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Nasal nitric oxide (NO) levels increase greatly during humming compared to silent exhalation. In this study, the physiological and anatomical factors that regulate NO release during humming have been characterised in 10 healthy subjects and in a model of the sinus and the nose.Single-breath humming caused a large initial peak in nasal NO output, followed by a progressive decline. The NO peak decreased in a step-wise manner during repeated consecutive humming manoeuvres but recovered completely after a silent period of 3 min. Topical nasal application of an NO synthase inhibitor reduced nasal NO by w50% but had no effect on the increase evoked by humming. Silently exhaled nasal NO measured immediately after repeated humming manoeuvres was between 5-50% lower than basal silent NO exhalation, suggesting variable continuous contribution from the sinuses to nasal NO. Among the factors known to influence normal sinus ventilation, ostium size was the most critical during humming, but humming frequency was also of importance.In conclusion, humming results in a large increase in nasal nitric oxide, which is caused by a rapid gas exchange in the paranasal sinuses. Combined nasal nitric oxide measurement with and without humming could be of use to estimate sinus ventilation and to better separate nasal mucosal nitric oxide output from sinus nitric oxide in health and disease. Eur Respir J 2003; 22: 323-329. This study was supported by a grant from the Swedish Heart-Lung Foundation, the Swedish Research Council and by a grant from University Federico II "Progetto scambi internazionali".Nitric oxide (NO) is released into the airway lumen [1], in particular in the upper airways [2][3][4]. The exact origin of NO found in nasal air and the relative contribution from different sources within the nasal airways are not known. The paranasal sinuses are major sources of NO in adult healthy subjects [5] and the concentrations in a healthy sinus may be very high, ranging 5-20 parts per million (ppm) [5]. The sinuses communicate with the nasal cavity through the ostia and the rate of gas exchange between these cavities is dependent on several factors, such as the size of the ostia, the volume of the sinus, the nasal airflow and intra-nasal pressure [6,7]. Proper ventilation is essential for maintenance of sinus integrity, and blockage of the ostium is a central event in the pathogenesis of sinusitis [8,9]. During normal ventilation, the time required to exchange all air in the sinuses is y30 min, with large inter-individual variation [7,10]. Sinus ventilation is much slower in patients with sinus disorders [10].Recently, the current authors have shown that nasal NO levels increase greatly during humming compared to normal silent nasal exhalation, probably by speeding up the sinus gas exchange, thereby increasing nasal NO output [11]. In a twocompartment model of the nose and sinus the authors demonstrated that pulsating airflow, created by humming, causes a dramatic increase in gas exchange between these cavities [11].In the ...
Nasal nitric oxide (NO) levels increase greatly during humming compared to silent exhalation. In this study, the physiological and anatomical factors that regulate NO release during humming have been characterised in 10 healthy subjects and in a model of the sinus and the nose.Single-breath humming caused a large initial peak in nasal NO output, followed by a progressive decline. The NO peak decreased in a step-wise manner during repeated consecutive humming manoeuvres but recovered completely after a silent period of 3 min. Topical nasal application of an NO synthase inhibitor reduced nasal NO by w50% but had no effect on the increase evoked by humming. Silently exhaled nasal NO measured immediately after repeated humming manoeuvres was between 5-50% lower than basal silent NO exhalation, suggesting variable continuous contribution from the sinuses to nasal NO. Among the factors known to influence normal sinus ventilation, ostium size was the most critical during humming, but humming frequency was also of importance.In conclusion, humming results in a large increase in nasal nitric oxide, which is caused by a rapid gas exchange in the paranasal sinuses. Combined nasal nitric oxide measurement with and without humming could be of use to estimate sinus ventilation and to better separate nasal mucosal nitric oxide output from sinus nitric oxide in health and disease. Eur Respir J 2003; 22: 323-329. This study was supported by a grant from the Swedish Heart-Lung Foundation, the Swedish Research Council and by a grant from University Federico II "Progetto scambi internazionali".Nitric oxide (NO) is released into the airway lumen [1], in particular in the upper airways [2][3][4]. The exact origin of NO found in nasal air and the relative contribution from different sources within the nasal airways are not known. The paranasal sinuses are major sources of NO in adult healthy subjects [5] and the concentrations in a healthy sinus may be very high, ranging 5-20 parts per million (ppm) [5]. The sinuses communicate with the nasal cavity through the ostia and the rate of gas exchange between these cavities is dependent on several factors, such as the size of the ostia, the volume of the sinus, the nasal airflow and intra-nasal pressure [6,7]. Proper ventilation is essential for maintenance of sinus integrity, and blockage of the ostium is a central event in the pathogenesis of sinusitis [8,9]. During normal ventilation, the time required to exchange all air in the sinuses is y30 min, with large inter-individual variation [7,10]. Sinus ventilation is much slower in patients with sinus disorders [10].Recently, the current authors have shown that nasal NO levels increase greatly during humming compared to normal silent nasal exhalation, probably by speeding up the sinus gas exchange, thereby increasing nasal NO output [11]. In a twocompartment model of the nose and sinus the authors demonstrated that pulsating airflow, created by humming, causes a dramatic increase in gas exchange between these cavities [11].In the ...
Otitis media, common in children, can result in middle ear structure alteration and hearing loss, and, hence, in language development deficiency. Physical anthropologists are qualified to do innovative research into the causes of this costly disease, which have not yet been delineated. The prevalence of otitis media appears related to age, sex, ethnicity, and environment. Investigation is warranted in areas such as the measurement of variability in eustachian tube, middle ear cleft, and mastoid process anatomy and physiology; the epidemiology and genetic mechanism of otitis media; and the microbiology and immunology as well as pathological studies of cranial variation as it relates to otitis media.Otitis media (OM), one of the most common diseases of childhood, is the problem most frequently seen by pediatricians in the US. Nearly 10% of all pediatric patients are those with OM, and if pediatricians dealt with children during their first year of life only, the estimate would be as high as 50% (Van Cauwenberge, 1985). Acute OM, the presence of fluid in the middle ear, may be accompanied by signs and symptoms including pain, hearing loss, irritability, fever, and malaise. The infection duration can vary from days to months and may result in alteration of middle ear structures, hearing loss, language development deficiency, and increased susceptibility to recurrence. Without the use of antibiotics, the sequelae of chronic OM often include labyrinthitis, meningitis, mastoiditis, tympanic membrane rupture, and cholesteatoma. The younger the age at which OM first occurs, the greater the risk of recurrences (Paradise, 1980). The condition may persist for weeks or months, even after the clinical signs of acute otitis media have already resolved (Shurin et al., 1979).Hearing loss, following from the presence of fluid and/or negative pressure in the middle ear, is a serious complication of OM, and many infected children spend prolonged periods during their first years of life with impaired or fluctuating conductive hearing losses. Chronic OM may also cause a sensorineural hearing lossoften irreversible (Bess, 1983). Katz (1978) even suggested (but never demonstrated) that the central deprivation caused by the peripheral conductive and/or sensorineural loss produces a form of auditory deprivation that can lead to anatomical and physiological changes in the brainstem and higher cortical areas.Of special concern are children who have OM from birth (Pestalozza, 1984) to age 3 years, a particularly common time of occurrence, as this period is critical for language acquisition (Lenneberg, 1967). Children with histories of OM during the first 3 years of life frequently have disturbances in auditory processing, an inconsistent auditory signal making the stream of speech difficult to segment. This difficulty creates confusion in the child's attempts to abstract word meanings and grammatical regularities (Berko-Gleason, 1983). Furthermore, the child's irritability, malaise, 0 1988 Alan R. Liss, Inc. [Vol. 31, 1988 and dec...
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.
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