Tracheobronchial mucosa

Decreased benzopyrene hydroxylase in lung and tracheobronchial mucosa... 

Muscarinic stimulants contract the smooth muscle of the bronchial tree. In addition, the glands of the tracheobronchial mucosa are stimulated to secrete. This combination of effects can occasionally cause symptoms, especially in individuals with asthma. The bronchoconstriction caused by muscarinic agonists is eliminated in knockout animals in which the M3... 

Erjefiilt, I. and Persson, C.G.A. (1991a). Allergen, bradylcinin, and capsaicin increase outward but not inward macro-molecular permeability of guinea-pig tracheobronchial mucosa. Clin. Exp. Allergy 21, 217-224. 

Inhalation of mustard vapor primarily affects the laryngeal and tracheobronchial mucosa. Evidence exists to suggest that mustard inhalation causes sustained respiratory difficulties even after the acute lesions have healed. Clinical follow-ups on 200 Iranian soldiers who were severely injured by mustard during the Iran-lraq War indicate that about one third had experienced persistent respiratory effects 2 years or more after initial exposure. Reported problems included chronic bronchitis, asthma, rhinopharyngitis, tracheobronchitis, laryngitis, recurrent pneumonia, bronchiectasis, and, in some cases, severe, unrelenting tracheobronchial stenosis. ... 

Transepithelial penetration of the nasal, laryngeal, and tracheobronchial mucosa by inhaled anti-ChEs will cause an accumulation of ACh at the parasympathetic M-cholinergic... 

After stent insertion, a final completion bronchoscopy with the use of the flexible endoscope should be done to check appropriate stent position, determine patency of bronchial ostia, rule out complications (e.g., bleeding, airway disruption, mucus impaction) and ascertain proper attachment of the proximal and distal stent ends to the tracheobronchial mucosa (see Fig. 12.If). 

The biological actions of capsaicin are primarily attributable to release of the neuropeptide substance P, calcitonin gene-related peptide (CGRP), and neurokinin A from sensory neurons. These transmitters from primary sensory neurons communicate witir other cell types. They produce alterations in the airway mucosa and neurogenic inflammation of the respiratory epithelium, airway blood vessels, glands, and smooth muscle. Alterations in multiple effector organs lead to bronchoconstriction, increased vascular permeability, edema of the tracheobronchial mucosa, elevated mucosal secretion, and neutrophil chemotaxis (Tominack and Spyker, 1987). Capsaicin-induced effects of bronchoconstriction, vasodilation, and plasma protein extravasation are mediated by substance P. In addition, substance P can cause bronchoconstriction through stimulation of c-fibers in pulmonary and bronchial circulation. 

Uddman, R, Alumets, J., Densert, O. etal. (1978). Occurrence and distribution of VIP nerves in the nasal mucosa and tracheobronchial wall. Acta Otolaryngol. (Stockh) 86, 443-448. 

Acute, heavy exposure to SM causes loss of the columnar cells of the upper respiratory tract, peribronchial edema, hyperemia of the blood vessels, cellular infiltrations in the submucosa, and intense vacuolization and disorganization of the cytoplasmic and nuclear structures (Emad and Rezaian, 1997, 1999). Pulmonary hemorrhage, pulmonary edema, and respiratory failure similar to ARDS may also occur. These cytotoxic effects are associated with acute thermal injury sustained by the airway mucosa and lead to scarring and development of stenosis of the tracheobronchial tree as was observed in 9.64% of the SM-exposed patients. 

Mustard produces dose-dependent damage to the mucosa of the respiratory tract, beginning with the upper airways and descending to the lower airways as the amount of mustard increases. The inflammatory reaction varies from mild to severe, with necrosis of the epithelium. When fully developed, the injury is characterized by an acute inflammation of the upper and lower airways, with discharge in the upper airway, inflammatory exudate, and pseudomembrane formation in the tracheobronchial tree. The injury develops slowly, intensifying over a period of days. 

Interaction of the metalhc stent and the tracheobronchial wall is expected unlike plastic tube stents. This leads to specific problems. Removal of a metalhc stent, which is incorporated into the mucosa several weeks after deployment is extremely difficult and sometimes requires laser destruction of the stent struts in order to remove the stent piece by piece . Similarly, repositioning of an embedded metal stent is more difficult than relocation of a silicone stent. Covered metal stents exert less problems regarding removal and repositioning than uncovered mesh stents, where the open mesh design can lead to complete inoculation of the small stent wires into the mucosa. 

Shlmamoto and Honjo concluded from animal studies that bromhexlne affects tracheobronchial secretions by an action on central nervous system structures, probably In the areas of the emetic center In the medulla oblongata occurring both as a direct effect and Indirectly via stimulation of the gastric mucous membrane. Other animal tests Indicated bronchial secretions were Increased by bromhexlne as a result of an Improved permeability ratio between the bronchial mucous membrane and Its blood supply. The lytic effect of bromhexlne on human bronchial mucosa, observed vitro by electron microscopy, appears due to Increased secretion... 

---