OJMIP  Vol.3 No.3 , August 2013
Discrimination between upper versus lower airway components to the rise of total airway resistance measured by Pennock’s method after nasal irritant challenge
Abstract: Terminals of the trigeminal afferents innervating nasal mucosa are called gate keepers, since these fibres detect substances entering the airways. Trigeminal excitation by irritants initiates airway defensive mechanisms, and it is also attributed to the influence of lower airways resistance in a term of nasobronchial reflex. This phenomenon is frequently under debate, because some investigators were unable to confirm its existence. The aim of our study was to determine, whether pharmacological approach could be useful to reach high accuracy and better interpretation of the data obtained by Pennock’s method. Pennock’s method, which is frequently used to measure airway resistance in vivo (Raw) in fact measures total airway resistance, however, the data are usually interpreted in a terms of bronchomotor response. The upper airway component, which represents approximately 40% of Raw, is commonly not considered as being important in this method. 30 Dunkin Hartley guinea pigs were exposed to nasal stimuli (TRPA1 agonist—irritant allylisothiocyanate (10 mM, AITC), TRPM8 agonist with cooling potential menthol (10-3 M) and saline as a control). Raw was measured pre challenge as baseline, after nasal provocation and further, after nasal inhalation of histamine and methacholine (10-6 M) each. The data showed rise of Raw only after nasal AITC challenge, with further increased responsiveness to histamine and methacholine (5.3 vs 10.18 vs 11.26 vs 17.32 cmH2O.s-1, p < 0.05). No significant changes were detected after saline, or menthol respectively. Data obtained in further experiment and its analysis showed that pre-treatment with nasal administration of 1% oxymetazoline but without salbutamol inhalation prevented the rise of Raw after nasal irritant challenges. Raw after nasal irritant challenges rises rather due to nasal response than due to narrowing of the lower airways.
Cite this paper: Biringerova, Z. , Gavliakova, S. , Hanuskova, E. , Buday, T. and Plevkova, J. (2013) Discrimination between upper versus lower airway components to the rise of total airway resistance measured by Pennock’s method after nasal irritant challenge. Open Journal of Molecular and Integrative Physiology, 3, 104-110. doi: 10.4236/ojmip.2013.33016.

[1]   Panneton, W.M., Hsu, H. and Gan, Q. (2010) Distinct central representations for sensory fibers innervating either the conjunctiva or cornea of the rat. Experimental Eye Research, 90, 388-396. doi:10.1016/j.exer.2009.11.018

[2]   Wallois, F., Macron, J.M., Jounieaux, V. and Duron, B. (1991) Trigeminal nasal receptors related to respiration and to various stimuli in cats. Respiration Physiology, 85, 111-125. doi:10.1016/0034-5687(91)90010-G

[3]   Sekizawa, S. and Tsubone, H. (1994) Nasal receptors responding to noxious chemical irritants. Respiration Physiology, 96, 37-48. doi:10.1016/0034-5687(94)90104-X

[4]   Taylor-Clark, T.E., Kollarik, M., MacGlashan Jr., D.W. and Undem, B.J. (2005) Nasal sensory nerve populations responding to histamine and capsaicin. The Journal of Allergy and Clinical Immunology, 116, 1282-1288. doi:10.1016/j.jaci.2005.08.043

[5]   Baraniuk, J.N. and Merck, S.J. (2008) Nasal reflexes: Implications for exercise, breathing and sex. Current Allergy & Asthma Reports, 8, 147-153. doi:10.1007/s11882-008-0025-7

[6]   Taylor-Clark, T.E. (2008) Insights into the mechanisms of histamine-induced inflammation in the nasal mucosa. Pulmonary Pharmacology & Therapeutics, 21, 455-460. doi:10.1016/j.pupt.2007.08.002

[7]   Sahin-Yilmaz, A. and Naclerio, R.M. (2011) Anatomy and physiology of the upper airway. Proceedings of American Thoracic Society, 8, 31-39. doi:10.1513/pats.201007-050RN

[8]   Kaufman, J., Chen, J.C. and Wright, G.W. (1970) The effect of trigeminal resection on reflex bronchoconstriction after nasal and nasopharyngeal irritation in man. The American Review of Respiratory Disease, 101, 768-769.

[9]   Togias, A. (1999) Mechanisms of nose lung interaction. Allergy, 54, 94-105.

[10]   Johansson, A., Bende, M., Milquist, E. and Bake, B. (2000) Nasobronchial relationship after cold air provocation. Respiratory Medicine, 94, 1119-1122. doi:10.1053/rmed.2000.0924

[11]   Fontanari, P., Burnet, H., Zattara-Hartmann, M.C. and Jammes, Y. (1996) Changes in airway resistance induced by nasal inhalation of cold dry, dry, or moist air in normal individuals. Journal of Applied Physiology, 81, 1739-1743.

[12]   Levi, L.R., Tyler, G.R., Olson, L.G. and Saunders, N.A. (1990) Lack of airway response to nasal iritation in normal and asthmatic subjects. Australian and New Zealand Journal of Medicine, 20, 578-582.

[13]   Little, N.T., Carlisle, C.C., Millman, R.P. and Braman, S.S. (1990) Changes in airway resistance following nasal provocation. The American Review of Respiratory Disease, 141, 580-583. doi:10.1164/ajrccm/141.3.580

[14]   Cole, P. (1998) Physiology of the nose and paranasal sinuses. Clinical Reviews in Allergy & Immunology, 16, 33-51. doi:10.1007/BF02739327

[15]   Plevkova, J., Kollarik, M., Brozmanova, M., Revallo, M., Varechova, S. and Tatar, M. (2004) Modulation of experimentally-induced cough by stimulation of nasal mucosa in cats and guinea pigs. Respiratory Physiology & Neurobiology, 142, 225-235. doi:10.1016/j.resp.2004.06.006

[16]   Tohda, Y., Muraki, M., Iwanaga, T., Haraguchi, R., Fukuoka, M. and Nakajima, S. (2000) Dualphase response model for bronchial asthma. Allergy and Asthma Proceedings, 21, 79-84. doi:10.2500/108854100778250851

[17]   Lofgren, J.L., Mazan, M.R., Ingenito, E.P., Lascola, K., Seavey, M., Walsh, A. and Hoffman, A.M. (2006) Restrained whole body plethysmography for measure of strain-specific and allergen induced airway responsiveness in conscious mice. Journal of Applied Physiology, 101, 1495-1505. doi:10.1152/japplphysiol.00464.2006

[18]   Pennock, B.E., Cox, C.P., Rogers, R.M., Cain, W.A. and Wells, J.H. (1979) A noninvasive technique for measurement of changes in specific airway resistance. Journal of Applied Physiology, 46, 399-406.

[19]   Agrawal, A. and Ram, A. (2007) Commentary on “restrained whole body plethysmography for measure of strain-specific and allergen-induced airway responsiveness in conscious mice”. Journal of Applied Physiology, 102, 2412-2413. doi:10.1152/japplphysiol.00134.2007

[20]   Bickford, L., Shakib, S. and Taverner, D. (1999) The nasal airways response in normal subjects to oxymetazoline spray: Randomized double-blind placebo-controlled trial. British Journal of Clinical Pharmacology, 48, 53-56. doi:10.1046/j.1365-2125.1999.00972.x

[21]   Gerhold, K.A. and Bautista, D.M. (2008) TRPA1: Irritant receptor of the airways. The Journal of Physiology, 586, 3303.

[22]   Sekizawa, S., Tsubone, H., Kuwahara, M. and Sugano, S. (1996) Nasal receptors responding to cold and l-menthol airflow in the guinea pig. Respiration Physiology, 103, 211-219. doi:10.1016/0034-5687(95)00091-7

[23]   Orani, G.P., Anderson, J.W., Sant’Ambrogio, G. and Sant’Ambrogio, F.B. (1991) Upper airway cooling and l-menthol reduce ventilation in the guinea pig. Journal of Applied Physiology, 70, 2080-2086.

[24]   Eccles, R. (1994) Menthol and related cooling compounds. The Journal of Pharmacy and Pharmacology, 46, 618-630.