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PubMed2006

Exhaled nitric oxide and airway caliber during exercise-induced bronchoconstriction.

Data on the relationship between exercise-induced bronchoconstriction (EIB) and exhaled nitric oxide (NO) in adult patients with asthma are controversial. It is unclear whether endogenous NO may act as either a protective or stimulatory factor in the airway response to exercise or whether changes in exhaled NO simply reflect acute narrowing of the airway. The aim of this study was to assess the changes in the fraction of exhaled nitric oxide (FE(NO)) before and after exercise challenge in patients with asthma and to analyze the relationship between FE(NO) and airway obstruction. Twenty-five non-smoking, steroid-naïve, atopic, adult patients with mild persistent asthma and 12 non-smoking, nonatopic, healthy subjects (control group) performed an exercise challenge on a cycloergometer, with monitored ventilation. FEV1 and FE(NO) were measured at baseline and 1, 5, 10, 15 and 20 minutes after the exercise challenge. Eleven of the asthmatic patients had exercise-induced bronchoconstriction (EIB group) and the remaining 14 did not (non-EIB group). Baseline FE(NO) was higher in the EIB and non-EIB asthmatic groups than in the control group. In the EIB group, FE(NO) was significantly lower 5, 10 and 15 minutes after exercise, and the changes in FE(NO) correlated with variation in FEV1 10 and 15 min after exercise. A significant correlation between baseline FE(NO) and maximal post-exercise decrease in FEV1 was found in asthmatic patients (EIB group). In conclusion, exhaled nitric oxide levels transiently decrease during exercise-induced bronchoconstriction in adult patients with asthma. Baseline FE(NO) might predict the airway obstruction resulting after exercise.

Adolescent↗
PubMed2005

Analysis of exhaled leukotrienes in nonasthmatic adult patients with seasonal allergic rhinitis.

BACKGROUND: Leukotrienes (LTs) are increased in exhaled breath condensate (EBC) in patients with asthma. So far no data have been reported about LT levels in nonasthmatic patients with seasonal allergic rhinitis (SAR). The aim of the study was to find out whether the LT levels in EBC were increased in the nonasthmatic adult patients with SAR both during and after the pollen season in comparison with healthy controls and to assess the changes of the LT levels after the pollen season. METHODS: Twenty-nine nonasthmatic adult patients with SAR underwent measurement of exhaled LTs in the EBC during and after the pollen season. Leukotrienes B(4), C(4), D(4) and E(4) were analysed by a specific and sensitive gas chromatography/mass spectrometry (GC/MS) assay and compared with 50 healthy nonsmoking controls. Spirometry, skin prick tests and nonspecific IgE were evaluated. RESULTS: Leukotrienes concentrations (B(4), E(4) but not D(4)) were significantly increased in and after the pollen season in patients with SAR in comparison with healthy controls. In most of the samples, LT C(4) was undetectable. The values of all exhaled LTs were significantly decreased after the pollen season compared with the seasonal baseline: LTB(4) (P = 0.023), LTD(4) (P = 0.020), LTE(4) (P = 0.047). CONCLUSIONS: Levels of exhaled LTB(4) and LTE(4) were higher in SAR patients than in healthy controls and decreased after the pollen season as compared with levels in season. The SAR patients with the highest in season LT levels had also the post-season levels elevated and this may be an early marker of inflammatory process in the lower airways despite the absence of clinical symptoms of asthma.

Adolescent↗
PubMed2006

Fractional exhaled nitric oxide concentration is increased in asbestosis and pleural plaques.

OBJECTIVE AND BACKGROUND: Asbestos exposure induces generation of reactive oxygen and nitrogen species. Nitric oxide is involved in asbestos-related lung toxicity in vitro and can be measured non-invasively in humans in exhaled breath. The authors hypothesized that fractional exhaled nitric oxide concentration (FENO) would be increased in subjects with asbestos-related lung disorders. METHODS: FENO was measured in 56 subjects with asbestos-related disorders (asbestosis: 12; pleural plaques: 32; asbestos-related diffuse pleural thickening: 12) and in 35 normal subjects. The authors also measured exhaled carbon monoxide, another marker of lung inflammation. RESULTS: Median (25-75 percentile) FENO was increased in subjects with asbestosis (7.9 (6.6-15.7) p.p.b.; P=0.001) and pleural plaques (6.3 (5.3-9) p.p.b.; P=0.03) compared with normal controls (4.6 (3.5-6) p.p.b.). Subjects with DPT had a median FENO of 5.6 p.p.b., similar to controls. No significant differences in exhaled carbon monoxide were observed between controls (1.0+/-0.3 p.p.m.) and subjects with asbestosis (1.3+/-0.3 p.p.m.), pleural plaques (1.2+/-0.3 p.p.m.) or diffuse pleural thickening (1.1+/-0.3 p.p.m.). CONCLUSIONS: FENO is raised in asbestosis consistent with lung inflammation, and also in pleural plaques.

Aged↗
PubMed2006

A simple technique to characterize proximal and peripheral nitric oxide exchange using constant flow exhalations and an axial diffusion model.

The most common technique employed to describe pulmonary gas exchange of nitric oxide (NO) combines multiple constant flow exhalations with a two-compartment model (2CM) that neglects 1) the trumpet shape (increasing surface area per unit volume) of the airway tree and 2) gas phase axial diffusion of NO. However, recent evidence suggests that these features of the lungs are important determinants of NO exchange. The goal of this study is to present an algorithm that characterizes NO exchange using multiple constant flow exhalations and a model that considers the trumpet shape of the airway tree and axial diffusion (model TMAD). Solution of the diffusion equation for the TMAD for exhalation flows >100 ml/s can be reduced to the same linear relationship between the NO elimination rate and the flow; however, the interpretation of the slope and the intercept depend on the model. We tested the TMAD in healthy subjects (n = 8) using commonly used and easily performed exhalation flows (100, 150, 200, and 250 ml/s). Compared with the 2CM, estimates (mean +/- SD) from the TMAD for the maximum airway flux are statistically higher (J'aw(NO) = 770 +/- 470 compared with 440 +/- 270 pl/s), whereas estimates for the steady-state alveolar concentration are statistically lower (CA(NO) = 0.66 +/- 0.98 compared with 1.2 +/- 0.80 parts/billion). Furthermore, CA(NO) from the TMAD is not different from zero. We conclude that proximal (airways) NO production is larger than previously predicted with the 2CM and that peripheral (respiratory bronchioles and alveoli) NO is near zero in healthy subjects.

Adult↗
PubMed2006

Markers of lung disease in exhaled breath: nitric oxide.

Management of airway inflammation requires proper monitoring and treatment to improve long-term outcomes. However, achieving this goal is difficult, as current methods have limitations. Although nitric oxide (NO) was first identified 200 years ago, its physiological importance was not recognized until the early 1980s. Many studies have established the role of NO as an essential messenger molecule in body systems. In addition, studies have demonstrated a significant relationship between changes in exhaled NO levels and other markers of airway inflammation. The technique used to measure NO in exhaled breath is noninvasive, reproducible, sensitive, and easy to perform. Consequently, there is growing interest in the use of exhaled NO in the management of asthma and other pulmonary conditions. The purpose of this review is to promote a basic understanding of the physiologic actions of NO, measurement techniques, and ways that research findings might translate to future application in clinical practice. Specifically, the article will review the role of exhaled NO in regard to its historical background, mechanisms of action, measurement techniques, and implications for clinical practice and research.

Asthma↗
PubMed2006

Genetic and environmental effects on exhaled nitric oxide and airway responsiveness in a population-based sample of twins.

Elevated levels of exhaled nitric oxide (eNO) and airway hyperresponsiveness are intermediate phenotypes of asthma. Using population-based data collected from a sample of twins, the present authors estimated the relative contribution of genes, family environment and nonshared environmental influences to variations in eNO and airway responsiveness (AR). In addition, the genetic and environmental sources of covariation between these two asthma-related phenotypes were investigated. The study population comprised a random sample of 377 adult twins identified through the Norwegian Twin Registry. The main outcome variables were eNO and AR to methacholine. Genetic effects accounted for 60% of the variation in eNO. Family environment accounted for 30% of the variation in AR, while nonshared environmental influences explained the remaining variation for both measures. For both eNO and AR, there were significant regression effects for atopy and smoking. The small, but significant association between eNO and AR was primarily explained by genetic factors. Sub-analyses restricted to atopic and nonsmoking twins strengthened the observation. In conclusion, variations in exhaled nitric oxide and airway responsiveness appear to be explained by different genetic and environmental variance structures. Variation in exhaled nitric oxide is explained by genetic and nonshared environmental effects, whereas an environmental model best explains the variation in airway responsiveness. Common genetic effects explain the small but significant association between exhaled nitric oxide and airway responsiveness.

Adult↗
PubMed2006

Saliva is one likely source of leukotriene B4 in exhaled breath condensate.

Leukotriene (LT)B4 in exhaled breath condensate (EBC) has been reported to be elevated in airway inflammation. The origin of leukotrienes in EBC is, however, not established. The aims of this study are to measure LTB4 levels in EBC collected in two challenges characterised by a strong neutrophilic airway inflammation and to compare LTB4 levels in EBC with levels in sputum and saliva. LTB4 and alpha-amylase were measured in EBC from 34 healthy subjects exposed in a pig confinement building or to a lipopolysaccharide provocation. These markers were also measured in induced sputum in 11 of the subjects. For comparison, LTB4 and alpha-amylase were measured in saliva from healthy subjects. Only four out of 102 EBC samples had detectable LTB4 (28-100 pg x mL(-1)). alpha-amylase activity was detected in the LTB4-positive samples. In contrast, LTB4 was detected in all examined sputum supernatants in the same study (median 1,190 pg x mL(-1)). The median LTB4 level in saliva was 469 pg x mL(-1). High levels of leukotriene B4 in saliva and the presence of leukotriene B4 in exhaled breath condensate only when alpha-amylase was detected, indicate that leukotriene B4 found in exhaled breath condensate is the result of saliva contamination. As leukotriene B4 was consistently present in sputum supernatants, exhaled breath condensate may be inappropriate for monitoring airway leukotriene B4.

Adult↗
PubMed2005

Latex allergen exposure increases exhaled nitric oxide in symptomatic healthcare workers.

The objective of this study was to investigate the clinical and diagnostic impact of baseline exhaled nitric oxide (eNO) levels and latex allergen-induced eNO changes in different healthcare worker groups. Healthcare workers, 31 latex-sensitised and 14 nonsensitised, underwent occupational-type challenge tests with powdered allergenic latex gloves. Sensitised as well as nonsensitised healthcare workers developed a significant eNO increase 1 h after challenge. Conversely, only latex-sensitised employees showed a significant eNO increase 22 h after challenge, which showed a significant relationship with bronchial obstruction (specific airway resistance changes). However, there was no difference in either baseline eNO level or eNO increase after 22 h between asthmatic (n = 13) and rhinitic only (n = 20) responders. The specificity and sensitivity of a 50% eNO increase after 22 h in responders were 100 and 56%, respectively. These results support the assumption that the whole respiratory tract is involved in a combined allergic rhinitis and asthma syndrome. Smoking healthcare workers showed reduced baseline exhaled nitric oxide levels, but, as shown for the first time, an allergen-induced exhaled nitric oxide increase comparable to that of nonsmokers. Corticosteroid therapy inhibited the allergen-induced exhaled nitric oxide change but not the clinical response in the challenge test. These findings suggest that cigarette smoke and corticosteroids initiate distinct molecular mechanisms influencing nitric oxide concentrations in the airways.

Adult↗
PubMed2006

Time course of exhaled hydrogen peroxide and nitric oxide during chemotherapy.

This study was designed to assess the effect of differential leukocyte depletion during chemotherapy by monitoring the levels of exhaled hydrogen peroxide H2O2 and nitric oxide (F(eNO)) present. In 39 patients with lung cancer (chronic obstructive pulmonary disorder up to stage II, median forced expiratory volume in one second 78% predicted), measurements were performed before a cycle of therapy (day 1), at least once during the cycle (day 8: n = 34; day 15: n = 19), and afterwards (days 21-29). There were significant changes in the level of H2O2, F(eNO) and peripheral blood cell differentials over the visits. The level of H2O2 was decreased only on day 15, with a median (difference between the upper and lower quartiles) fall of 31 (57)%, while F(eNO) was reduced only on day 8, by 22 (40)%. Neutrophil numbers were unchanged on day 8 and decreased by 59 (48)% on day 15, while monocyte numbers were decreased on day 8 by 87 (39)%. On days 21-29, values had returned to baseline. Taken together with previous findings, the parallel course of levels of exhaled hydrogen peroxide and neutrophil counts suggests that a major part of exhaled hydrogen peroxide is due to neutrophils via the conducting airways. In contrast, the production of exhaled nitric oxide seems to be primarily associated with monocytes.

Exhalation↗
PubMed2005

Correlation of exhaled breath temperature with bronchial blood flow in asthma.

In asthma elevated rates of exhaled breath temperature changes (Deltae degrees T) and bronchial blood flow (Qaw) may be due to increased vascularity of the airway mucosa as a result of inflammation.We investigated the relationship of Deltae degrees T with Qaw and airway inflammation as assessed by exhaled nitric oxide (NO). We also studied the anti-inflammatory and vasoactive effects of inhaled corticosteroid and beta2-agonist.Deltae degrees T was confirmed to be elevated (7.27 +/- 0.6 Delta degrees C/s) in 19 asthmatic subjects (mean age +/- SEM, 40 +/- 6 yr; 6 male, FEV1 74 +/- 6 % predicted) compared to 16 normal volunteers (4.23 +/- 0.41 Delta degrees C/s, p < 0.01) (30 +/- 2 yr) and was significantly increased after salbutamol inhalation in normal subjects (7.8 +/- 0.6 Delta degrees C/ s, p < 0.05) but not in asthmatic patients. Qaw, measured using an acetylene dilution method was also elevated in patients with asthma compared to normal subjects (49.47 +/- 2.06 and 31.56 +/- 1.6 mul/ml/min p < 0.01) and correlated with exhaled NO (r = 0.57, p < 0.05) and Deltae degrees T (r = 0.525, p < 0.05). In asthma patients, Qaw was reduced 30 minutes after the inhalation of budesonide 400 mug (21.0 +/- 2.3 mul/ml/min, p < 0.05) but was not affected by salbutamol.Deltae degrees T correlates with Qaw and exhaled NO in asthmatic patients and therefore may reflect airway inflammation, as confirmed by the rapid response to steroids.

Adult↗
PubMed2006

An audible indication of exhalation increases delivered tidal volume during bag valve mask ventilation of a patient simulator.

Self-inflating manual resuscitators (SIMRs) can mislead caregivers because the bag, unlike a Mapleson-type device, reinflates even without patient exhalation. We added a whistle as an audible indicator to the exhalation port of a SIMR. In randomized order, each participant provided two sets of breaths via mask ventilation with a SIMR, one with and one without audible feedback, to a Human Patient Simulator modified to log lung volume changes. The last three breaths in each set were used to compare average tidal volume (Vt) under both conditions. Eighty-seven advanced cardiac life support trainees (54 males, 33 females) with clinical experience averaging 6.4 +/- 9.4 yr were recruited. Average Vt delivered with the standard SIMR was 486 +/- 166 mL and 624 +/- 96 mL with the modified SIMR. Average Vt delivered by a modified SIMR was significantly larger by 40% when it followed standard SIMR use and 19% when using the modified SIMR first. Use of a SIMR with an audible indicator of exhalation significantly (P < 0.001) increased mask ventilation of a patient simulator, suggesting that mask ventilation of a patient with a SIMR may also be increased by objective, real-time feedback of exhaled Vt.

Acoustic Stimulation↗
PubMed2003

8-Isoprostane, a marker of oxidative stress, is increased in exhaled breath condensate of patients with obstructive sleep apnea after night and is reduced by continuous positive airway pressure therapy.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) is characterized by recurrent apnea during sleep that may compromise oxidative balance. Oxidative stress is increased in the blood and in the airways of OSA patients. DESIGN: The aim of this study was to investigate whether oxidative stress is determined by nocturnal apneas and could be reduced by CPAP therapy, and whether there is a relation between local and systemic oxidative stress in these patients. PATIENTS AND METHODS: Eighteen patients with OSA (13 men; mean [+/- SD] age, 48 +/- 3 years) and 12 healthy age-matched and weight-matched subjects (8 men; mean age, 46 +/- 7 years) were recruited. 8-Isoprostane was measured in exhaled breath condensate and blood by a specific enzyme immunoassay. MEASUREMENTS AND RESULTS: Higher concentrations of 8-isoprostane were found in the morning exhaled condensate (9.5 +/- 1.9 pg/mL) and plasma (9.7 +/- 1.5 pg/mL) of OSA patients compared to healthy obese subjects (6.7 +/- 0.2 and 7.1 +/- 0.3 pg/mL, respectively; p < 0.0001). Elevated mean concentrations of exhaled 8-isoprostane were observed in the OSA patients at 8:00 AM (9.5 +/- 1.9 pg/mL) but not at 8:00 PM (7.6 +/- 0.8 pg/mL; p < 0.0005), and a significant reduction was seen after continuous positive airway pressure (CPAP) therapy (7.7 +/- 0.9 pg/mL; before treatment, 9.6 +/- 1.7 pg/mL; p < 0.005). A positive correlation was found between morning exhaled 8-isoprostane levels and the apnea-hypopnea index (r = 0.8; p < 0.0001), and 8-isoprostane levels and neck circumference (r = 0.6; p < 0.0001). CONCLUSIONS: These findings suggest that systemic and local oxidative stress are increased in OSA patients, and that they are higher after nocturnal apnea and reduced by CPAP therapy.

Breath Tests↗
PubMed2003

Comparison of exhaled breath condensate from nasal and oral collection.

BACKGROUND: Analysis of exhaled breath condensate may provide new insights into pulmonary inflammatory processes. A new collection method via suction of nasally expired air especially suitable for younger children was presented recently. Here we compare this nasal suction method with the more widely used oral collection method regarding the amount of condensate collected as well as the concentrations of hydrogen peroxide (H2O2), nitrite and nitrate, respectively. MATERIALS AND METHODS: Exhaled breath condensate was collected from 11 healthy adults for the measurements of the amount of condensate and H2O2 concentration and from 17 children for the measurements of nitrite and nitrate. Condensate was collected via nasal suction and oral exhalation from each subject. RESULTS: Overall, no differences between both collection methods were found for all variables assessed except the concentration of H2O2, whereas the latter closely correlated (Spearman r = 0.88, p = 0.0007) between both collection methods. No correlation was found for the amount of condensate collected and the concentration of nitrite and nitrate. The Bland-Altman limits of agreement scattered over a wide range with clinical impact, proving significant differences between both collection methods for all variables measured. CONCLUSIONS: Although nasal and oral collection method proved again suitable for the collection of exhaled breath condensate, the variability of the results obtained precludes the interchangeable usage of the inflammatory markers assessed here.

Adult↗
PubMed2003

[Effect of cigarette smoking on exhaled nitric oxide levels in healthy volunteers and patients with coronary heart disease].

UNLABELLED: Exhaled air contains nitric oxide in very low concentrations reaching several parts per billion. There are many factors which can influence exhaled nitric oxide levels (eNO), one of them is cigarette smoking. MATERIAL AND METHODS: We investigated 78 patients: Group I (n = 26)--smokers, divided in two subgroups--I A healthy volunteers (n = 13) and I B--patients with coronary heart disease (CAD) (n = 13) Group II (n = 52)--nonsmokers. They were also divided in two subgroups--II A healthy volunteers (n = 21) and II B patients with CAD taking nitrates orally (n = 31) We use NO analyzer NOA 280 (Sievers Boulder Col. USA) with chemo-luminescence method RESULTS: We found that eNO levels were significantly lower in smoking group than in nonsmokers. This fact was noticed in whole investigated population and in both subgroups, CONCLUSION: 1. Cigarette smoking significantly lowers exhaled nitric oxide levels and should be always taken into account during interpretation of the results. 2. Cigarette smoking significantly lowers exhaled nitric oxide levels even with of oral nitrates therapy.

Administration, Oral↗
PubMed2003

[Concentration of nitric oxide exhaled air (eNO) in patients with COPD and bronchiectasis].

UNLABELLED: Exhaled nitric oxide (eNO) concentration measurement may allow for noninvasive estimation of severity of airways inflammation in respiratory tract diseases. Exhaled nitric oxide concentration is a sensitive marker of bronchial inflammation in asthma. The purpose of this study was: to evaluate eNO concentration in patients with COPD and bronchiectasis; to evaluate correlation between eNO concentration and the degree of airways obstruction in patients with COPD as well as correlation between eNO and extent of bronchiectasis in HRCT; to evaluate the effect of smoking on eNO concentration in COPD group. There were two groups of patients and the control group. The first group consisted of 20 patients with COPD (17 men, 3 women aged 41-68 yr). Ten patients were ex-smokers, and ten were current smokers. The second group consisted of 15 nonsmokers (10 men, 5 women aged 45-72 yr) with the diagnosis of bronchiectasis based on high-resolution CT criteria. The control group consisted of 11 healthy, nonsmoking subjects who had no respiratory disease or allergy, aged 28-52 years. Exhaled NO was measured by means of SIEVERS 280 Nitric Oxide Analyser (Boulder, Colorado, USA). RESULTS: The highest eNO concentration was found in patients with bronchiectasis (9.83 ppb +/- 3.09; median 8.0). It was significantly elevated compared to the values found in patients with COPD (5.3 ppb +/- 0.57, median 4.46; p = 0.002) or in the control group (5.17 ppb +/- 0.73, median 4.32; p = 0.007). Ex-smokers with COPD had higher eNO levels (6.3 ppb +/- 0.73; median 5.7) than did active smokers with COPD (4.3 ppb +/- 0.80; median 3.39; p = 0.017). Exhaled NO did not differ between exsmokers and healthy nonsmokers. There was no correlation between eNO and number of packyears (r = -0.022; p = 0.928). The extent of bronchiectasis expressed as CT score did not correlate with eNO concentration. There was also no significant relationship between eNO and FEV1 (r = -0.046; p = 0.87).

Adult↗
PubMed2006

[Measurement of exhaled nitric oxide: methodology].

INTRODUCTION: The singular relationship between the exhaled nitric oxide (NO) fraction and the expiratory flow rate has both technical (subject of international guidelines) and theoretical (modelling of pulmonary NO exchange) implications. STATE OF THE ART: Guidelines recommend the measurement of exhaled NO at a single, defined, expiratory flow rate (V') against a positive expiratory pressure to ensure velum closure, providing a fraction of exhaled NO, FE(NO,V'). With some oversimplifications concerning the relationship between FENO and V', NO exchange parameters independent of the expiratory flow rate can be calculated based on a two-compartment model: maximum conducting airway NO flux (J'awNO), alveolar NO concentration (CalvNO), and in some conditions, airway NO diffusing capacity (DawNO) and epithelial NO concentration of conducting airways (CawNO). PERSPECTIVES: Technical progress has provided the pulmonologist with simple equipment to allow the determination of the NO output from the respiratory tract. The two-compartment model provides the physiologist with a non-invasive technique for evaluating the contribution of alveolar space and conducting airways. CONCLUSION: The measurement of exhaled NO allows the non-invasive evaluation of a key mediator involved in the regulation of biological processes.

Endothelium-Dependent Relaxing Factors↗
PubMedDate not supplied

Exhaled nitric oxide decreases upon acute exposure to high-altitude hypoxia.

Nitric oxide (NO) is a vasodilator that plays a role in blood flow and oxygen delivery. Acute hypoxia down regulates NO synthesis, a response that may exacerbate hypoxic stress by decreasing blood flow. This study was designed to test the hypotheses that pulmonary NO decreases upon acute exposure to high-altitude hypoxia and that relatively low levels of NO at altitude are associated with greater stress as reflected in more symptoms of acute mountain sickness (AMS). A sample of 47 healthy, adult, nonsmoking, sea-level residents provided measurements at sea level, at 2,800 m, and at 0-, 2-, and 3-h exposure times at 4,200 m altitude on Mauna Kea, Hawaii. Measurements were made of exhaled NO, oxygen saturation of hemoglobin, heart rate, and reported symptoms of AMS. The partial pressure of NO concentration in exhaled breath decreased significantly from a sea level mean of 4.2 nmHg to 3.8 nmHg at 2,800 m and 3.4 nmHg at 4,200 m. NO concentration in exhaled breath did not change significantly over a 3-h exposure at 4,200 m and recovered to pre-exposure baseline upon return to sea level. There was no significant association between the level of NO exhaled and the number of self-reported symptoms of AMS during this brief exposure.

Altitude Sickness↗
PubMedDate not supplied

Reduction of hepatic tetrahydrofolate and inhibition of exhalation of 14CO2 formed from [dimethylamino-14C]aminopyrine in nitrous oxide-treated rats.

The exhalation of 14CO2 after the administration of [dimethylamino-14C]aminopyrine to an organism is assumed to reflect the demethylation of aminopyrine by hepatic mixed-function oxidase activity. The formaldehyde formed as a result of the demethylation of aminopyrine is then sequentially oxidized to formic acid and CO2. The last step in the pathway, i.e., formate oxidation, is dependent upon tetrahydrofolate; thus, factors which alter hepatic tetrahydrofolate potentially may modify 14C-aminopyrine metabolism to 14CO2 in vivo. Exposure of rats to nitrous oxide (N2O) produces a significant reduction in hepatic tetrahydrofolate as a result of the inhibition of 5-methyltetrahydrofolate:homocysteine methyltransferase activity (E.C. 2.1.1.13). In the present study, exposure of rats to N2O/O2 (1:1) for 4 hr prior to the administration of 14C-aminopyrine (40 or 400 mumoles per kg) produced a 60% reduction in the peak rate of 14CO2 exhalation and a 45% decrease in the total 14CO2 exhaled within 2 hr. In control experiments, exposure of rats to nitrogen/O2 (1:1) produced no effect on 14C-aminopyrine metabolism to 14CO2. Administration of methionine (1.3 mmoles per kg) 30 min prior to 14C-aminopyrine administration reversed the inhibition of 14CO2 exhalation and reduction in hepatic tetrahydrofolate observed in N2O-exposed animals. Aminopyrine (400 mumoles per kg) administration to air-breathing rats did not affect the level of urinary formate, but exposure to N2O produced a 40-fold increase. Aminopyrine administration to N2O-exposed rats produced a 75% increase in urinary formate as compared to rats treated with N2O alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine↗