The tracheobronchial vasculature: a possible role in asthma.
The tracheobronchial microcirculation consists of a subepithelial capillary network and in some species deeper capacitance vessels and an adventitial network. Postcapillary venules are the main site of plasma extravasation in inflammatory conditions. There are surprising species differences. The subepithelial capillary network is dense in species such as sheep and dog but relatively scanty in rabbit and humans. Sheep have conspicuous capacitance vessels or blood sinuses, especially in the trachea and at points of bronchial branching with walls that lack smooth muscle. The rabbit also has a well-developed capacitance system but the blood sinuses have thick muscular walls. Although the capacitance system in humans has not been studied much it is probably present with muscular walls. It is absent in rats but present in guinea pigs. Thus, in some species the tracheobronchial vasculature may give the mucosa an erectile capacity, as in the nose of each species. Arteriovenous anastomoses (AVA) cannot be demonstrated physiologically in sheep but they seem to be present as thoroughfare vessels in rats and guinea pigs. Whether they exist in humans is not known. The absence of AVA might indicate a weak or absent thermoregulatory and air conditioning role for the lower airway vasculature. Extensive studies of neurogenic inflammation in rodents show that sensory neuropeptides can open gaps between the endothelial cells of postcapillary venules and the same change can be caused by a large number of inflammatory mediators. These opened gaps cause extravasation of plasma into the interstitium. Small increases in interstitial pressure lead to spaces opening between the epithelial cells and exudation of plasma into the airway lumen. The role of the airway microvasculature in asthma is controversial. Cold and hyperosmolar solutions cause vasodilatation as do the mediators released in the mucosal inflammation of asthma. However, quantitation of the thickening of the airway wall due to vascular engorgement, mucosal edema, or increased luminal liquid does not prove that these changes are a cause of airway obstruction. The contraction of airway smooth muscle superimposed on the mucosal inflammatory pathology might lead to a synergistic mechanism to increase airway resistance.
Widdicombe
J
J
Department of Physiology, St. George's Hospital Medical School, London, England.
D000403:Airway Resistance; D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D001980:Bronchi / Q000098:blood supply* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid; D002199:Capillary Permeability; D003080:Cold Temperature / Q000009:adverse effects; D016207:Cytokines / Q000378:metabolism; D004285:Dogs; D005122:Exudates and Transudates; D006168:Guinea Pigs; D006801:Humans; D006982:Hypertonic Solutions / Q000494:pharmacology; D007365:Intercellular Junctions / Q000378:metabolism; D008833:Microcirculation; D009092:Mucous Membrane / Q000098:blood supply; D009479:Neuropeptides / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D012756:Sheep / Q000033:anatomy & histology; D013045:Species Specificity; D014132:Trachea / Q000098:blood supply* / Q000503:physiopathology; D014630:Vagus Nerve / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects
D016207:Cytokines; D006982:Hypertonic Solutions; D009479:Neuropeptides