Inhalation Of Dry Air Research Articles

Reduction of peak expiratory flow after a 5-meter dive with extreme exertion

The effects of physically exerting scuba dives on the airways are expected to affect the respiratory system and therefore the spirometric flow indices directly after surfacing. After on-air open-sea dives, the flow indices were examined with standard spirometry (maximal forced expiration) within 10 minutes pre- and post-dive. Twenty volunteers, age 49 ± 14 years (m ± SD) equipped with a dive computer to record the dive profile, cylinder pressures and water temperature (27°C), as well as a heart rate monitor, performed 5-meter dives of 27 minutes at maximal swimming velocity (v). Mean pulmonary ventilation (PV) was 48 ± 10 ambient L/minute (aL.min-1). Mean v was 34 ± 6 meters/minute and mean heart rate 143 beats per minute, about 80% of the on-land theoretical maximum. None of the flow variables changed except a decrease of 7.1% ± 8.3 (p=0.001) of the peak expiratory flow (PEF), pre-dive of 11.2 ± 2.7 L/minute. A likely major cause of the reduction of PEF is expiratory muscle fatigue. A small contribution of subclinical pulmonary edema cannot be excluded. The inhalation of dry air and the cooling of the airways are expected to affect PEF minimally. Although the change is normally clinically irrelevant, during emergency it may be of importance.

Low ambient humidity impairs barrier function and innate resistance against influenza infection

In the temperate regions, seasonal influenza virus outbreaks correlate closely with decreases in humidity. While low ambient humidity is known to enhance viral transmission, its impact on host response to influenza virus infection and disease outcome remains unclear. Here, we showed that housing Mx1 congenic mice in low relative humidity makes mice more susceptible to severe disease following respiratory challenge with influenza A virus. We find that inhalation of dry air impairs mucociliary clearance, innate antiviral defense, and tissue repair. Moreover, disease exacerbated by low relative humidity was ameliorated in caspase-1/11-deficient Mx1 mice, independent of viral burden. Single-cell RNA sequencing revealed that induction of IFN-stimulated genes in response to viral infection was diminished in multiple cell types in the lung of mice housed in low humidity condition. These results indicate that exposure to dry air impairs host defense against influenza infection, reduces tissue repair, and inflicts caspase-dependent disease pathology.

Impact of Vocal Fold Dehydration on Vocal Function and Its Treatment.

The change of vocal function after vocal fold dehydration due to dryness was discussed along with the treatment effect of different atomizing agents. Forty-eight staffs from The Central Hospital of Wuhan were recruited. All volunteers breathed dry air for vocal fold dehydration. After dry air inhalation, the subjects were randomly divided into four groups, with 12 cases each. Three groups were treatment groups, receiving 0.9% normal saline (IS), 5% hypertonic saline (HS) and double-distilled water (SW) atomizing inhalation therapy, respectively, and the last group was the control group without treatment. Voice data were collected for all subjects before and immediately after dry air inhalation using the Multi-Dimensional Voice Program (MDVP) system. Atomizing inhalation therapy was given 10 min after dry air inhalation, and voice data were collected using MDVP system at the following time points after atomizing inhalation treatment: 5 min, 20 min, 35 min, 50 min, 65 min, 80 min, 95 min, 110 min. In the control group, voice data were collected at the same time points and compared with those of treatment groups. The vocal function parameters collected before and after dry air inhalation as well as after treatment were subjected to test using SPSS 16.0 software. In the four groups, jitter (fundamental frequency perturbation), shimmer (amplitude perturbation), and amplitude perturbation quotient (APQ) were significantly increased after dry air inhalation (P<0.05). In IS, HS and SW groups, after atomizing inhalation treatment, there was an obvious reduction in jitter, shimmer and APQ, showing significant differences as compared with those after dry air inhalation (P<0.05). Moreover, these parameters were significantly lower than those in the control group (P<0.05). The jitter, shimmer and APQ in the IS group were significantly lower than those in the HS and SW groups (P<0.05). We are led to a conclusion: Vocal fold dehydration induced by dryness can reduce the stability of voice; such decreased voice stability can be improved by atomizing inhalation therapy; without proper treatment, voice stability caused by vocal fold dehydration cannot heal spontaneously; of three atomizing agents namely, IS, HS and SW, IS had the best treatment effect for decreased voice stability caused by vocal fold dehydration.

Humidification therapy; long-term effects in COPD and OSAS patients.

Humidification therapy is widely used in patients during invasive ventilation and the importance of heating and humidifying the inhaled air is well defined in both the acute and long term setting. On the other hand the continuous usage of humidification in noninvasive ventilation is controversial and the long term effects are still not well defined. The usage of noninvasive ventilation is especially important in hypercapnic Chronic obstructive pulmonary disease (COPD) and also the obstructive sleep apnea syndrome (OSAS) patients and compliance to this treatment is essential in long term. Limited number of studies have shown that heated humidification is preferred by COPD patients and might help in mucus clearance, reduce mucus viscosity and help in expectoration, but there was shown no priority as far as concerns the lung function or blood gas parameters. Humidification might also be important in long term oxygen treatment since the inhalation of dry air can lead to ciliary dysfunction, alterations in mucus properties and mucociliary clearance impairment. Studies concerning OSAS patients showed that humidification helps to reduce the nasal symptoms but plays no role in increasing the compliance of patients in long term. Multi-center studies with large number of patients are needed to identify patients' groups who are likely to benefit from the addition of humidification to noninvasive therapy.

Year in review 2016: Interstitial lung disease, pulmonary vascular disease, pulmonary function, paediatric lung disease, cystic fibrosis and sleep.

Year in review 2016: Interstitial lung disease, pulmonary vascular disease, pulmonary function, paediatric lung disease, cystic fibrosis and sleep.

Exercise-Induced Bronchoconstriction and Vocal Cord Dysfunction

Patients are referred often because of self-reported symptoms of dyspnea and wheeze during exercise. The two common causes of exercise-induced dyspnea are exercise-induced bronchoconstriction (EIB) and vocal cord dysfunction (VCD). It can be extraordinarily difficult to differentiate between the two, especially because they may coexist in the same patient. EIB is caused by bronchial smooth muscle constriction in the lower airways due to the inhalation of dry air or allergens during exercise; it is associated with the release of bronchoconstricting mediators from airway cells. EIB can occur in patients with or without persistent asthma. In contrast, VCD is associated with the paradoxical adduction of the vocal cords, especially during inhalation, which may produce inspiratory stridor. VCD can be solitary or comorbid with asthma and/or EIB. EIB classically is most severe after the cessation of exercise, while VCD typically occurs during exercise and resolves quickly upon exercise cessation. However, history is not adequate to differentiate between EIB and VCD, and appropriate challenge tests and flexible laryngoscopy during exercise are often necessary for diagnosis. This article examines our current understanding of these entities and discusses the mechanism, prevalence, diagnosis, and treatment.

The effect of relative humidity of inhaled air onacoustic parameters of voice in normal subjects

The hypothesis that relative humidity (RH) of air exerts an effect on voice has been widely accepted. The aim of this study has been to assess whether this can be demonstrated. Eight healthy subjects inhaled during ten minutes three different air conditions: dry, standard room, and humidified air. After inhalation, the subjects produced repeatedly a sustained /a/ of controlled pitch and loudness, which was analyzed for perturbation and noise-to-harmonic parameters. Perturbation measures increased after inhalation of dry air. No significant differences existed between standard and humidified air. No significant difference in the noise-to-harmonic ratio was found among the three conditions. We conclude that the human voice is very sensitive to decreases in RH of inhaled air, because even after a short provocation with dry air, a significant increase in perturbation measures was found.

Exercise-induced asthma and the use of hypertonic saline aerosol as a bronchial challenge.

Exercise induced asthma is a common complaint and the prevalence appears to be increasing worldwide. Once confined to the research domain of university teaching hospitals, the study of EIA has extended into the school playground, defence force establishments and sports institutions. Standardized protocols have been developed to study EIA in the laboratory and in the field. A surrogate challenge using eucapnic or isocapnic hyperventilation with dry air is becoming popular because it has advantages over exercise, at least for adults. The stimulus that leads the airways to narrow is caused by the inhalation of dry air during hyperventilation and exercise, during which water is evaporated from the airways in order to condition the inspired air. The mechanism whereby the airways narrow is thought to be due to the dehydrating effects of water loss, particularly in relation to its potential to cause the airways to become hyperosmolar. Mast cell mediators such as histamine and the leucotrienes are probably involved in EIA because specific antagonists reduce severity. As a result of the osmotic theory of EIA, studies were carried out to determine whether subjects with EIA were sensitive to the effects of increasing airway osmolarity by inhalation of hyperosmolar aerosols of sodium chloride. A challenge protocol using an aerosol of 4.5% sodium chloride, generated from an ultrasonic nebulizer, has been used to identify persons with asthma and to assess response to drug therapy. There are many similarities between responses to exercise, hyperventilation and hypertonic saline in the physiological and biochemical responses and the responses to drugs. Challenge with hypertonic saline is easier and cheaper to use because expensive equipment and a source of dry air is not required as with exercise or hyperventilation. The ability to obtain a dose-response curve rather than a single response and the ability to collect inflammatory cells at the same time make challenge with hypertonic saline an attractive technique to study patients suspected of having asthma.

Effect of a leukotriene B4 receptor antagonist SC-53228 on ozone-induced airway hyperresponsiveness and inflammation in dogs.

The importance of the potent neutrophil chemoattractant leukotriene (LT)B4 in causing ozone-induced bronchoconstriction, airway inflammation, and airway hyperresponsiveness in dogs was studied using the LTB4-receptor antagonist SC-53228. Seven dogs from random sources were studied three times, at least 2 wk apart. On each occasion, acetylcholine (Ach) airway responsiveness was measured before and 1 h after ozone (3 ppm, 30 min) or dry air inhalation, followed by a bronchoalveolar lavage (BAL). On the first day, dogs were treated with SC-53228 (0.4 mg/kg intravenously) followed by a continuous intravenous infusion of 1.2 mg/kg/h before ozone inhalation. On the other two days, diluent was infused followed by ozone or dry air inhalation. Cell counts were measured in BAL and cell activation was measured by spontaneous and by phorbol myristate acetate-stimulated (PMA) (2.4 mumol/L) oxygen radical release, measured from washed BAL cells (4 x 10(6) cells) by lucigenin-enhanced chemiluminescence. Ozone inhalation caused bronchoconstriction and airway hyperresponsiveness. SC-53228 inhibited the ozone-induced airway hyperresponsiveness (p = 0.006), but not the bronchoconstriction. Spontaneous (p = 0.004) and PMA-stimulated (p = 0.04) lucigenin-enhanced chemiluminescence were increased after ozone inhalation. The ozone-induced increases in PMA-stimulated chemiluminescence were significantly attenuated by treatment with SC-53228 (p = 0.04). These results suggest that LTB4 is involved in the pathogenesis of ozone-induced airway hyperresponsiveness, possibly through activation of airway inflammatory cell.

High altitude exposure reduces bronchial responsiveness to hypo-osmolar aerosol in lowland asthmatics.

It is well-known that many patients with asthma undergo clinical improvement during a stay at high altitude. At high altitude, the atmospheric and climatic conditions (such as hypoxia, cold and dry air inhalation) could modify the bronchial responsiveness in asthmatics. Our study was designed to assess the difference in bronchial responsiveness to hypotonic aerosol between sea level and high altitudes in nonresident asthmatic subjects. The results were obtained during two mountaineering expeditions above 4,000 m i.e. at 4,559 m on Mt Rosa, Italy; and at 5,050 m near the Mt Everest base camp in Nepal. Eleven mild asthmatics performed standard bronchial challenges with ultrasonically nebulized distilled water (5 min inhalation, delivery 2 mL-min-1) at sea level and after staying at least 72 h at the above mentioned altitudes. The decrease in forced expiratory volume in one second (FEV1) from baseline was used as index of bronchial response. There was no significant difference in pre-challenge FEV1 between sea level and high altitude in either study. However, the bronchoconstriction response to ultrasonically nebulized distilled water was significantly reduced at high altitude in both studies. At sea level the mean FEV1 decrease was 22.2% (range 15-35%), whereas as the maximal altitude it was 6.7% (range 2-11%). Our results indicate that there is a reduction in bronchial responsiveness to hypoosmolar aerosol at high altitude. This suggests that atmospheric and climatic conditions, or physiological adaptations, via mediators such as atrial natriuretic peptide, are beneficial to patients with asthma at high altitude.

Ozone-induced oxygen radical release from bronchoalveolar lavage cells and airway hyper-responsiveness in dogs.

1. Ozone inhalation causes airway hyper-responsiveness and airway inflammation in dogs. The purpose of this study was to determine whether these effects are associated with increases in oxygen radical production from bronchoalveolar lavage (BAL) cells. 2. Twelve randomly selected dogs were studied twice, 4 weeks apart. On each study day, acetylcholine (ACh) airway responsiveness was measured before and 1 h after ozone (3 p.p.m., 30 min) or dry air inhalation, followed by BAL. The response to ACh was expressed as the concentration causing an increase in lung resistance of 5 cmH2O l-1 s-1 above baseline. Spontaneous and phorbol myristate acetate (PMA) (2.4 mumol l-1)-stimulated oxygen radical release from washed BAL cells (4 x 10(6) cells ml-1) was measured by luminol-enhanced chemiluminescence in a luminometer at 37 degrees C. 3. Ozone inhalation caused airway hyper-responsiveness. The concentration of ACh causing an increase in lung resistance of 5 cmH2O l-1 s-1 (the 'provocative' concentration) fell from 4.68 mg ml-1 (% S.E.M., 1.43) before, to 0.48 mg ml-1 (% S.E.M., 1.60) after ozone (P < 0.0001). Spontaneous chemiluminescence area under the curve (AUC) significantly increased after ozone from 4.08 mV (10 min) (% S.E.M., 1.28) after dry air to 8.25 mV (10 min; % S.E.M., 1.29) after ozone (P = 0.007). Ozone inhalation also increased PMA-stimulated chemiluminescence AUC from 18.97 mV (10 min; % S.E.M., 1.18) after dry air to 144.03 mV (10 min; % S.E.M., 1.45) after ozone (P = 0.0001). The increase in PMA-stimulated chemiluminescence was significantly correlated with ozone-induced ACh airway hyper-responsiveness (r = 0.83, P < 0.001). 4. These results indicate that inhaled ozone increases oxygen radical release from BAL cells and suggest that oxygen radicals are important in causing ozone-induced airway hyper-responsiveness.

Effect of inhaled budesonide on ozone-induced airway hyperresponsiveness and bronchoalveolar lavage cells in dogs.

Inhaled corticosteroids are known to reduce components of the airway inflammation characteristic of asthma and improve airway hyperresponsiveness. However, the effect of inhaled corticosteroids on ozone-induced airway responses is unknown. Eight dogs inhaled budesonide [2.74 +/- 0.25 (SE) mg/day] or lactose powder twice daily for 7 days before inhaling ozone (3 ppm for 30 min) or dry air. Acetylcholine airway responsiveness was measured before and 1 h after ozone, followed by a bronchoalveolar lavage (BAL). The response to acetylcholine was expressed as the concentration causing an increase in lung resistance of 5 cmH2O.l-1.s above baseline (acetylcholine provocation concentration). Budesonide pretreatment significantly attenuated the ozone-induced increase in pulmonary resistance (P = 0.003) and neutrophil influx into BAL (P = 0.001) and significantly reduced BAL eosinophils (P = 0.026). However, budesonide pretreatment had no significant effect on ozone-induced airway hyperresponsiveness. After budesonide, the acetylcholine provocative concentration fell from 5.96 mg/ml (%SE 1.46) before to 1.11 mg/ml (%SE 1.63) after ozone (P = 0.006). After lactose, the acetylcholine provocative concentration fell from 5.34 mg/ml (%SE 1.40) before to 0.50 mg/ml (%SE 1.85) after ozone (P = 0.001). Dry air inhalation did not cause airway hyperresponsiveness (P = 0.68). These results suggest that ozone-induced airway hyperresponsiveness is steroid resistant and that airway neutrophils or eosinophils are not important in its pathogenesis.

Theophylline Minimally Inhibits Bronchoconstriction Induced by Dry Cold Air Inhalation in Asthmatic Subjects

The aim of this study was to evaluate the effect of a sustained-release theophylline preparation on bronchial responsiveness to cold dry air inhalation in asthmatic subjects. Sixteen adult subjects with asthma in a clinical steady state underwent 3 isocapnic cold air challenges on 3 consecutive days at a time when they had not received oral theophylline medication over the past 3 days. The dose of cold air causing a 20% (PD20) fall in FEV1 was obtained from each subject's dose-response curve. Subjects were then administered active or placebo sustained-release theophylline preparations according to a double-blind, randomized, two-treatment crossover design. Medication was given for a minimum of 3 consecutive days. PD20 was reassessed on 4 different days, 3 to 4 h after receiving active or placebo medication (two visits for each medication). We found a significant bronchodilator effect of theophylline as compared to the placebo (mean +/- SD differences in changes of FEV1 of 8.8 +/- 1.9%). We also documented a significant blocking effect of the active medication as opposed to the placebo on PD20 (p = 0.01). This difference (mean = 0.18 on the loge scale) was statistically beyond the intraindividual between-day variability observed on the 3 control days (p less than 0.001) but was physiologically minimal. This blocking effect was also partially related to changes in airway caliber. We conclude that theophylline showed a blocking effect on bronchial responsiveness to dry cold air, which was physiologically minimal and was partially related to changes in airway caliber.

Studies on the allergic and nonallergic nasal inflammation

Nasal lavage after antigenic and nonantigenic nasal stimulation has become an important tool for the study of inflammatory phenomena in the upper airway. Biochemical and cytologic information is relatively easily obtainable, and pharmacologic manipulations can be readily monitored. This article is of several studies aiming toward a more profound understanding of the mechanisms of allergic and nonallergic rhinitis by the use of laboratory-challenge procedures and nasal-lavage techniques. An early and a late reaction are detected clinically in the nose after antigen challenge of allergic individuals. In addition, the sensitivity to antigen significantly increases after the initial challenge, and this phenomenon is not obligatorily linked to the presence of a late-phase reaction (LPR). Inflammatory mediators, mostly mast cell- and/or basophil-derived, are detected in the nasal washes and correlate with the symptomatology in both the early and the late reactions. The allergen-induced LPR is marked by an early influx of eosinophils and, later, basophils and neutrophils. Elevation of major basic protein and histamine, but not prostaglandin D 2, is detected during the LPR, giving evidence of active eosinophil and basophil participation. Systemic steroids can effectively suppress the clinical, biochemic, and cellular manifestations of antigen-induced LPR. Topical steroids have a similar effect but are also capable of suppressing the early reaction to antigen. A nonallergic form of rhinitis can be induced in the laboratory by nasal inhalation of dry air at freezing temperatures in individuals who report sensitivity to cold and windy environments. Early and late reactions are also detectable with this stimulus, and the panel of mediators appears to be identical with that of antigen-induced rhinitis, indicating activation of the same cell type(s). This stimulus, however, appears to act through different mechanisms, since pharmacologic agents that control the allergen response are inactive against cold, dry air (CDA) reactions. Studies on the mechanism of CDA-induced rhinitis have detected elevations in the osmolality of nasal secretions after CDA challenge. This occurs only in CDA-sensitive subjects and not in CDA nonresponders or antigen-challenged allergic individuals. Elevated osmolality correlates with mediator release, suggesting a role of nasal fluid tonicity in mast cell activation. The above pieces of information offer significant insight in the mechanisms of allergic and nonallergic inflammation of the nose and the upper airways. Reconstitution of that information into a persuasive model of the naturally occurring disease and development of new therapeutic modalities will be our tasks in the future.