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旨在减少气道平滑肌生长的治疗干预措施。

Therapeutic interventions aimed at reducing airway smooth muscle growth.

作者信息

Martin J G, Greenstone E A, Maghni K

机构信息

Meakins-Christie Laboratories, Dept of Medicine, McGill University, Montreal, Quebec, Canada.

出版信息

Monaldi Arch Chest Dis. 2000 Aug;55(4):311-6.

PMID:11057085
Abstract

The airways of asthmatic subjects undergo complex changes which affect all compartments of the airway wall. The airway smooth muscle (ASM) is particularly affected and is increased in mass. Both hyperplasia and hypertrophy probably contribute to the altered mass of muscle which is a potential cause of airway hyperresponsiveness. The impedance to smooth muscle shortening resulting from the constitutive properties of the airway wall and the elasticity of the parenchyma may be more easily overcome by the excess muscle of the asthmatic airway. The ASM may also undergo important changes in its functional characteristics as a result of allergic sensitization and challenge. Increases in maximal shortening velocity, phospholipase C activity and membrane potential are some of the changes in the characteristics of sensitized ASM. The ASM may also change its phenotype from a contractile to a secretory tissue in response to the stimulus of airway inflammation and in doing so may contribute to the inflammatory process itself. The current therapies for asthma have the potential to counter some of the adverse effects of airway modelling, in particular in so far as the ASM is concerned. These effects should be kept in mind when considering the rationale for effective maintenance therapy for asthma.

摘要

哮喘患者的气道会发生复杂变化,影响气道壁的所有部分。气道平滑肌(ASM)受到的影响尤为显著,其质量增加。增生和肥大可能都导致了肌肉质量的改变,这是气道高反应性的一个潜在原因。哮喘气道中过多的肌肉可能更容易克服由气道壁的固有特性和实质弹性导致的平滑肌缩短阻力。由于过敏致敏和激发,ASM的功能特性也可能发生重要变化。致敏ASM的特征变化包括最大缩短速度、磷脂酶C活性和膜电位增加。ASM也可能因气道炎症刺激而从收缩性组织转变为分泌性组织,进而可能促进炎症过程本身。目前的哮喘治疗方法有可能对抗气道重塑的一些不良影响,特别是就ASM而言。在考虑哮喘有效维持治疗的基本原理时,应牢记这些影响。

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