Deep inspiration (DI)-induced bronchodilation is the first line of defense against bronchoconstriction in healthy subjects. A hallmark of asthma is the lack of this beneficial effect of DI. The mechanism underlying the bronchodilatory effect of DI is not clear. Understanding the mechanism will help us unravel the mystery of asthma pathophysiology. It has been postulated that straining airway smooth muscle (ASM) during a DI could lead to bronchodilation and bronchoprotection. The hypothesis is currently under debate, and a central question is whether ASM is sufficiently stretched during a DI for its contractility to be compromised. Besides bronchoconstriction, another contributor to lung resistance is airway heterogeneity. The present study examines changes in airway diameter and heterogeneity at different lung volumes. Freshly explanted sheep lungs were used in plethysmographic measurements of lung resistance and elastance at different lung volumes while the airway dimensions were measured by computed tomography (CT). The change in airway diameter informed by CT measurements was applied to isolated airway ring preparations to determine the strain-induced loss of ASM contractility. We found that changing the transpulmonary pressure from 5 to 30 cmH₂O led to a 51%-increase in lung volume, accompanied by a 46%-increase in the airway diameter with no change in airway heterogeneity. When comparable airway strains measured in the whole lung were applied to isolated airway rings in either relaxed or contracted state, a significant loss of ASM contractility was observed, suggesting that DI-induced bronchodilation and bronchoprotection can result from strain-induced loss of ASM contractility.

中文翻译：

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离体羊肺中不同跨肺压下的气道直径：对深吸气诱导的支气管扩张和支气管保护的影响

深吸气 (DI) 诱导的支气管扩张是健康受试者对抗支气管收缩的第一道防线。哮喘的一个标志是缺乏 DI 的这种有益作用。DI 的支气管扩张作用的机制尚不清楚。了解其机制将有助于我们解开哮喘病理生理学的奥秘。据推测，在 DI 期间使气道平滑肌 (ASM) 紧张可能导致支气管扩张和支气管保护。该假设目前正在辩论中，一个核心问题是 ASM 在 DI 期间是否被充分拉伸以使其收缩性受到损害。除了支气管收缩，另一个导致肺阻力的因素是气道异质性。本研究检查了不同肺容量下气道直径和异质性的变化。新鲜移植的羊肺用于体积描记测量不同肺容量下的肺阻力和弹性，同时通过计算机断层扫描 (CT) 测量气道尺寸。CT 测量通知的气道直径变化应用于隔离气道环制剂，以确定应变引起的 ASM 收缩性损失。我们发现将跨肺压从 5 cmH 改变为 30 cmH₂ O 导致肺容量增加 51%，同时气道直径增加 46%，气道异质性没有变化。当在整个肺中测量的可比气道应变应用于处于放松或收缩状态的孤立气道环时，观察到 ASM 收缩力的显着丧失，这表明 DI 诱导的支气管扩张和支气管保护可能是由应变诱导的 ASM 收缩力丧失引起的。