Gilbert I A, Fouke J M, McFadden E R
Airway Disease Center, Cleveland, Ohio.
J Appl Physiol (1985). 1987 Oct;63(4):1681-91. doi: 10.1152/jappl.1987.63.4.1681.
To explore the relationship between the flux of heat and water within the respiratory tract during exercise and recovery to the development of exercise-induced asthma (EIA), we recorded airstream temperature at multiple points throughout the tracheobronchial tree in 10 normal and 10 asthmatic subjects before, during, and after cycle ergometry. In both groups, the intra-airway temperature fell progressively as ventilation increased, and there were no significant differences between the thermal profiles of the two populations at rest or during exercise. Calculation of water losses and the osmolality of the airway surface fluid failed to demonstrate significant airway drying in either group. With cessation of the work load, the airstream temperature increased abruptly, rising two times more rapidly in the asthmatics than the normals. Since the major source of heat in these experiments is the bronchial circulation, our findings suggest a reaction sequence consisting of vasoconstriction and airway cooling during exercise followed by a rapid resupply of heat when exercise ceases. The latter may cause the hyperplastic capillary bed in the airways of asthmatics to develop an exaggerated rebound hyperemia which may lead to airway edema and EIA.
为了探究运动及恢复过程中呼吸道内热量与水分通量和运动诱发哮喘(EIA)发展之间的关系,我们在10名正常受试者和10名哮喘受试者进行自行车测力计运动前、运动期间和运动后,记录了整个气管支气管树多个点的气流温度。在两组中,随着通气量增加气道内温度逐渐下降,且在静息或运动期间两组的热分布无显著差异。对两组气道表面液体的水分流失和渗透压进行计算,结果未能显示出两组存在显著的气道干燥现象。随着工作负荷停止,气流温度突然升高,哮喘患者气流温度升高速度比正常受试者快两倍。由于这些实验中热量的主要来源是支气管循环,我们的研究结果提示了一个反应序列,即在运动期间由血管收缩和气道冷却组成,运动停止后则迅速重新供热。后者可能导致哮喘患者气道中增生的毛细血管床出现过度的反弹充血,进而可能导致气道水肿和运动诱发哮喘。