Rubin Bruce K
Department of Pediatrics, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1081, USA.
Respir Care. 2002 Jul;47(7):818-22.
The airway mucosa responds to infection and inflammation in a variety of ways. This response often includes surface mucous (goblet) cell and submucosal gland hyperplasia and hypertrophy, with mucus hypersecretion. Products of inflammation, including neutrophil-derived deoxyribonucleic acid (DNA) and filamentous actin (F-actin), effete cells, bacteria, and cell debris, all contribute to mucus purulence and, when this mucus is expectorated it is called sputum. Mucoactive medications are intended to serve one of 2 purposes; either to increase the ability to expectorate sputum or to decrease mucus hypersecretion. Mucoactive medications have been classified according to their proposed mechanisms of action. Increased knowledge of the properties of mucus has given us tools to better understand the mechanisms of airway disease and mucoactive therapy. Expectorants are thought to increase the volume or hydration of airway secretions. Systemic hydration and classic expectorants have not been demonstrated to be clinically effective. Modifiers of airway water transport are being clinically investigated as expectorants. Mucolytics degrade polymers in secretions. The classic mucolytics have free thiol groups to degrade mucin. Peptide mucolytics break pathologic filaments of neutrophil-derived DNA and actin in sputum. Nondestructive mucolysis includes mucin dispersion by means of charge shielding. Mucokinetics are medications that increase mucociliary efficiency or cough efficiency. Cough flow can be increased by bronchodilators in patients with airway hyperreactivity. Abhesives such as surfactants decrease mucus attachment to the cilia and epithelium, augmenting both cough and mucociliary clearance. Mucoregulatory agents reduce the volume of airway mucus secretion and appear to be especially effective in hypersecretory states such as bronchorrhea, diffuse panbronchiolitis, and some forms of asthma. Mucoregulatory agents include anti-inflammatory agents (indomethacin, glucocorticosteroids), anticholinergic agents, and some macrolide antibiotics. Classifying mucoactive agents should help us to develop and evaluate new types of therapy and to better direct therapy toward the patients who are most likely to benefit.
气道黏膜会以多种方式对感染和炎症作出反应。这种反应通常包括表面黏液（杯状）细胞和黏膜下腺的增生及肥大，并伴有黏液分泌过多。炎症产物，包括中性粒细胞衍生的脱氧核糖核酸（DNA）和丝状肌动蛋白（F-肌动蛋白）、衰老细胞、细菌和细胞碎片，都会导致黏液化脓，当这种黏液咳出时就称为痰液。黏液活性药物旨在实现两个目的之一；要么提高咳痰能力，要么减少黏液分泌过多。黏液活性药物已根据其假定的作用机制进行了分类。对黏液特性的更多了解为我们提供了更好地理解气道疾病机制和黏液活性治疗的工具。祛痰剂被认为可增加气道分泌物的量或水分含量。全身补水和传统祛痰剂尚未被证明具有临床疗效。气道水转运调节剂正在作为祛痰剂进行临床研究。黏液溶解剂可降解分泌物中的聚合物。传统的黏液溶解剂具有游离巯基以降解黏蛋白。肽类黏液溶解剂可分解痰液中中性粒细胞衍生的DNA和肌动蛋白的病理性细丝。非破坏性黏液溶解包括通过电荷屏蔽使黏蛋白分散。黏液动力学药物可提高黏液纤毛效率或咳嗽效率。对于气道高反应性患者，支气管扩张剂可增加咳嗽流量。表面活性剂等黏附剂可减少黏液与纤毛和上皮的附着，增强咳嗽和黏液纤毛清除功能。黏液调节药物可减少气道黏液分泌量，在黏液分泌过多的状态如支气管溢液、弥漫性泛细支气管炎和某些形式的哮喘中似乎特别有效。黏液调节药物包括抗炎药（吲哚美辛、糖皮质激素）、抗胆碱能药物和一些大环内酯类抗生素。对黏液活性药物进行分类应有助于我们开发和评估新型治疗方法，并更好地将治疗针对最可能受益的患者。
