Nasal blood vessels

In order to understand the pathological changes that occur in allergic and vasomotor rhinitis, it is necessary to consider in some detail the vasculature of the nose. It consists of four groups of blood vessels: 1 ) precapillary resistance vessels, 2) capillaries. 3) veins and venous erectile tissue with venous sinusoids, and 4) arteriovenous anastomoses. Transudation of albumin occurs in nasal inflammation. This very stable protein may give a more reliable estimate of the inflammation than the relatively unstable mediators. The venous erectile tissue ma> be filled with blood. This filling determines the stare of con gestion of the mucosa which will regulate the nasal resistance to air flow.

Blood flow through the blood vessels is controlled by the autonomic innervation of the nasal mucosa. The nasal blood vessels receive a dense sympathetic innervation so that stimulation causes reduction in nasal blood flow and pronounced decongestion. The sympathetic tone of the nasal venous erectile tissue exhibits a cyclic reciprocal activity. The nasal mucosa seems to undergo a rest period every 2-4 h in humans. It is not surprising, therefore, that patients may state that one and then the other side of the nose becomes obstructed. The tickling sensation, sneezing and hypersecretion caused by allergen challenge is due to stimulation of the sensory nerve endings in the nasal mucosa with histamine from the mast cells being the main mediator.

Prostaglandin E2 is formed in an allergic response but as it is a potent constrictor of nasal venous erectile tissue, it presumably does not reach this tissue. There is an increase in nasal secretion and glandular vasodilation which is caused by reflex activation of the parasympathetic nervous system so that unilateral stimulation produces a bilateral effect yet the vascular response remains local and unilateral. Nerve fibers containing vasoactive intestinal polypeptide (VIP) are richly distributed in the nasal mucosa. The fibers are especially numerous around seromucous glands and beneath the surface epithelium. Probably VIP is mainly involved in vasodilation of blood vessels serving the glands.

The neuromediator substance P seems to be involved in many of the inflammatory responses elicited in the nose in animals, but not at all in humans. Much more information is required about the anatomy and physiology of nasal blood vessels. It may be that prostaglandin E2, which is known to inhibit norepinephrine release from sympathetic nerve endings, has a role as a modulator of sympathetic tone to nasal blood vessels.

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