Search PubMed⌕ Search

Biomedical subjects

N Zamel

Publications and source records attributed to N Zamel.

180 records · Page 10Linked to original sources

EEG alpha reactivity and self-regulation correlates of smoking and smoking deprivation.

Twelve nonsmokers, ten ex-smokers, ten deprived smokers (2-3 hours), and ten nondeprived smokers were exposed to a short-term (18-sec) vigilance task and underwent 6 min of biofeedback-assisted alpha amplitude enhancement and suppression training. Cigarette smoking was found to be associated with decreased alpha suppression to the vigilance task. However, no consistent role of cigarette smoking in alpha self-regulation emerged from the results.

Adult↗

Effect of high dose inhaled acetic acid on airway responsiveness in Fischer rats.

BACKGROUND: Sudden, severe airway injury has been associated with an acute, and at times persisting, airway hyper-responsiveness with clinical features of asthma, termed reactive airways dysfunction syndrome (RADS). An attempt was made to develop a rat model of RADS by exposing inbred Fischer rats to inhaled 8 N acetic acid for 2 mins (13 N inhalation was lethal). METHODS: Lung resistance (RL) and lung elastance (EL) were measured in 14 eight- to 10-week old male rats. Baseline responsiveness to methacholine was quantified by calculating the dose required for doubling of RL. The next day, the study group (n=11) was exposed to aerosolized acetic acid. Control animals (n=3) were similarly exposed to buffered saline solution. RESULTS: Acetic acid exposure resulted in a significant (P<0.02) increase in RL (by 80%) and EL (by 67%), lasting less than 10 mins postexposure, but no significant change in methacholine responsiveness at one day and seven days postexposure. CONCLUSIONS: Failure to induce persistent airway hyper-responsiveness may relate to the choice of animal, choice of irritant, or insufficient level or duration of exposure, or may reflect a lack of individual predisposing cofactors such as smoking or underlying asthmatic predisposition.

Acetic Acid↗

Nasal nitric oxide is not altered by topical anesthesia.

This prospective study was undertaken to determine whether topical nasal anesthetic agents affect nasal nitric oxide (NO) output in healthy adults. Seven volunteers (aged: 29-56 (40.6 +/- 10.7) years, six male), were recruited. A topical anesthetic (4% lidocaine or 0.5% tetracaine) was sprayed into the subject's right nostril while the left nostril served as a control. Unilateral nasal NO and nasal volume were measured before administration of the anesthetic and at 15 and 30 minutes after the administration. The mean (+/- SD) unilateral nasal NO output was 307 +/- 45.9 nL/minute from the right nostril (exposure side) before the topical application of lidocaine. At 30 minutes after topical application (n = 6), it was 295.5 +/- 41.5 in the right nostril and 297.5 +/- 39.8 in the left (control side). In the tetracaine group (n = 7), the mean (+/- SD) unilateral nasal NO output was 302 +/- 53.3 before the administration and 307 +/- 39.7 at 30 minutes after the administration in the right nostril. The mean NO output in the left nostril at 30 minutes after the administration was 297.7 +/- 40.75. In neither group was there any significant difference in nasal NO output between either the pre- and postlocal anesthetic application on the exposure side (Group 1, P = 0.76; group 2, P = 0.41) or the two nostrils after topical anesthesia application (group 1, P = 0.83; group 2, P = 0.62). Topical anesthesia with either lidocaine or tetracaine does not alter nasal NO output. NO measurement should not be affected in circumstances that require topical anesthesia of the nasal cavity.

Administration, Inhalation↗

Acoustic rhinometric assessment of the nasal valve.

The aims of this study are to assess nasal valve cross-sectional areas in healthy noses and in patients with nasal obstruction after rhinoplasty and to evaluate the effect of an external nasal dilator on both healthy and obstructive nasal valves. Subjects consisted of (i) volunteers with no nasal symptoms, nasal cavities unremarkable to rhinoscopy and normal nasal resistance and (ii) patients referred to our clinic complaining of postrhinoplasty nasal obstruction. All subjects were tested before and after topical decongestion of the nasal mucosa and with an external nasal dilator. In 79 untreated healthy nasal cavities the nasal valve area showed two constrictions: the proximal constriction averaged 0.78 cm2 cross-section and was situated 1.18 cm from the nostril, the distal constriction averaged 0.70 cm2 cross-section at 2.86 cm from the nostril. Mucosal decongestion increased cross-sectional area of the distal constriction significantly (p < 0.0001) but not the proximal. External dilation increased cross-sectional area of both constrictions significantly (p < 0.0001). In 26 post-rhinoplasty obstructed nasal cavities, only a single constriction was detected, averaging 0.34 cm2 cross-section at 2.55 cm from the nostril and 0.4 cm2 at 2.46 cm from the nostril, before and after mucosal decongestion respectively. External dilation increased the minimum cross-sectional area to 0.64 cm2 in these nasal cavities (p < 0.0001). We conclude that the nasal valve area in patients with postrhinoplasty nasal obstruction is significantly smaller than in healthy nasal cavities as shown by acoustic rhinometry. Acoustic rhinometry objectively determines the structural and mucovascular components of the nasal valve area and external dilation is an effective therapeutical approach in the management of nasal valve obstruction.

Acoustics↗

Nasal nitric oxide is independent of nasal cavity volume.

This study was performed to evaluate the relationship between nasal nitric oxide (NO) and changes in nasal cavity volume resulting from the topical application of xylometazoline and saline and between upright and supine posture. Nasal NO was measured using a fixed high flow technique that avoids contamination with lower airways NO. In nine healthy subjects nasal NO concentration was measured by a rapid response chemiluminescent analyzer. A tapered tube was inserted in one nostril, into which room air was insufflated to produce a constant flow of 100 mL/second; another tube was inserted into the opposite nostril for NO sampling (air exit side). Subjects were instructed to keep the vellum closed while NO was sampled through a sideport connected to the analyzer. Nasal cavity volume was measured by acoustic rhinometry from a segment of the acoustic pathway, 2 to 5 cm from the nostril. Nasal cavity volume and NO measurements were made at baseline, 15 minutes, and 60 minutes after intervention (administration of saline 0.9%, xylometazoline or posture changes on 3 consecutive days). Xylometazoline produced a significant increase in nasal cavity volume, together with a significant reduction in NO level at 15 and 60 minutes after intervention. In addition, the change from seated to supine position decreased the total nasal volume significantly, but without changes in nasal NO. No correlation was found between the magnitudes of changes in nasal NO and the changes in nasal volume. Topical application of xylomethazoline resulted in increased nasal cavity volume and reduced NO output. In contrast to previous published reports, a technique using high flow rate insufflation demonstrated an abscence of correlation between the magnitudes of changes in nasal NO and nasal cavity volume brought about by decongestant, saline, or posture.

Acoustic Stimulation↗

Nasal nitric oxide: a comparison of measurement techniques.

Nasal nitric oxide measurement may be a surrogate marker of upper airway inflammation. There is, however, no standardized measurement technique; and this led us to examine measurement techniques for acceptability and reproducibility. In five subjects we examined the flow dependence of nasal NO. In 13 healthy volunteers, nasal NO was measured on-line by five methods: 1) Tidal nasal and oral breathing: NO sampling during exclusive nasal followed by exclusive oral tidal breathing; 2) Fixed flow exhalation: NO sampling during exclusive nasal followed by exclusive oral exhalation at 100 mL/second from total lung capacity; 3) Nasal-oral aspiration: air aspirated from the mouth via both nares at 100 mL/second with glottis closure; 4) Aspiration from one nares: air aspirated from one nares at 3.3 mL/second using nitric oxide analyzer sample line with velum closure; 5) Nasal Insufflation: NO sampled at one nares as air insufflated into the other nares at a flow of 100 mL/second with velum closure. Acceptability of all methods was assessed by subjects and technicians. Nasal NO concentration showed a significant inverse correlation with transnasal flow rate. All methods showed excellent reproducibility as assessed by the intraclass correlation coefficient except tidal breathing, which showed highly variable breath-to-breath NO levels, although mean breath values were reproducible. Mean nasal NO concentrations with methods 1, 2, 3, 4, and 5 were 32.1, 50.2, 62.8, 1381, and 60.0 ppb, respectively. Velum closure was not always achieved in methods 4 and 5, whereas methods 1 and 2 required separate nasal and oral procedures. Method 5 had reduced acceptability. NO concentrations were similar with methods that used the same airflow (2, 3, and 5). Nasal NO can be sampled in different ways with excellent reproducibility. In view of the flow dependence of nasal NO, it is vital to use a constant flow rate, and lower airway NO contribution must be excluded or subtracted. The fixed flow exhalation appears to be the preferred method as it is highly reproducible and acceptable.

Analysis of Variance↗

Acoustic rhinometry: a study of transient and continuous noise techniques with nasal models.

The objective of this study is to compare the properties of two of the most frequently used acoustic rhinometers: the EcoVision (Hood Laboratories, USA) using the transient technique, and the Rhin2100 (RhinoMetrics, Denmark) using the continuous wide-band technique. In the wide-band rhinometer (Rhin2100), the transient analog signals of traditional rhinometers (EcoVision), are replaced by a digitally produced continuous wide-band noise signal. Tubular models and a plastic model produced by stereolithography (SLA), representing the true replicate of the nasal anatomy, were used to compare the accuracy of the two rhinometers. The effect of increasing angling (0-50 degrees) between the sound wave tube and the cavity was evaluated in a tubular model. The curves obtained with the two rhinometers showed close similarity, and the acoustically derived volumes correlated well with the volumes of tubular (% error < 4%) as well as the complex nasal model (% error < 10.5%). Both rhinometers underestimated the minimum cross-sectional area (MCA) of the complex nasal model (mean % error complex model: Rhin2100 = -7.6%, EcoVision = -13%). The effect of increasing the angle between the nose adapter and the tubular models was small for both rhinometers (CV < 3% for MCA and CV < 1% for volumes). The similar, and in general, high accuracy of the two rhinometers evaluated, particularly in the complicated geometry of the SLA model, is an indication of the reliability of both. The small effect of changing the angle between the nose adapter and the models was unexpected and very encouraging. Nevertheless, some minor differences in performance and capabilities of the two rhinometers might influence interpretation and comparison of results. Further comparisons in a clinical setting are under current investigation.

Acoustics↗

Reproducibility of acoustic rhinometry and rhinomanometry in normal subjects.

The reproducibility of nasal patency measurements was assessed by acoustic rhinometry and active rhinomanometry using previously described Toronto methodologies. Six subjects with normal upper airways were tested with both procedures on six separate occasions within a 2-month period. Topical decongestant was applied to minimize the effects of mucosal variation on the nasal airway. The mean coefficients of variation (mean +/- s.d; %) over time of the measurements were 8.1 +/- 4.1 and 9.7 +/- 5.2 for minimal unilateral cross-sectional area and 4.8 +/- 1.8 and 5.5 +/- 3.5 for nasal volume (0-5 cm) of the right and left sides, respectively. For active rhinomanometry, the mean coefficients of variation (mean +/- s.d.; %) over time of the measurements were 15.9 +/- 7.3, 12.9 +/- 4.6, and 8.5 +/- 2.8 for right, left and combined nasal airflow resistance. The intraclass correlation coefficient was 0.76, 0.70, and 0.96 for right, left, and combined nasal resistance, 0.91 and 0.87 for right and left minimal cross sectional area, and 0.86 and 0.69 for right and left nasal volumes, respectively, also confirming a high level of reproducibility for both methods. In conclusion, performed by an experienced operator under controlled circumstances, the reproducibility of both methods of nasal patency assessment compared favorably with many widely accepted clinical tests.

Acoustics↗

Nitrogen and bolus closing volumes: the effect of beta-agonist bronchodilator aerosol.

Studies of the effect of beta-agonist bronchodilators on closing volume in normal subjects have produced conflicting results. We studied the possibility that these differences might be due to the different methods of measuring closing volume. We measured closing volume by both the nitrogen washout and the bolus techniques in 19 healthy nonsmoking adults before and after inhalation of salbutamol aerosol. Prior to salbutamol, closing volume measured by the nitrogen method (N2 CV) was significantly smaller (p less than 0.02) than the closing volume measured by the bolus method (bolus CV). After salbutamol inhalation, N2 CV increased significantly (p less than 0.05); however, bolus CV did not change, so that following inhalation of salbutamol there was no significant difference between N2 CV and bolus CV. The increase in N2 CV after salbutamol inhalation was associated with an increase in the slope of phase IV (p less than 0.05). We suggest that beta-agonist bronchodilator aerosol has no effect on closing volume in normal individuals and the apparent increase in N2 CV after bronchodilator is probably an artefact.

Adrenergic beta-Agonists↗

Effect of a simulated 3,048 meter altitude on the single-breath transfer factor.

The single-breath transfer factor (TLCO) was measured in ten healthy subjects at sea level and at a simulated altitude of 3,048 m. Measurements were made at sea level using 21% oxygen and at altitude using both 21% and 31% oxygen in the test gas. At 3,048 m altitude (PB = 69.7 kPa), the mean TLCO increased 14% or about 2.3% per kPa (0.3% per mmHg) decrease in inspired oxygen pressure. Our data also suggests that altering the test gas oxygen concentration to account for the change in PAO2 due to altitude results in a TLCO equivalent to that obtained at sea level.

Adult↗

Pharyngeal and glottic changes following methacholine challenge in normal subjects.

Recent evidence indicates that some normal subjects exhibit glottic narrowing following experimentally induced bronchospasm. Similar findings have been observed during episodes of bronchospasm in asthmatics. The exact mechanism of this effect is unknown but it is thought to occur as part of a generalized reflex response associated with constriction of intrapulmonary airways. We tested the hypothesis that in addition to the glottic changes, coincident with intrapulmonary airway constriction which occurred after inhalation of methacholine, the pharynx would show similar changes. Pharyngeal and glottic cross-sectional areas were measured using the acoustic reflection technique in seven healthy subjects before and after inhalation of metacholine. Before methacholine, pharyngeal and glottic areas (mean +/- SE) were 5.0 +/- 0.2 cm2 and 2.4 +/- 0.3 cm2 respectively. After inhalation of methacholine, these areas were reduced to 4.6 +/- 0.3 cm2 and 1.9 +/- 0.3 cm2 respectively (p less than 0.05). We conclude that inhalation of methacholine induces similar reductions in glottic and pharyngeal areas. The role of local or reflex mechanisms accounting for this reduction remains unclear.

Adult↗

Absence of habituation of airway dilation following lung inflation.

In order to test the possibility that airway dilation following lung inflation (ADFLI) could exhibit habituation, partial and complete maximum expiratory flow-volume curves were obtained in 12 healthy individuals before and after inhaling methacholine aerosol in a dose that reduced in each individual the partial expiratory flows to approximately 50% of baseline values. Following methacholine inhalation, the difference in flows between complete and partial flow-volume curves at 40% VC was 64 +/- 22% (mean +/- SD) of partial curves after a single full lung inflation and 79 +/- 36% after 12 consecutive full inflations (p = NS). The absence of demonstrable habituation (tachyphylaxis) of ADFLI makes it unlike that ADFLI is due to a release of mediators and supports the view that it may be due to the intrinsic properties of the airway smooth muscle.

Adult↗

Improved expiratory airflow dynamics with smoking cessation.

Lung recoil, Pst(1), dependence and gas density dependence of maximum expiratory flow (Vmax) using air and an 80% helium + 20% oxygen (HeO2) gas mixture before and 60 +/- 4 (means +/- SD) days after cessation of smoking were determined in five male and five female subjects (33.4 +/- 6.4 years). Pst(1) dependence of Vmax, a relationship dependent on airway elastance at the "choke", was estimated by measuring the slope and the zero flow intercept using the maximum flow-static recoil (MFSR) curve. MFSR slope was unchanged by abstinence. The intercept showed no difference between air and HeO2 before or after cessation of smoking. Density independence of the zero flow intercept is deducible from wave speed theory if there is no change at the "choke" and the slope truly reflects the elastic behaviour of the "choke". This correspondence of theory and measurement suggests that the "choke" was not changed by abstinence. The reduction of Pst(1) with smoking cessation, without any fall in Vmax at the same lung volume, suggests a complementary reduction in lung recoil and frictional energy loss upstream of the "choke". This would suggest that a decrease in small airway muscle tone was the single cause of a reduction of Pst(1) and peripheral airway resistance.

Adult↗