Lutchen K R, Jensen A, Atileh H, Kaczka D W, Israel E, Suki B, Ingenito E P
Respiratory and Physiological Systems Identification Laboratory, Biomedical Engineering, Boston University, 44 Cummington Street, Boston, MA 02215, USA.
Am J Respir Crit Care Med. 2001 Jul 15;164(2):207-15. doi: 10.1164/ajrccm.164.2.2008119.
Measurements of lung resistance and elastance (RL and EL) from 0.1 to 8 Hz reflect both the mean level and pattern of lung constriction. The goal of this study was to establish a relation between a deep inspiration (DI) and the heterogeneity of constriction in healthy versus asthmatic subjects. Constriction pattern was assessed from measurements of the RL and EL from 0.1 to 8 Hz in seven healthy subjects and in 12 asthmatics. These data were acquired before and after a DI and before and after a standard methacholine challenge versus a modified challenge in which a DI is prohibited. Generally, avoidance of a DI increased responsiveness. In healthy subjects and in those with mild-to-moderate baseline asthma a bronchial challenge, especially during self-inhibited DI, produced a heterogenous pattern of constriction inclusive of randomly distributed airway closures or near closures. Nevertheless, such subjects were able to reopen their airways via a DI. In contrast, in subjects with severe baseline asthma, there is a more extreme heterogeneous constriction pattern with random airway closures even at baseline. Further, there is no residual bronchodilatory effect of a DI either before or after bronchial challenge. We conjecture that inflammation and wall-remodeling facilitate a dangerous degree of heterogeneous constriction inclusive of airway closures or near closures, and contribute to the prevention of a DI from having a residual bronchodilatory effect.
在0.1至8赫兹范围内测量肺阻力和弹性（RL和EL），可反映肺收缩的平均水平和模式。本研究的目的是确定深吸气（DI）与健康受试者和哮喘受试者收缩异质性之间的关系。通过测量7名健康受试者和12名哮喘患者在0.1至8赫兹范围内的RL和EL来评估收缩模式。这些数据在深吸气前后、标准乙酰甲胆碱激发前后以及禁止深吸气的改良激发前后获取。一般来说，避免深吸气会增加反应性。在健康受试者和基线为轻度至中度哮喘的受试者中，支气管激发，尤其是在自我抑制的深吸气期间，会产生包括随机分布的气道关闭或近乎关闭的异质性收缩模式。然而，这些受试者能够通过深吸气重新打开气道。相比之下，在基线为重度哮喘的受试者中，即使在基线时也存在更极端的异质性收缩模式，伴有随机的气道关闭。此外，在支气管激发前后，深吸气均无残余的支气管扩张作用。我们推测，炎症和气道壁重塑促进了包括气道关闭或近乎关闭在内的危险程度的异质性收缩，并导致深吸气无法产生残余的支气管扩张作用。
