Noble Peter B, McFawn Peter K, Mitchell Howard W
Physiology, School of Biomedical, Biomolecular, and Chemical Sciences, Univ. of Western Australia, 35 Stirling Hwy., Crawley, Perth, Western Australia, 6009, Australia.
J Appl Physiol (1985). 2007 Sep;103(3):787-95. doi: 10.1152/japplphysiol.00314.2007. Epub 2007 May 17.
In vivo, breathing movements, including tidal and deep inspirations (DIs), exert a number of beneficial effects on respiratory system responsiveness in healthy humans that are diminished or lost in asthma, possibly as a result of reduced distension (strain) of airway smooth muscle (ASM). We used bronchial segments from pigs to assess airway responsiveness under static conditions and during simulated tidal volume oscillations with and without DI and to determine the roles of airway stiffness and ASM strain on responsiveness. To simulate airway dilations during breathing, we cycled the luminal volume of liquid-filled segments. Volume oscillations (15 cycles/min) were set so that, in relaxed airways, they produced a transmural pressure increase of approximately 5-10 cmH(2)O for tidal maneuvers and approximately 5-30 cmH(2)O for DIs. ACh dose-response curves (10(-7)-3 x 10(-3) M) were constructed under static and dynamic conditions, and maximal response and sensitivity were determined. Airway stiffness was measured from tidal trough-to-peak pressure and volume cycles. ASM strain produced by DI was estimated from luminal volume, airway length, and inner wall area. DIs produced substantial ( approximately 40-50%) dilation, reflected by a decrease in maximal response (P < 0.001) and sensitivity (P < 0.05). However, the magnitude of bronchodilation decreased significantly in proportion to airway stiffening caused by contractile activation and an associated reduction in ASM strain. Tidal oscillations, in comparison, had little effect on responsiveness. We conclude that DI regulates airway responsiveness at the airway level, but this is limited by airway stiffness due to reduced ASM strain.
在体内，呼吸运动，包括潮式呼吸和深吸气（DI），对健康人的呼吸系统反应性具有多种有益作用，而在哮喘患者中这些作用会减弱或丧失，这可能是由于气道平滑肌（ASM）的扩张（应变）减少所致。我们使用猪的支气管段来评估静态条件下以及在有和没有DI的模拟潮气量振荡期间的气道反应性，并确定气道僵硬度和ASM应变在反应性中的作用。为了模拟呼吸过程中的气道扩张，我们对充满液体的支气管段的管腔容积进行循环操作。设定容积振荡频率为每分钟15次循环，以便在松弛的气道中，潮式呼吸动作产生的跨壁压力增加约5 - 10 cmH₂O，深吸气时产生的跨壁压力增加约5 - 30 cmH₂O。在静态和动态条件下构建乙酰胆碱剂量反应曲线（10⁻⁷ - 3×10⁻³ M），并确定最大反应和敏感性。通过潮气量低谷到峰值的压力和容积循环来测量气道僵硬度。根据管腔容积、气道长度和内壁面积估算由深吸气产生的ASM应变。深吸气产生了显著的（约40 - 50%）扩张，表现为最大反应（P < 0.001）和敏感性（P < 0.05）降低。然而，支气管扩张的程度与收缩激活导致的气道僵硬度增加以及相关的ASM应变减少成比例地显著降低。相比之下，潮式振荡对反应性影响很小。我们得出结论，深吸气在气道水平调节气道反应性，但由于ASM应变减少导致的气道僵硬度限制了这种调节作用。
