Showing posts with label physiology. Show all posts
Showing posts with label physiology. Show all posts

Wednesday, January 20, 2010

Nitric oxide in the nasal airway: a new dimension in otorhinolaryngology.

Am J Otolaryngol. 2001 Jan-Feb;22(1):19-32.

Djupesland PG, Chatkin JM, Qian W, Haight JS.

University of Oslo, Norway.
The discovery that the gas nitric oxide (NO) is an important signaling molecule in the cardiovascular system earned its Nobel prize in 1998. NO has since been found to play important roles in a variety of physiologic and pathophysiologic processes in the body including vasoregulation, hemostasis, neurotransmission, immune defense, and respiration. The surprisingly high concentrations of NO in the nasal airway and paranasal sinuses has important implications for the field of otorhinolaryngology. NO provides a first-line defense against micro-organisms through its antiviral and antimicrobial activity and by its upregulation of ciliary motility. Nasal treatments such as polypectomy, sinus surgery, removal of hypertrophic adenoids and tonsils, and treatment of allergic rhinitis may alter NO output and, therefore, the microbial colonization of the upper airways. Nasal surgery aimed at relieving nasal obstruction may do the same but would also be expected to improve pulmonary function in patients with asthma and upper airway obstruction. NO output rises in a number of conditions associated with chronic airway inflammation, but not all of them. Concentrations are increased in asthma, allergic rhinitis, and viral respiratory infections, but reduced in sinusitis, cystic fibrosis, primary ciliary dysfunction, chronic cough, and after exposure to tobacco and alcohol. Therefore, NO, similar to several other inflammatory mediators, probably subserves different functions as local conditions dictate. At present, it seems that the measurement of NO in the upper airway may prove valuable as a simple, noninvasive diagnostic marker of airway pathologies. The objective of this review is to highlight some aspects of the origin, physiology, and functions of upper airway NO, and to discuss the particular methodological problems that result from the complex anatomy.

PMID: 11172211 [PubMed - indexed for MEDLINE]

Nitric oxide and the paranasal sinuses.

Anat Rec (Hoboken). 2008 Nov;291(11):1479-84.
Lundberg JO.

Karolinska Institutet, Department of Physiology and Pharmacology, Stockholm, Sweden. Jon.Lundberg@ki.se
The discovery within the paranasal sinuses for the production of nitric oxide (NO) has altered the traditional explanations of sinus physiology. This review article reports the ongoing investigation of sinus physiology beginning with the discovery of NO gas production in the paranasal sinuses that occurred in 1995, and the impact that finding has had both in the basic science and clinical arenas. It was shown that healthy paranasal sinus epithelium expresses an inducible NO synthase that continuously generates large amounts of NO, a pluripotent gaseous messenger with potent vasodilating, and antimicrobial activity. This NO can be measured noninvasively in nasally exhaled breath. The role of NO in the sinuses is likely to enhance local host defense mechanisms via direct inhibition of pathogen growth and stimulation of mucociliary activity. The NO concentration in a healthy sinus exceeds those that are needed for antibacterial effects in vitro. In patients with primary ciliary dyskinesia (PCD) and in cystic fibrosis, nasal NO is extremely low. This defect NO generation likely contributes to the great susceptibility to chronic sinusitis in these patients. In addition, the low-nasal NO is of diagnostic value especially in PCD, where nasal NO is very low or absent. Intriguingly, NO gas from the nose and sinuses is inhaled with every breath and reaches the lungs in a more diluted form to enhance pulmonary oxygen uptake via local vasodilation. In this sense NO may be regarded as an "aerocrine" hormone that is produced in the nose and sinuses and transported to a distal site of action with every inhalation. Copyright 2008 Wiley-Liss, Inc.

PMID: 18951492 [PubMed - indexed for MEDLINE]

Friday, November 27, 2009

The physiology of the nose

Clin Chest Med. 1986 Jun;7(2):159-70.
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Widdicombe JG.

The nose, as an organ initiating reflexes affecting itself and the rest of the body, and as a target organ of control, is highly complex. Its innervation includes parasympathetic, sympathetic, sensory/afferent, and somatic motor nerves, which combine in a variety of morphologic pathways. The vasculature of the nose contains capacitance vessels such as sinusoids and distensible venules, as well as arteriovenous anastomoses, arterioles, capillaries, and venules. The secretory tissue of the nose includes epithelial cells, submucosal glands, and relatively large anterior or lateral serous glands; in addition, some species have specialized secretory glands. The nose is the source of many powerful reflexes, including the diving response, sneeze and sniff reflexes, and reflexes affecting autonomic nervous function to the cardiovascular system, airways in the lungs, the larynx, and other organs. Axon reflex control of the nasal vasculature is also important. The nasal vasculature can be shown to be under parasympathetic and sympathetic control, but there is little precise information concerning the effect of nerves on different types of blood vessels. Pharmacologic experiments show that vascular resistance and vascular volume can be separately influenced by nerves and mediators, and that vascular resistance and airway resistance are not necessarily inversely related. Nasal secretion is also under the influence of both parasympathetic and sympathetic nerves, and can be induced by a wide range of neurotransmitters and mediators. In general, the concentrations needed to promote secretion are considerably higher than those that affect vascular resistance, at least with regard to the lateral nasal gland of the dog. In humans, nasal patency is affected by several nervous inputs, presumably acting via vascular beds. The nasal cycle is the alternation of resistances between the two sides of the nose, on which other changes are superimposed. In exercise and hyperpnea, nasal airflow resistance decreases, presumably with vascular decongestion. Recent studies of the crutch reflex (the ipsilateral nasal congestion caused by stimulation of the axilla) show that some of the reflex inputs to the nose can be unilateral.

PMID: 3522066 [PubMed - indexed for MEDLINE]