Role of Endogenous Nitric Oxide in Airflow Obstruction in Smokers

doi:10.1378/chest.110.4.927

Chest

Volume 110, Issue 4, October 1996, Pages 927-929

https://doi.org/10.1378/chest.110.4.927 Get rights and content

Objective

The aim of this study was to examine the relationship between endogenous nitric oxide (NO) level and airflow obstruction in smokers using single-breath measurement of exhaled NO with the sequential breath-holding method.

Setting

A university hospital.

Patients

Nine nonsmoking and ten smoking healthy volunteers.

Measurements

NO in exhaled air was measured using a chemiluminescence analyzer. Pulmonary function tests were performed using an autospirometer.

Results

The level of exhaled NO was higher in nonsmokers than in smokers, and the difference became larger as the breath-holding time increased. To evaluate the correlation between endogenous NO level and the degree of airflow obstruction in smokers, we used a new parameter, the NO concentration difference (ΔNO). Our findings indicate that reduced level of NO in exhaled air is an indicator of decreased NO synthesis within the respiratory system and is associated with the development of airflow obstruction in smokers (r=0.678; p<0.01).

Conclusions

ANO is a good indicator of the synthesis of endogenous NO within the respiratory system, and it appears likely that the reduced synthesis of NO may be a contributing factor to airflow obstruction in smokers.

Section snippets

Materials and Methods

The experiments were approved by the human ethics committee of our university, and informed consent for participation was obtained from each subject. Nineteen healthy volunteers (all male) were allocated to two groups (Table 1): nonsmoking (n=9, mean [SE] 32.3 [3.4] years) and smoking (n=10,35.1 [1.7] years) subjects. Subjects with an asthmatic component, hypertension, or respiratory infection within the 2 weeks preceding the study were excluded. Smokers were asked not to smoke during the 2-h

Results

The two groups were age matched, and in both, pulmonary function was within the normal range, but FEV_1.0% and maximum expiratory flow at 25% and 50% vital capacity were significantly lower in smokers than in nonsmokers. In nonsmokers, the concentration of exhaled NO increased after breath-holding in a time-dependent manner (Fig 1). However, the concentration of exhaled NO was not affected by breathholding in smokers. The level of exhaled NO was higher in nonsmokers than in smokers, and this

Discussion

In this study, we examined healthy male volunteers who were relatively young and had normal pulmonary function to evaluate the effect of smoking alone. We used the difference in NO concentration (ΔNO) as a parameter to determine the degree of airflow obstruction because it is a sensitive indicator of NO synthesis in the respiratory tract. In nonsmokers, the increase in NO in exhaled air after breath-holding was probably due to accumulation of basally excreted NO, since the amount of NO in

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Single-breath nitric oxide measurements in asthmatic patients and smokers
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Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.
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Inhaled nitric oxide for the adult respiratory distress syndrome
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Am Rev Respir Dis
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Cited by (20)

Lycopene mitigates pulmonary emphysema induced by cigarette smoke in a murine model
2019, Journal of Nutritional Biochemistry
Citation Excerpt :
One minute after cessation of smoking, levels of expired nitric oxide increase in smokers. Two hours after smoking, however, levels of expired nitric oxide are lower in smokers than nonsmokers [1,63]. This sustained reduction in expired nitric oxide in smokers may result from superoxide and peroxynitrite-dependent inflammatory and conversion processes [1].
Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by a non-fully reversible airflow limitation comprising chronic bronchitis and pulmonary emphysema both being induced by cigarette smoke (CS) exposure. Lycopene has shown antioxidant and anti-inflammatory properties that can prevent acute lung inflammation and emphysema. We hypothesized that administration with lycopene would repair lung damage in emphysema caused by CS exposure. Mice were administered with two different doses of lycopene (25 or 50 mg/kg/day, diluted in sunflower oil by orogastric gavage) and then exposed to 60 days of CS or not (CG). Lycopene promoted a reduction in the number of total leukocytes and it improved pulmonary emphysema. Lycopene was able to minimize redox processes by decreasing lipid peroxidation and DNA damage, and by having an increase in the activities of SOD, CAT and GSH content. Furthermore, it decreased levels of TNF-α, IFN-γ and IL-10. In addition, it was able to decrease MPO activity and nitrite content. In conclusion, our data elucidated the role of lycopene as an antioxidant and anti-inflammatory agent in mice exposed to CS.
Measurement of exhaled nitric oxide in humans and animals
1999, Pulmonary Pharmacology and Therapeutics
Exhaled pentane and nitric oxide levels in patients with obstructive sleep apnea
1997, Chest
Upper airway inflammation is present in patients with obstructive sleep apnea (OSA).
To determine whether exhaled pentane and nitric oxide (NO) levels, two nonspecific markers of inflammation, are increased in patients with OSA.
Exhaled nasal and oral pentane and NO levels were determined before and after sleep in 20 patients with OSA (apnea-hypopnea index, 48±7; mean±SEM) and eight healthy control subjects.
In patients with OSA, exhaled nasal and oral pentane levels after sleep were significantly higher than presleep values (6.1 ±1.2 nM vs 3.4±0.4 nM, and 7.0±1.3 nM vs 4.2±0.4 nM, respectively; p<0.05). Likewise, exhaled nasal and oral NO levels after sleep were significantly higher than presleep values in patients with OSA (39.7±3.8 ppb vs 28.4±2.9 ppb and 10.9±1.5 ppb vs 6.6±0.8 ppb, respectively; p<0.05). By contrast, there were no significant differences in exhaled nasal and oral pentane, and nasal NO levels before and after sleep in control subjects. Exhaled oral NO levels were significantly increased after sleep in comparison to presleep values in control subjects (p<0.05).
Exhaled nasal pentane and NO levels are increased after sleep in patients with moderate-severe OSA. These data suggest that upper airway inflammation is present in these patients after sleep.
Atorvastatin and Simvastatin Promoted Mouse Lung Repair After Cigarette Smoke-Induced Emphysema
2017, Inflammation
Modulation of lung function by increased nitric oxide production
2017, Journal of Clinical and Diagnostic Research
A study of fraction of exhaled nitric oxide levels as a diagnostic marker in patients with bronchial asthma
2013, Journal, Indian Academy of Clinical Medicine

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Chest

Objective

Setting

Patients

Measurements

Results

Conclusions

Section snippets

Materials and Methods

Results

Discussion

References (16)

Endogenous nitric oxide is present in the exhaled air of rabbits, guinea pigs and humans

Biochem Biophy Res Commun

Single-breath nitric oxide measurements in asthmatic patients and smokers

Lancet

Nitric oxide: physiology, pathophysiology and pharmacology

Pharmacol Rev

Nitric oxide as a secretory product of mammalian cells

FASEB J

Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.

Acta Physiol Scand

Inhaled nitric oxide for the adult respiratory distress syndrome

N Engl J Med

Bronchodilator action of nitric oxide in guinea pigs

J Clin Invest

Endogenous nitric oxide in single exhalations and the change during exercise

Am Rev Respir Dis

Cited by (20)

Lycopene mitigates pulmonary emphysema induced by cigarette smoke in a murine model

Measurement of exhaled nitric oxide in humans and animals

Exhaled pentane and nitric oxide levels in patients with obstructive sleep apnea

Atorvastatin and Simvastatin Promoted Mouse Lung Repair After Cigarette Smoke-Induced Emphysema

Modulation of lung function by increased nitric oxide production

A study of fraction of exhaled nitric oxide levels as a diagnostic marker in patients with bronchial asthma

Chest

Clinical Investigations: Smoking and Nitric Oxide: ArticlesRole of Endogenous Nitric Oxide in Airflow Obstruction in Smokers

Objective

Setting

Patients

Measurements

Results

Conclusions

Section snippets

Materials and Methods

Results

Discussion

Biochem Biophy Res Commun

Lancet

Nitric oxide: physiology, pathophysiology and pharmacology

Pharmacol Rev

Nitric oxide as a secretory product of mammalian cells

FASEB J

Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.

Acta Physiol Scand

Inhaled nitric oxide for the adult respiratory distress syndrome

N Engl J Med

Bronchodilator action of nitric oxide in guinea pigs

J Clin Invest

Endogenous nitric oxide in single exhalations and the change during exercise

Am Rev Respir Dis

Clinical Investigations: Smoking and Nitric Oxide: Articles
Role of Endogenous Nitric Oxide in Airflow Obstruction in Smokers