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PubMed1995

Exhaled nitric oxide concentration and amniotic fluid nitrite concentration during pregnancy.

We have assessed fetal and maternal nitric oxide (NO) production in pregnancy. Exhaled NO and amniotic fluid nitrite concentrations were measured by chemiluminescence between 10 and 42 weeks of pregnancy. Exhaled NO concentrations did not alter significantly during gestation. In contrast, there was a significant change in mean amniotic fluid nitrite concentration in late pregnancy (P < 0.001). The finding of decreased amniotic nitrite concentrations after 37 weeks of gestation support the hypothesis that reduced NO production may contribute to increased uterine activity in late pregnancy.

Adolescent↗
PubMed2004

Effect of inhalation aspirin challenge on exhaled nitric oxide in patients with aspirin-inducible asthma.

BACKGROUND: A complex relationship between arachidonic acid metabolites and nitric oxide (NO) synthesis has been reported in asthma. The effects of inhaled aspirin on fractional exhaled NO (FENO) in patients with aspirin-tolerant (ATA) and aspirin-inducible (AIA) asthma compared with normal controls have been investigated. METHODS: The FENO was measured baseline, after saline and lysine-aspirin (L-ASA) bronchial challenge in 10 patients with ATA and in 10 patients with AIA [mean (PD(20)FEV(1) L-ASA): 14.7 +/- 12.7 mg], who had comparable age and baseline FEV(1). Ten healthy subjects served as controls. Sputum eosinophils were counted after saline and after L-ASA challenge in the two groups of asthmatics. RESULTS: Asthmatic patients had baseline FENO significantly higher than controls (29.7 +/- 6.8 vs 9.8 +/- 2.05 p.p.b. respectively, P < 0.0001). No difference was observed in methacholine PD(20)FEV(1) and baseline FENO between ATA and AIA patients. After L-ASA inhalation, FENO increased significantly only in patients with AIA, reaching the peak value 4 h after bronchoconstriction (from 31.1 +/- 6 to 43 +/- 4.8 p.p.b., P < 0.001), while no change was observed in patients with ATA and in controls. Sputum eosinophils increased significantly after L-ASA inhalation only in patients with AIA (from 8.1 +/- 2.7 to 11.1 +/- 2.8%, P < 0.005) and there was a significant relationship between the increase in sputum eosinophils and the increase in FENO after ASA challenge. CONCLUSION: Exhaled NO may indicate eosinophilic airway inflammation during ASA exposure in patients with ASA inducible asthma.

Administration, Inhalation↗
PubMed2006

Exhaled breath condensate pH measurement in children with asthma, allergic rhinitis and atopic dermatitis.

Recent studies have shown that the pH of exhaled breath condensate (EBC) could be predictive of asthma exacerbation. Moreover, it has been documented that both allergic rhinitis and atopic dermatitis constitute risk factors for the occurrence of asthma in a progression of disease known as atopic march. The aim of our study was to establish if condensate pH could be used as a valuable mean of monitoring of asthma in atopic children. We studied 34 atopic children with acute asthma, 70 with stable asthma, 35 children with allergic rhinitis, and 17 with atopic dermatitis. Thirty healthy children were used as controls. All children underwent skin prick tests and lung function tests. Exhaled breath condensate samples were collected with a condensing device and de-aerated with argon. The pH of EBC was measured using a pH meter. Children with acute asthma were treated with inhaled steroids and bronchodilators. We found that the pH of condensate in patients with acute asthma was lower than that of patients with stable asthma, rhinitis, and controls (7.25 vs. 7.32, p < 0.05; 7.25 vs. 7.48, p < 0.02; 7.25 vs. 7.78, p < 0.0001, respectively). Patients with stable asthma, rhinitis, and eczema had also lower pH than that of controls (7.32, 7.48, and 7.44 vs. 7.78; p < 0.0001, p < 0.006, p < 0.04, respectively). Patients with acute asthma normalized their pH after treatment (7.82 vs. 7.25; p < 0.0001). Finally, patients with acute asthma showed a positive correlation between pH and lung functional parameters (forced expiratory volume in 1 s; r = 0.39, p = 0.04). Our study shows that EBC pH measurement may be a promising marker for assessing airway inflammation and monitoring response to anti-inflammatory treatment in asthmatic children. Furthermore, we report the first evidence of airways acidification in children with allergic rhinitis and atopic dermatitis. Therefore, EBC pH assessment may be useful in the evaluation of progression of the atopic march toward the development of asthma later in life. Further studies are recommended in order to confirm this indication.

Adolescent↗
PubMed1986

Lipid peroxidation in vivo monitored as ethane exhalation and malondialdehyde excretion in urine after oral administration of chloroform.

In vivo lipid peroxidation was studied in phenobarbital pretreated rats exposed for chloroform. Lipid peroxidation was monitored as ethane exhalation or malondialdehyde (MDA) excretion in urine. A single oral dose of chloroform (0.7 ml/kg b.wt.) showed a marked increase in ethane exhalation in animals starved for 48 hours prior to chloroform treatment. This increase became evident after a lag-period of about 100 min. Pretreatment with diethylmaleate (1 ml/kg b.wt.) 1 hour prior to chloroform treatment gave a similar result. MDA excretion in urine from non-starved animals, exposed to chloroform, markedly increased after 4 hours and after 24 hours 115 nmol/kg had been excreted. In animals starved for 48 hours prior to chloroform treatment about 270 nmol/kg excreted within 24 hours. Small molecular weight thiols were measured in liver, kidneys and lungs. Chloroform decreased the thiol content of the liver by 43.2% within 100 min. while the concentration in the kidneys and the lungs were less affected. It is suggested that chloroform may act as a potent inducer of lipid peroxidation in vivo. The synergistic effects of the pretreatments and the lag phase indicate that glutathione depletion in the liver was an essential factor in this response.

Administration, Oral↗
PubMed1975

The physiological effects of inhaling exhaled cigarette smoke in relation to attitude of the nonsmoker.

Fifty-six nonsmoking college students were exposed, in a closed environment, for a period of 20 minutes to the exhaled cigarette smoke of two smokers. After intervals of 5, 10, 15 and 20 minutes of being exposed to the exhaled smoke, heart rates and systolic and diastolic blood pressures were monitored. Differences between times on systolic pressure was the only statistically significant finding. The subjects were then divided into two distinct attitude groups: (1) those who objected ("disliked") to being in the presence of cigarette smoke, and (2) those who did not mind ("indifferent") being in the presence of cigarette smoke. Variances attributable to between groups was statistically significantly different for heart rate. The "dislike" group had the higher rate in comparison to the "indifferent" group. Between times was statistically different for both groups for systolic pressure. Between group systolic pressures were not significantly different. As expected, there was no significant finding concerning diastolic changes.

Attitude↗
PubMed2005

Exhaled breath measures of inflammation: are they useful in neonatal chronic lung disease?

Neonatal chronic lung disease is a common problem for surviving infants of extreme prematurity. Although the precise pathophysiology is still not known, it is clear that inflammation provides a common link that amplifies the injury to the premature lung. Current invasive measures of pulmonary inflammation include markers in blood and airway effluent, with the cellular composition of tracheal fluid being the "gold standard". In this article available exhaled breath measures, particularly nitric oxide, carbon monoxide, volatile hydrocarbons, and exhaled breath condensate, are reviewed with particular reference to sample collection, analysis, and common pitfalls as they apply to the ventilated premature newborn at risk of chronic lung disease. Although they have great potential, all measures require thorough validation before being used clinically.

Biomarkers↗
PubMed2003

Safety and success of exhaled breath condensate collection in asthma.

BACKGROUND: Exhaled breath condensate (EBC) is a rapidly expanding area of research to study airway inflammation through the detection of volatile and non-volatile substances in the airways. AIMS: To determine the safety and feasibility of EBC procedure in a group of children with asthma of varying severity. METHODS: In a cross sectional study of children aged 4-17 years, 18 healthy and 91 asthmatic children (69 in stable condition and 22 with asthma exacerbation) underwent the EBC procedure. Outcomes assessed included completion of the procedure, decrease in FEV1, change in fractional exhaled nitric oxide (FE(NO)), and adverse effects. No pretreatment with beta2 agonists was given. All children were able to successfully complete the EBC procedure. RESULTS: Median fall in FEV1 after the procedure was -1% (IQR -3.5, 1.8) in asthmatics and was comparable to that observed in healthy children. In only one asthmatic child did the drop in FEV1 exceed 12%. No significant changes in FE(NO) were observed after EBC. CONCLUSION: This study suggests that EBC is a simple and well tolerated method for evaluating biological samples from the lower airway. The procedure was safe in children with asthma exacerbation, and the success rate was 100% in children aged 4 years and above.

Adolescent↗
PubMed1996

Airway and cough responsiveness and exhaled nitric oxide in non-smoking patients with stable chronic heart failure.

OBJECTIVE: To investigate the airway and cough responsiveness in non-smoking patients with stable chronic heart failure. Cough and wheeze, features associated with hyper-responsive airways, are not uncommon especially in decompensated chronic heart failure. Bronchial hyperresponsiveness has previously been demonstrated in chronic heart failure but this may have been confounded by smoking and acute decompensation. DESIGN: Case-control study. SETTING: Tertiary specialist hospital. PATIENTS AND INTERVENTIONS: Airway responsiveness to methacholine (a direct stimulant of smooth muscle in the airways), sodium metabisulphite (a putative stimulant of airway sensory nerves), and exercise was examined in 10 non-smoking patients with stable chronic heart failure (age 56.5 (3.2) (SEM) years; 7 men; radionuclide left ventricular ejection fraction 20.8 (2.9)%; radiographic cardiothoracic ratio 0.56 (0.02)). Exhaled nitric oxide, a product of the action of proinflammatory cytokines, was also measured to assess the contribution of local inflammation to airway responsiveness. The cough responses to low-concentration chloride solutions and to capsaicin were studied. Because all patients were receiving angiotensin-converting enzyme inhibitors, which may influence airway responsiveness and cough, 8 asymptomatic non-smoking controls taking angiotensin-converting enzyme inhibitors for essential hypertension were also studied (age 54.3 (2.8) years; 6 men; radiographic cardiothoracic ratio 0.46 (0.01)). RESULTS: The mean provocative concentration that induced a 20% decrease in forced expiratory volume in 1 second (FEV1) was 67.6 v 79.8 mg/ml (P = 0.71) for methacholine and 276.7 v 290.4 mg/ml (P = 0.79) for sodium metabisulphite in chronic heart failure patients and controls respectively. The change in FEV1 after maximal cardiopulmonary exercise testing was +1.44% in patients and +2.53% in controls (P = 0.47), indicating that there was no exercise-induced bronchospasm in either group (peak oxygen consumption was 16.9 (1.3) v 26.5 (2.3) ml/kg/min respectively, P < 0.01). Exhaled nitric oxide concentration was not increased in chronic heart failure (12.3 (1.7) v 16.2 (3.3) ppb, P = 0.32). The median cough counts after nebulised 0 mM and 37.5 mM chloride solutions were 2.5 v 1.0 (P = 0.6) and 5.5 v 5.5 (P = 0.5) respectively and the capsaicin concentration causing two or more coughs was 13.5 v 6.5 microM (P = 0.5). CONCLUSION: Airway hyper-responsiveness is not a predominant feature in non-smoking patients with stable chronic heart failure treated with, and tolerant to, angiotensin-converting enzyme inhibitors. It is unlikely to contribute to the exertional dyspnoea seen in these patients.

Adult↗
PubMed1978

Ethanol-increased exhalation of mercury in mice.

CBA/J mice injected three days beforehand with 203HgCl2 were given ethanol or water by gavage and placed in a chamber designed to collect exhaled mercury. Ethanol treatment led to an eight-fold increase of counts accumulated on a filter over a four-hour period, compared with water-treated mice. The mercury-collection apparatus tested for extracorporeal contribution of volatilised mercury indicated that the counts originated from the air exhaled by the mice.

Animals↗
PubMed2001

Effect of pulmonary rehabilitation on exhaled nitric oxide in patients with chronic obstructive pulmonary disease.

BACKGROUND: In patients with mild to moderate chronic obstructive pulmonary disease (COPD) the exercise induced increase in exhaled nitric oxide (eNO) parallels that observed in normal untrained subjects. There is no information on the effects of the level of exercise tolerance on eNO in these patients. The aim of this study was to evaluate the effect of a pulmonary rehabilitation programme including exercise training on eNO in patients with COPD. METHODS: In 14 consecutive male patients with stable COPD of mean (SD) age 64 (9) years and forced expiratory volume in one second (FEV1) 55 (14)% predicted, fractional eNO concentration (FeNO), peak work rate (Wpeak) and oxygen uptake (VO2peak) were assessed at baseline (T-1), at the end of a 1 month run in period (T0), and after an 8 week outpatient multidisciplinary pulmonary rehabilitation programme (T1) including cycloergometer training. RESULTS: FeNO did not significantly differ at T-1 and T0 (mean (SE) 4.3 (0.6) and 4.4 (0.6) ppb, respectively), whereas it rose significantly at T1 to 6.4 (0.7) ppb (p<0.02). Compared with T0, both Wpeak and VO2 were significantly (p<0.05) increased at T1 (mean (SE) Wpeak from 89 (5.6) W to 109 (6.9) W); VO2peak from 1.27 (0.1) l/min to 1.48 (0.1) l/min). A significant correlation was found between baseline FEV1 and the change in FeNO following the rehabilitation programme (r=-0.71; p<0.05) and between changes in FeNO and Wpeak from T0 to T1(r=0.60; p<0.05). CONCLUSIONS: Pulmonary rehabilitation in patients with mild to moderate COPD is associated with an increase in exhaled nitric oxide.

Aged↗
PubMed2002

Caffeine decreases exhaled nitric oxide.

BACKGROUND: Caffeine is known to inhibit phosphodiesterases, to mobilise intracellular calcium, and to act as an antagonist at adenosine receptors, all of which can potentially alter nitric oxide (NO) production. It was therefore hypothesised that caffeine may alter exhaled NO (eNO) levels. METHODS: In a randomised, single blind, crossover manner, 12 normal subjects consumed either (1) coffee and a placebo capsule, (2) decaffeinated coffee and a capsule of 200 mg caffeine, or (3) decaffeinated coffee and a placebo capsule. Serum caffeine levels were measured at baseline and 1 hour later. Exhaled NO levels were also measured at baseline and each hour for 4 hours. RESULTS: A significant percentage fall in mean (SE) eNO from baseline was seen 1 hour after either caffeinated coffee or a caffeine capsule when compared with placebo (13.5 (4.0)%, p=0.009 and 19.0 (3.8)%, p=0.001, respectively). CONCLUSION: Caffeine causes a significant decrease in eNO which will need to be considered when designing trials to measure eNO levels. The mechanism may be via adenosine receptor antagonism or by altering levels of cGMP.

Adult↗
PubMed2003

Effect of bradykinin on allergen induced increase in exhaled nitric oxide in asthma.

BACKGROUND: Exposure of patients with atopic asthma to allergens produces a long term increase in exhaled nitric oxide (FENO), probably reflecting inducible NO synthase (NOS) expression. In contrast, bradykinin (BK) rapidly reduces FENO. It is unknown whether BK suppresses increased FENO production after allergen exposure in asthma, and whether it modulates FENO via NOS inhibition. METHODS: Levels of FENO in response to aerosolised BK were studied before (day 3) and 48 hours after (day 10) randomised diluent (diluent/placebo/BK (Dil/P/BK)), allergen (allergen/placebo/BK (All/P/BK), and allergen/L-NMMA/BK (All/L/BK)) challenges (day 8) in 10 atopic, steroid naïve, mild asthmatic patients with dual responses to inhaled house dust mite extract. To determine whether BK modulates FENO via NOS inhibition, subjects performed pre- and post-allergen BK challenges after pretreatment with the NOS inhibitor L-NMMA in the All/L/BK period. RESULTS: Allergen induced a fall in FENO during the early asthmatic reaction (EAR) expressed as AUC(0-1) (ANOVA, p=0.04), which was followed by a rise in FENO during the late asthmatic reaction (LAR) expressed as AUC(1-48) (ANOVA, p=0.008). In the Dil/P/BK period, FENO levels after BK on pre- and post-diluent days were lower than FENO levels after placebo (difference 23.5 ppb (95% CI 6.2 to 40.9) and 22.5 ppb (95% CI 7.3 to 37.7), respectively; p<0.05). Despite the long lasting increase in FENO following allergen challenge in the LAR, BK suppressed FENO levels at 48 hours after allergen challenge in the All/P/BK period, lowering the increased FENO (difference from placebo 54.3 ppb (95% CI 23.8 to 84.8); p=0.003) to the baseline level on the pre-allergen day (p=0.51). FENO levels were lower after L-NMMA than after placebo on pre-allergen (difference 10.85 ppb (95% CI 1.3 to 20.4); p=0.03) and post-allergen (difference 36.2 ppb (95% CI 5.5 to 66.9); p=0.03) days in the All/L/BK and All/P/BK periods, respectively. L-NMMA did not significantly potentiate the pre- and post-allergen reduction in BK induced FENO. CONCLUSIONS: Bradykinin suppresses the allergen induced increase in exhaled NO in asthma; this is not potentiated by L-NMMA. Bradykinin and L-NMMA may follow a common pathway in reducing increased NO production before and after experimental allergen exposure. Reinforcement of this endogenous protective mechanism should be considered as a therapeutic target in asthma.

Administration, Inhalation↗
PubMed2003

Exhaled nitric oxide and asthma: complex interactions between atopy, airway responsiveness, and symptoms in a community population of children.

BACKGROUND: Exhaled nitric oxide (FE(NO)) is raised in asthmatic children, but there are inconsistencies in the relationship between FE(NO) and characteristics of asthma, including atopy, increased airway responsiveness (AR), and airway inflammation. The aim of this study was to investigate the relationship between FE(NO) and asthma, atopy, and increased AR in children. METHODS: One hundred and fifty five children (79 boys) of mean age 11.5 years underwent an assessment that included FE(NO) measurements, spirometric tests, inhaled histamine challenge, and a skin prick test. Blood was collected for eosinophil count. Current and past asthma like symptoms were determined by questionnaire. RESULTS: In multiple linear regression analyses FE(NO) was associated with atopy (p<0.001), level of AR (p = 0.005), blood eosinophil count (p = 0.007), and height (p = 0.002) but not with physician diagnosed asthma (p = 0.1) or reported wheeze in the last 12 months (p = 0.5). Separate regression models were conducted for atopic and non-atopic children and associations between FE(NO) and AR, blood eosinophils and height were only evident in atopic children. Exhaled NO was raised in children with a combination of atopy and increased AR independent of symptoms. CONCLUSION: Raised FE(NO) seems to be associated with an underlying mechanism linking atopy and AR but not necessarily respiratory symptoms.

Adolescent↗
PubMed2003

Exhaled nitric oxide rather than lung function distinguishes preschool children with probable asthma.

BACKGROUND: Respiratory function and airway inflammation can be evaluated in preschool children with special techniques, but their relative power in identifying young children with asthma has not been studied. This study was undertaken to compare the value of exhaled nitric oxide (FE(NO)), baseline lung function, and bronchodilator responsiveness in identifying children with newly detected probable asthma. METHODS: Ninety six preschool children (age 3.8-7.5 years) with asthmatic symptoms or history and 62 age matched healthy non-atopic controls were studied. FE(NO) was measured with the standard online single exhalation technique, and baseline lung function and bronchodilator responsiveness were measured using impulse oscillometry (IOS). RESULTS: Children with probable asthma (n=21), characterised by recent recurrent wheeze, had a significantly higher mean (SE) concentration of FE(NO) than controls (22.1 (3.4) ppb v 5.3 (0.4) ppb; mean difference 16.8 ppb, 95% CI 12.0 to 21.5) and also had higher baseline respiratory resistance, lower reactance, and larger bronchodilator responses expressed as the change in resistance after inhalation of salbutamol. Children with chronic cough only (n=46) also had significantly raised mean FE(NO) (9.2 (1.5) ppb; mean difference 3.9 ppb, 95% CI 0.8 to 7.0) but their lung function was not significantly reduced. Children on inhaled steroids due to previously diagnosed asthma (n=29) differed from the controls only in their baseline lung function. The analysis of receiver operating characteristics (ROC) showed that FE(NO) provided the best power for discriminating between children with probable asthma and healthy controls, with a sensitivity of 86% and specificity of 92% at the cut off level of 1.5 SD above predicted. CONCLUSIONS: FE(NO) is superior to baseline respiratory function and bronchodilator responsiveness in identifying preschool children with probable asthma. The results emphasise the presence of airway inflammation in the early stages of asthma, even in young children.

Airway Resistance↗
PubMed2002

Exhaled NO is reduced at an early stage of hypoxia-induced pulmonary hypertension in newborn piglets.

Altered nitric oxide (NO) production could contribute to the pathogenesis of hypoxia-induced pulmonary hypertension. To determine whether parameters of lung NO are altered at an early stage of hypoxia-induced pulmonary hypertension, newborn piglets were exposed to room air (control, n = 21) or 10% O(2) (hypoxia, n = 19) for 3-4 days. Some lungs were isolated and perfused for measurement of exhaled NO output and the perfusate accumulation of nitrite and nitrate (NOx-), the stable metabolites of NO. Pulmonary arteries (20-600-microm diameter) and their accompanying airways were dissected from other lungs and incubated for NOx- determination. Abundances of the nitric oxide synthase (NOS) isoforms endothelial NOS and neural NOS were assessed in homogenates of PAs and airways. The perfusate NOx- accumulation was similar, whereas exhaled NO output was lower for isolated lungs of hypoxic, compared with control, piglets. The incubation solution NOx- did not differ between pulmonary arteries (PAs) of the two groups but was lower for airways of hypoxic, compared with control, piglets. Abundances of both eNOS and nNOS proteins were similar for PA homogenates from the two groups of piglets but were increased in airway homogenates of hypoxic compared with controls. The NO pathway is altered in airways, but not in PAs, at an early stage of hypoxia-induced pulmonary hypertension in newborn piglets.

Animals↗
PubMed1999

Inducible nitric oxide synthase in the lung and exhaled nitric oxide after hyperoxia.

The effect of hyperoxia on nitric oxide (NO) production in intact animals is unknown. We described the effects of hyperoxia on inducible nitric oxide synthase (iNOS) expression and NO production in the lungs of rats exposed to high concentrations of oxygen. Animals were placed in sealed Plexiglas chambers and were exposed to either 85% oxygen (hyperoxic group) or 21% oxygen (negative control group). Animals were anesthetized after 24 and 72 h of exposure and were ventilated via a tracheotomy. We measured NO production in exhaled air (E(NO)) by chemiluminescence. The lungs were then harvested and processed for detection of iNOS by immunohistochemistry and Western blotting analysis. The same experiments were repeated in animals exposed to hyperoxia for 72 h after they were infused with L-arginine. We used rats that were injected intraperitoneally with Escherichia coli lipopolysaccharide to induce septic shock as a positive control group. Hyperoxia and septic shock induced expression of iNOS in the lung. However, E(NO) was elevated only in septic shock rats but was normal in the hyperoxic group. Exogenous infusion of L-arginine after hyperoxia did not increase E(NO). To exclude the possibility that in the hyperoxic group NO was scavenged by oxygen radicals to form peroxynitrite, lungs were studied by immunohistochemistry for the detection of nitrotyrosine. Nitrotyrosine was found in septic shock animals but not in the hyperoxic group, further suggesting that NO is not synthesized in rats exposed to hyperoxia. We conclude that hyperoxia induces iNOS expression in the lung without an increase in NO concentration in the exhaled air.

Animals↗
PubMed1995

Cold dry air-induced rhinitis: effect of inhalation and exhalation through the nose.

Ten subjects with a history of cold air-induced nasal symptoms participated in a randomized two-period crossover study to evaluate the occurrence and magnitude of the reaction induced by inhalation and exhalation of cold dry air through the nose. The protocol involved breathing of either warm moist or cold dry air for 45 min at resting breathing rates. The nasal response was quantified by determining the amount of produced secretions as well as by measuring histamine and N-alpha-p-tosyl-L-arginine methyl (TAME) esterase activities in recovered nasal lavage fluids. Symptom scores were obtained. Warm moist air did not increase symptoms nor did it result in any significant changes in secretions or mediator levels. Compared with baseline, cold dry air induced significant rhinorrhea and increased both secretion weights (9.6 +/- 1.3 vs. 28.1 +/- 6.5 mg; P = 0.01) and the levels of histamine (3.9 +/- 1.2 vs. 10.6 +/- 2.7 ng/ml; P = 0.02) and TAME esterase activity (3.1 +/- 0.8 vs. 7.0 +/- 2.0 counts.min-1.10(-3); P = 0.01). We conclude that bidirectional nasal breathing of cold dry air results in a reaction that is qualitatively similar to that induced when air is only inhaled through the nose and exhaled through the mouth.

Adult↗
PubMed1997

Exhalation of gaseous nitric oxide by rats in response to endotoxin and its absorption by the lungs.

Rats injected with a lipopolysaccharide endotoxin produce detectable concentrations of nitric oxide gas (NO) in the expired air within 60 min. The concentration of NO reaches a plateau at 3 h. Production of the NO is dose dependent on lipopolysaccharide, and at a dose of 1 mg/kg i.v., lipopolysaccharide alveolar concentrations of > 260 parts per billion are observed. NO synthase inhibitors suppress this NO production in response to endotoxin. Experiments were conducted to ascertain the site of origin of this NO and to measure the capacity of the lungs to absorb NO from alveolar air. Results indicate that the endotoxin-induced NO originates from within the lungs themselves and that the lungs have the capacity to absorb > 60% of NO that is presented to them. Lung tissues absorb approximately 44-47% of the NO load, blood carries away between 15 and 19%, while the remainder is exhaled in the expired air. It is proposed that the exhalation of NO might prove useful as an early biomarker for acute lung injury.

Animals↗