测量肺阻力、弹性和容积。采用DI操作,包括快速充气至肺活量,然后放气至0经肺压,以解决空气潴留。分别记录注射前后肺阻力和弹性。实验也在支气管扩张剂沙丁胺醇存在的情况下进行,以评估ASM的作用。结果:不使用DI通气可增加肺阻力和弹性,并增加气潴留。DI有效地解决了空气捕获问题,将阻力和弹性恢复到初始值。沙丁胺醇也减轻了肺阻力、弹性和空气捕获的增加。结论:DI能有效地阻止体外绵羊在潮汐通气时肺的空气捕获,降低肺阻力和弹性,其作用与药物支气管扩张剂相似。
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来源期刊
CiteScore
9.20
自引率
4.10%
发文量
146
审稿时长
2 months
期刊介绍: The American Journal of Physiology-Lung Cellular and Molecular Physiology publishes original research covering the broad scope of molecular, cellular, and integrative aspects of normal and abnormal function of cells and components of the respiratory system. Areas of interest include conducting airways, pulmonary circulation, lung endothelial and epithelial cells, the pleura, neuroendocrine and immunologic cells in the lung, neural cells involved in control of breathing, and cells of the diaphragm and thoracic muscles. The processes to be covered in the Journal include gas-exchange, metabolic control at the cellular level, intracellular signaling, gene expression, genomics, macromolecules and their turnover, cell-cell and cell-matrix interactions, cell motility, secretory mechanisms, membrane function, surfactant, matrix components, mucus and lining materials, lung defenses, macrophage function, transport of salt, water and protein, development and differentiation of the respiratory system, and response to the environment.
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