The ultrastructure and permeability of tracheobronchial blood vessels in health and disease.

Studies using morphological methods, some contemporary and others traditional, have revealed that part of the distinctive behaviour of the airway mucosa under normal and pathological conditions can be explained by the characteristics of the microvasculature. For example, the terminal arterioles of the airway mucosa are innervated not only by sympathetic and parasympathetic nerves but also by sensory nerves. The sensory nerves release tachykinins such as substance P which dilate arterioles and can increase vascular permeability through an action on postcapillary venules. The increase in vascular permeability produced by these mediators results from gaps in the endothelium that permit the extravasation of plasma proteins into the mucosal connective tissue and even into the airway lumen. The magnitude of the response of postcapillary venules to pro-inflammatory mediators is influenced by numerous factors. Among these are airway infections which can potentiate the response by causing the proliferation of mediator-sensitive venules, by decreasing the breakdown of peptide mediators by neutral endopeptidase, and perhaps by increasing the number of tachykinin receptors on venules.