King G G, Paré P D, Seow C Y
University of British Columbia Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, Canada.
Respir Physiol. 1999 Oct 15;118(1):1-13. doi: 10.1016/s0034-5687(99)00076-6.
Although non-specific bronchial hyperresponsiveness (NSBH) is a basic mechanism underlying the excessive, labile airway narrowing which is characteristic of asthma, its mechanism remains unknown. It is still unclear if the phenomenon is due to fundamental changes in the phenotype of the smooth muscle or is caused by structural and/or mechanical changes in the non-contractile elements of the airway wall or by alterations in the relationship of the airway wall to the surrounding lung parenchyma. Although airway wall remodeling may contribute to NSBH there is increasing evidence that the bronchodilating response to cyclic and periodic stretch is impaired in asthma. There are at least two different mechanisms by which periodic length and force oscillations could influence airway smooth muscle shortening and airway narrowing. These processes which have been called 'perturbed equilibrium of myosin binding' and 'plasticity' have different biochemical and mechanical mechanisms and consequences. They have the potential to interact and to have a fundamental effect on the shortening capacity of airway smooth muscle and its ultimate ability to cause excessive airway narrowing.
尽管非特异性支气管高反应性(NSBH)是哮喘所特有的过度、易变气道狭窄的基本机制,但其机制仍不清楚。目前仍不清楚该现象是由于平滑肌表型的根本变化,还是由气道壁非收缩成分的结构和/或机械变化,或气道壁与周围肺实质关系的改变所致。尽管气道壁重塑可能导致NSBH,但越来越多的证据表明,哮喘患者对周期性拉伸的支气管舒张反应受损。周期性长度和力振荡至少有两种不同机制可影响气道平滑肌缩短和气道狭窄。这些过程被称为“肌球蛋白结合的平衡紊乱”和“可塑性”,具有不同的生化和机械机制及后果。它们有可能相互作用,并对气道平滑肌的缩短能力及其导致过度气道狭窄的最终能力产生根本性影响。