Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content +++ Nasal Function ++ Warming and humidification Air is humidified to high relative humidity Air is warmed through heat diffusion and convection Optimum mucociliary clearance is facilitating by temperature of 37°C Regulation of nasal secretions and airway resistance Proteins in nasal secretions Plasma proteins Albumin Immunoglobulins (IgG, IgM, IgA) Serous cell products Antibacterial defense molecules Lysozymes Lactoferrin Secretory component Mucous cell products Mucoglycoproteins Mucins Epithelial goblet cell products Macromolecules and ions Proteins are dissolved or suspended in epithelial lining fluid Modified by epithelial ion pumps Plasma extravasation controlled by interepithelial tight junctions Dependent on rate of blood flow and plasma transudation Arterial vasodilation and filling of venous sinusoidal vessels results in plasma extravasation, thickened nasal mucosa, increased airway resistance. Vasoconstriction reduces mucosal blood flow, reduces plasma extravasation, relieves venous sinusoidal congestion. Autonomic innervation Vidian nerve Formed at junction of greater superficial petrosal (preganglionic parasympathetic fibers) and deep petrosal nerves (postganglionic sympathetic fibers) Postganglionic sympathetic and parasympathetic fibers carried in the nerve of the vidian canal and join branches of sphenopalatine nerve Parasympathetic neurons Cotransmitter to acetylcholine (vasointestinal peptide [VIP]) Vasodilation at arterial and sinusoidal vessels Enhanced secretory activity Mast cell degranulation – Release of histamine, bradykinin, arachidonic acid metabolites, ions Sympathetic fibers join branches of sphenopalatine nerve and artery Cotransmitter to noradrenaline (neuropeptide Y) Vasoconstriction of venous sinusoidal vessels Nonadrenergic, noncholinergic responses Trigeminal sensory neurons use peptides as neurotransmitters Secreted by macrophages, eosinophils, lymphocytes, dendritic cells Substance P, neurokinin A, calcitonin gene-related peptide (CGRP) Induce vasodilation Increase vascular permeability Increase nasal resistance Stimulate glandular secretion Leukocyte chemotaxis Mast cell degranulation Nasal cycle Cyclical vascular phenomenon that occurs in 80% of normal individuals Alternating congestion/decongestion every 3 to 7 hours Centrally mediated autonomic tone of capacitance vessels of erectile mucosa Other influences on nasal resistance Exercise decreases nasal resistance Irritants (dust, smoke), cold/dry air, alcohol, pregnancy, hypothyroidism, and medications can cause congestion of capacitance vessels Medications that can cause nasal congestion Antihypertensives (alpha and beta blockers) Oral contraceptives Antidepressants Nonsteroidal anti-inflammatory medications Decongestants in excess may result in rhinitis medicamentosa Atrophic rhinitis Chronic, degenerative disorder characterized by nasal crusting, malodorous discharge, and nasal obstruction Atrophy of serous and mucinous glands Loss of cilia and goblet cells Inflammatory cell infiltrates Possible causes Underlying chronic inflammatory disease Granulomatous disorders Irradiation Bacterial and viral infection Excessive nasal surgery Nasal airflow At low flow rates, airflow is laminar. Maximum velocity occurs in the nasal valve region. Bernoulli principle Airflow velocity is greatest at the narrowest segment. Increased airflow velocity leads to negative pressure and nasal valve collapse. Poiseuille law Airflow resistance is inversely proportional to fourth power of the radius. Small decrease in cross-sectional area produces large increase in airway resistance. Relatively slow flow rates found in olfactory region with quiet breathing During inspiration, main flow stream occurs in the lower and middle airway (space between middle meatus and nasal septum) During expiration, maximum velocity is lower but expiratory air is evenly distributed across inferior, middle, and olfactory regions... Your Access profile is currently affiliated with [InstitutionA] and is in the process of switching affiliations to [InstitutionB]. Please select how you would like to proceed. Keep the current affiliation with [InstitutionA] and continue with the Access profile sign in process Switch affiliation to [InstitutionB] and continue with the Access profile sign in process Get Free Access Through Your Institution Learn how to see if your library subscribes to McGraw Hill Medical products. Subscribe: Institutional or Individual Sign In Error: Incorrect UserName or Password Username Error: Please enter User Name Password Error: Please enter Password Sign in Forgot Password? Forgot Username? Sign in via OpenAthens Sign in via Shibboleth You already have access! Please proceed to your institution's subscription. Create a free profile for additional features.