Lung airways secretion

Puchelle E, Girod de Bentzmann S, Higenbottam T (1995) Airway secretion and lung liquids. In Brewis RAL, Corrin B, Geddes DM, Gibson GJ (eds.) Respiratory Medicine. WB Saunders Company Ltd, London, pp 97-111. 

The prolonged retention of viscous airway secretions in the diseased lung (e.g., CF and COPD) can lead to recurring bacterial infections, resulting in a viscous, more purulent sputum [155]. Increased mucus viscoelasticity may be attributed to extensive disulphide and lectin bonding, poor hydration, and/or excess concentrations of extracellular DNA or actin [155], In these situations, therapeutics have been used to reduce the viscosity of airway secretions to improve the rate of mucociliary clearance. 

Three of the cell types in the epithelium have secretory functions. These cells are the mucous (goblet) cells, serous cells, and Clara cells. These cells contribute to the secretion of airway mucus, a complex mixture of water, glycoproteins, immunoglobulins, lipids, and salts. The secretion of mucus is a defense function that contributes to the removal of foreign objects from lung airways via the mucociliary transport process, as described in later sections of this chapter. Excess mucus secretion can be detrimental, however, since it can obstruct the movement of air through the airways and is a component of certain pulmonary diseases such as asthma, emphysema, chronic bronchitis, and cystic fibrosis. A hypertrophy of secretory cells in the epithelial layer of the airways is often characteristic of these diseases. 

The flow-resistive properties of the airways are of major relevance to aerosol therapy in that they directly influence the pattern of distribution and deposition of inhaled particles within the lungs. Airway resistance increases, and hence aerosol delivery will be reduced, if the airways become partially blocked or narrowed by factors such as bronchospasm, inflammation, or secretions. Small changes in airway caliber can have dramatic effects on airway resistance. In a healthy adult, airway resistance is approximately 0.2 kPa/L/s (2 cmHp/L/s)... 

The carotid body is the primary sensor of hypoxemia across many species. When stimulated by a decrease in Pa02 or hypoxic perfusates, it promotes many cardiopulmonary responses. Ventilation, static lung volumes, airway resistance, and airway secretions increase. The hypoxic pulmonary vasoconstrictor response and the systemic vascular vasodilator responses are attenuated bronchial vascular resistance decreases (for review see Ref 1). A current question is How does the carotid body transduce a low Pa02 stimulus into increased neural output traveling to the nucleus tractus sohtarii Here the increased neural traffic is processed and distributed to various other nuclei responsible for the increased breathing and the autonomicaUy regulated changes in the cardiopulmonary system. 

Chest wall compliance may be reduced in kyphoscoliosis, fibrothorax, or spinal cord injury and lung compliance may be reduced in pulmonary edema, pulmonary fibrosis, and acute respiratory distress syndrome (ARDS) and COPD in the presence of hyperinflation. Airway secretions or bronchoconstriction may contribute to increased airway resistance. Respiratory drive and muscle function may be compromised by anesthetics, sedation, coma, or hypercapnia, and muscle dysfunction may occur in the presence of malnutrition, hypophosphatemia, disuse atrophy, sepsis, myopathies, or limited oxygen delivery (9). The factors that led to a tracheostomy must be optimized prior to decannulation. 

Pneumocystis carinii Pneumonia Second Edition, eckted byP.D. Walzer 70. Fluid and Solute Transport in the Airspaces of the Lungs, edited by RM.Effros and H.K.Chang 71. Sleep and Breathing Second Edition, edited by N.A.Saunders andC.E.Sullivan 72. Airway Secretion Physiological Bases for the Control of Mucous Hypersecretion, edited by T.Takishima andS.Shimura... 

Biochemical studies have demonstrated the presence of surface-active components, predominantly phospholipids, in airway secretions (42). Bernhard et al. (43,44) studied the conductive airway phospholipids in the tracheobronchial secretions of adult pigs and compared their results with analyses of bronchoalveolar lavage (B AL) fluid, tracheobronchial epithelium, and lung parenchyma. The composition of the PC and PL molecular species of the tracheal aspirates was similar... 

Infection of the trachea and bronchi causes hyperemic and edematous mucous membranes and an increase in bronchial secretions. Destruction of respiratory epithelium can range from mild to extensive and may affect bronchial mucociliary function. In addition, the increase in bronchial secretions, which can become thick and tenacious, further impairs mucociliary activity. Recurrent acute respiratory infections may be associated with increased airway hyperreactivity and possibly the pathogenesis of chronic obstructive lung disease. 

The 5-lipoxygenase pathway of arachidonic acid metabolism is responsible for production of cysteinyl leukotrienes. Leukotrienes C4, D4, and E4 are released during inflammatory processes in the lung and produce broncho-spasm, mucus secretion, microvascular permeability, and airway edema. 

Until recently, epithelial cells were considered to function solely as the ciliated barrier lining in the airways and as conduits for gas exchange at the air/blood interphase. As techniques have improved to isolate and culture these cells and measure their gene products, it has become clear that they have a key role in lung defense and repair. Epithelial cells secrete a number of anti-microbial compounds and immunoregulatory cytokines [52], and are also capable of ingesting and killing bacteria [53],... 

---