Wang Lu, Paré Peter D
Department of Physiology, University of Manitoba, Winnipeg, MB, Canada.
Respir Physiol Neurobiol. 2003 Sep 16;137(2-3):169-78. doi: 10.1016/s1569-9048(03)00145-9.
In normal subjects a deep inspiration (DI) taken during bronchoconstriction substantially reduces airway narrowing (bronchodilation) and a DI taken prior to bronchoconstriction attenuates subsequent airway narrowing (bronchoprotection). Although the exact mechanism(s) for these phenomena are unclear the time course of these effects supports the hypothesis that they are mediated through actions of airway smooth muscle (ASM). There is convincing evidence that both the bronchodilation and bronchoprotection actions of DI are deficient or absent in asthmatic subjects. Various theories have been proposed such as a failure of transmission of stress and strain to the ASM in asthma, stretch-induced contraction of smooth muscle in asthmatics, a failure to release bronchodilating substances and differential effects on cross-bridge dynamics or contractile element rearrangement. In this brief review we focus on the mechanical consequences of DI on the ASM. We suggest that a failure of plastic rearrangement of the contractile apparatus following DI is at the basis of the abnormal response to DI in asthma.
在正常受试者中，支气管收缩期间进行的深呼吸（DI）可显著减轻气道狭窄（支气管舒张），而在支气管收缩之前进行的深呼吸可减轻随后的气道狭窄（支气管保护）。尽管这些现象的确切机制尚不清楚，但这些效应的时间进程支持了它们是通过气道平滑肌（ASM）的作用介导的这一假说。有令人信服的证据表明，哮喘患者中DI的支气管舒张和支气管保护作用均不足或缺乏。已经提出了各种理论，例如哮喘中应力和应变向ASM的传递失败、哮喘患者平滑肌的拉伸诱导收缩、支气管舒张物质释放失败以及对横桥动力学或收缩元件重排的不同影响。在这篇简短的综述中，我们关注DI对ASM的机械后果。我们认为，DI后收缩装置的塑性重排失败是哮喘患者对DI异常反应的基础。
