scholarly journals Traffic-related air pollution and alveolar nitric oxide in southern California children

2016 ◽  
Vol 47 (5) ◽  
pp. 1348-1356 ◽  
Author(s):  
Sandrah P. Eckel ◽  
Zilu Zhang ◽  
Rima Habre ◽  
Edward B. Rappaport ◽  
William S. Linn ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Air Pollution ◽  
Southern California ◽  
Airway Wall ◽  
Acute Effects ◽  
Estimated Parameters ◽  
Free Air ◽  
Distal Airway ◽  
Airway Response ◽  
The Mean

Mechanisms for the adverse respiratory effects of traffic-related air pollution (TRAP) have yet to be established. We evaluated the acute effects of TRAP exposure on proximal and distal airway inflammation by relating indoor nitric oxide (NO), a marker of TRAP exposure in the indoor microenvironment, to airway and alveolar sources of exhaled nitric oxide (FeNO).FeNO was collected online at four flow rates in 1635 schoolchildren (aged 12–15 years) in southern California (USA) breathing NO-free air. Indoor NO was sampled hourly and linearly interpolated to the time of the FeNO test. Estimated parameters quantifying airway wall diffusivity (DawNO) and flux (J′awNO) and alveolar concentration (CANO) sources of FeNO were related to exposure using linear regression to adjust for potential confounders.We found that TRAP exposure indoors was associated with elevated alveolar NO. A 10 ppb higher indoor NO concentration at the time of the FeNO test was associated with 0.10 ppb higher average CANO (95% CI 0.04–0.16) (equivalent to a 7.1% increase from the mean), 4.0% higher J′awNO (95% CI −2.8–11.3) and 0.2% lower DawNO (95% CI −4.8–4.6).These findings are consistent with an airway response to TRAP exposure that was most marked in the distal airways.

At high cardiac output, diesel exhaust exposure increases pulmonary vascular resistance and decreases distensibility of pulmonary resistive vessels

2015 ◽  
Vol 309 (12) ◽  
pp. H2137-H2144 ◽  
Author(s):  
Aurélien Wauters ◽  
Marco Vicenzi ◽  
Benjamin De Becker ◽  
Jean-Philippe Riga ◽  
Fatemeh Esmaeilzadeh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Air Pollution ◽  
Cardiac Output ◽  
Diesel Exhaust ◽  
Stress Echocardiography ◽  
Decompensated Heart Failure ◽  
Dobutamine Stress ◽  
Fractional Exhaled Nitric Oxide ◽  
High Cardiac Output ◽  
The Mean

Air pollution has recently been associated with the development of acute decompensated heart failure, but the underlying biological mechanisms remain unclear. A pulmonary vasoconstrictor effect of air pollution, combined with its systemic effects, may precipitate decompensated heart failure. The aim of the present study was to investigate the effects of acute exposure to diesel exhaust (DE) on pulmonary vascular resistance (PVR) under resting and stress conditions but also to determine whether air pollution may potentiate acquired pulmonary hypertension. Eighteen healthy male volunteers were exposed to ambient air (AA) or dilute DE with a particulate matter of <2.5 μm concentration of 300 μg/m3 for 2 h in a randomized, crossover study design. The effects of DE on PVR, on the coefficient of distensibilty of pulmonary vessels (α), and on right and left ventricular function were evaluated at rest ( n = 18), during dobutamine stress echocardiography ( n = 10), and during exercise stress echocardiography performed in hypoxia ( n = 8). Serum endothelin-1 and fractional exhaled nitric oxide were also measured. At rest, exposure to DE did not affect PVR. During dobutamine stress, the slope of the mean pulmonary artery pressure-cardiac output relationship increased from 2.8 ± 0.5 mmHg·min·l−1 in AA to 3.9 ± 0.5 mmHg·min·l−1 in DE ( P < 0.05) and the α coefficient decreased from 0.96 ± 0.15 to 0.64 ± 0.12%/mmHg ( P < 0.01). DE did not further enhance the hypoxia-related upper shift of the mean pulmonary artery pressure-cardiac output relationship. Exposure to DE did not affect serum endothelin-1 concentration or fractional exhaled nitric oxide. In conclusion, acute exposure to DE increased pulmonary vasomotor tone by decreasing the distensibility of pulmonary resistive vessels at high cardiac output.

scholarly journals Exercise-induced bronchoconstriction alters airway nitric oxide exchange in a pattern distinct from spirometry

2006 ◽  
Vol 291 (6) ◽  
pp. R1741-R1748 ◽  
Author(s):  
Hye-Won Shin ◽  
Christina D. Schwindt ◽  
Anna S. Aledia ◽  
Christine M. Rose-Gottron ◽  
Jennifer K. Larson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Forced Expiratory Volume ◽  
Healthy Controls ◽  
Airway Wall ◽  
Exercise Challenge ◽  
Exhaled No ◽  
Forced Expiratory Flow ◽  
The Mean ◽  
Exercise Induced ◽  
Exchange Parameters

Exhaled nitric oxide (NO) is altered in asthmatic subjects with exercise-induced bronchoconstriction (EIB). However, the physiological interpretation of exhaled NO is limited because of its dependence on exhalation flow and the inability to distinguish completely proximal (large airway) from peripheral (small airway and alveolar) contributions. We estimated flow-independent NO exchange parameters that partition exhaled NO into proximal and peripheral contributions at baseline, postexercise challenge, and postbronchodilator administration in steroid-naive mild-intermittent asthmatic subjects with EIB (24–43 yr old, n = 9) and healthy controls (20–31 yr old, n = 9). The mean ± SD maximum airway wall flux and airway diffusing capacity were elevated and forced expiratory flow, midexpiratory phase (FEF25–75), forced expiratory volume in 1 s (FEV1), and FEV1/forced vital capacity (FVC) were reduced at baseline in subjects with EIB compared with healthy controls, whereas the steady-state alveolar concentration of NO and FVC were not different. Compared with the response of healthy controls, exercise challenge significantly reduced FEV1 (−23 ± 15%), FEF25–75 (−37 ± 18%), FVC (−12 ± 12%), FEV1/FVC (−13 ± 8%), and maximum airway wall flux (−35 ± 11%) relative to baseline in subjects with EIB, whereas bronchodilator administration only increased FEV1 (+20 ± 21%), FEF25–75 (+56 ± 41%), and FEV1/FVC (+13 ± 9%). We conclude that mild-intermittent steroid-naive asthmatic subjects with EIB have altered airway NO exchange dynamics at baseline and after exercise challenge but that these changes occur by distinct mechanisms and are not correlated with alterations in spirometry.

Acute effects of air pollution on asthma hospitalization in Shanghai, China

2014 ◽  
Vol 191 ◽  
pp. 139-144 ◽  
Author(s):  
Jing Cai ◽  
Ang Zhao ◽  
Jinzhuo Zhao ◽  
Renjie Chen ◽  
Weibing Wang ◽  
...  
Keyword(s):  
Air Pollution ◽  
Acute Effects ◽  
Asthma Hospitalization

Effects of Intermittent Sequential Compression in Venous Hypertensive Microangiopathy

1994 ◽  
Vol 9 (3) ◽  
pp. 99-103 ◽  
Author(s):  
G. V. Belcaro ◽  
A. N. Nicolaides
Keyword(s):  
Venous Insufficiency ◽  
Marked Change ◽  
Venous Hypertension ◽  
Horizontal Position ◽  
Acute Effects ◽  
Doppler Flowmetry ◽  
Vasomotor Activity ◽  
The Mean ◽  
Intermittent Sequential Compression ◽  
Normal Controls

Objective: To investigate the acute effects of sequential compression on the microcirculation in limbs with chronic venous hypertension causing venous microangiopathy. Design: One group of patients with venous hypertension and a group of normal, comparable subjects were treated with intermittent sequential pneumatic compression applied for 30 min. Skin blood flow was measured by laser Doppler flowmetry at the perimalleolar region at rest (horizontal position) and on standing. The measurements were repeated at 0, 30 and 60 min after cessation of the compression. As criteria of inclusion, only limbs with high perimalleolar skin flux and decreased venoarteriolar response were included. Setting: St Mary's Hospital, London (teaching hospital). Patients, participants: Sixteen limbs in 16 patients with chronic venous hypertension and 12 limbs of comparable healthy volunteers were studied. Results: At rest, in the normal controls, the mean (SD) flux was 0.56 (0.3) units; it decreased on average by 35% on standing (venoarteriolar response). There was normal vasomotor activity. In patients, the mean flux was 1.45 (0.8) ( p < 0.025) and the median venoarticular response only 7%. There was very limited vasomotor activity. Vasomotor activity started 10 min after the commencement of compression. At the end of the compression period there was a marked change towards normality. Resting flux was 0.90 (0.5) (significantly decreased) and the venoarteriolar response had increased to 23% ( p < 0.025) with an improvement in vasomotor activity. These changes persisted at 30 and 60 min. Conclusions: The findings offer an explanation of the effect of sequential compression on the healing of leg ulcers in chronic venous insufficiency.

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