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PubMed2003

A comparison of the rate of recovery of 13CO2 in exhaled breath with 2H in body water following ingestion of [2H/13C]octanoic acid in a dog.

The objective of this study was to assess post-gastric processing of octanoic acid (OA) by comparing the rate of recovery of 13C in breath with the rate of recovery of 2H in saliva following ingestion of [2H/13C]OA. A test meal with 100mg [13C]OA and 750 mg [2H]OA was ingested on two separate occasions by one dog. Exhaled breath and saliva samples were collected at set time points for 6h following ingestion of the test meal. Two indices were computed, half recovery time (t(1/2)) and the time of peak excretion (t(max)). Recovery of 2H in saliva was quicker than recovery of 13C in breath as determined by the difference in the indices for each isotope; 1.33 and 1.59 h for t(1/2) and t(max), respectively. These findings suggest that the post-gastric processing of OA imposes a delay on the recovery of 13C in breath in the dog, as occurs in man and in the horse.

Animals↗
PubMed2002

Exhaled nitric oxide: a marker of pulmonary hemodynamics in heart failure.

OBJECTIVES: We sought to test the hypothesis that patients with decompensated heart failure (HF) lose a compensatory process whereby nitric oxide (NO) maintains pulmonary vascular tone. BACKGROUND: Exhaled nitric oxide (eNO) partially reflects vascular endothelial NO release. Levels of eNO are elevated in patients with compensated HF and correlate inversely with pulmonary artery pressures (PAP), reflecting pulmonary vasodilatory activity. METHODS: We measured the mean mixed expired NO content of a vital-capacity breath using chemiluminescence in patients with compensated HF (n = 30), decompensated HF (n = 7) and in normal control subjects (n = 90). Pulmonary artery pressures were also measured in patients with HF. The eNO and PAP were determined sequentially during therapy with intravenous vasodilators in patients with decompensated HF (n = 7) and in an additional group of patients with HF (n = 13) before and during administration of milrinone. RESULTS: The eNO was higher in patients with HF than in control subjects (9.9 +/- 1.1 ppb vs. 6.2 +/- 0.4 ppb, p = 0.002) and inversely correlated with PAP (r = -0.81, p < 0.00001). In marked contrast, patients with decompensated HF exhibited even higher levels of eNO (20.4 +/- 6.2 ppb) and PAP, but there was a loss of the inverse relationship between these two variables. During therapy (7.3 +/- 6 days) with sodium nitroprusside and diuresis, hemodynamics improved, eNO concentrations fell (11.2 +/- 1.2 ppb vs. before treatment, p < 0.05), and the relationship between eNO and PAP was restored. After milrinone, eNO rose proportionally with decreased PAP (p < 0.05). CONCLUSIONS: Elevated eNO may reflect a compensatory circulatory mechanism in HF that is lost in patients with clinically decompensated HF. The eNO may be an easily obtainable and quantifiable measure of the response to therapy in advanced HF.

Adult↗
PubMed2003

Exhaled nitric oxide during exercise and dobutamine stress echocardiography in patients with mitral stenosis.

BACKGROUND: Pulmonary hypertension (PH) is an important limiting factor of exercise tolerance in patients with mitral stenosis (MS). We wished to investigate the relationship between respiratory nitric oxide (NO), a potent vasodilator, and exercise tolerance in patients with moderate MS. In the same patients, we wondered whether acute change in pulmonary hemodynamics could affect respiratory NO. METHODS: Ten patients with moderate MS (valve area 1.4+/-0.2 cm(2)) were studied at rest, during incremental cycle ergometry exercise, and during dobutamine stress echocardiography (DSE). The concentration of NO in exhaled air (FE(NO)) and NO output (V'(NO)) were measured at baseline, at the end of exercise, and at the end of DSE. Eight healthy subjects served as normal controls for NO output during exercise. RESULTS: During exercise, FE(NO) decreased both in patients and in controls, while V'(NO) increased in both. At the end of exercise, both VO(2) max and V'(NO) were significantly higher in controls than in patients. The increase in V'(NO) during exercise was significantly correlated with VO(2) max, both in patients and in controls. During DSE, cardiac output (CO), pulmonary artery pressure (PAP), and mitral valve gradient increased. No changes in mean FE(NO), V'(NO), or ventilation were observed during DSE. There was a significant inverse correlation between FE(NO) and mitral valve gradient at the end of DSE. CONCLUSIONS: In patients with moderate MS, exercise performance is correlated with respiratory NO output. In the same patients, during DSE, the increase in CO, which is not accompanied by an increase in ventilation, is not associated with an increase in respiratory V'(NO).

Journal Article↗
PubMed2003

Exhaled breath condensate acidification in acute lung injury.

Lung injury in ventilated lungs may occur due to local or systemic disease and is usually caused by or accompanied by inflammatory processes. Recently, acidification of exhaled breath condensate pH (EBC-pH) has been suggested as marker of inflammation in airway disease. We investigated pH, ammonia, Lactate, pCO2, HCO3-, IL-6 and IL-8 in EBC of 35 ventilated patients (AECC-classification: ARDS: 15, ALI: 12, no lung injury: 8). EBC-pH was decreased in ventilated patients compared to volunteers (5.85 +/- 0.32 vs. 7.46 +/- 0.48; P < 0.0001). NH4+, lactate, HCO3-, pCO2, IL-6 and IL-8 were analyzed in EBC and correlated with EBC-pH. We observed correlations of EBC-pH with markers of local (EBC IL-6: r = -0.71, P < 0.0001, EBC IL-8: r = -0.68, P < 0.0001) but not of systemic inflammation (serum IL-6, serum IL-8) and with indices of severity of lung injury (Murray's Lung Injury Severity Score; r = -0.73, P < 0.0001, paO2/FiO2; r = 0.54, P < 0.001). Among factors potentially contributing to pH of EBC, EBC-lactate and EBC-NH4+ were found to correlate with EBC-pH. Inflammation-induced disturbances of regulatory mechanisms, such as glutaminase systems may result in EBC acidification. EBC-pH is suggested to represent a marker of acute lung injury caused by or accompanied by pulmonary inflammation.

Acute Disease↗
PubMed2003

Effect of switching from cyclosporine to tacrolimus on exhaled nitric oxide and pulmonary function in patients with chronic rejection after lung transplantation.

BACKGROUND: Previous studies have demonstrated that shifting immunosuppressive therapy from cyclosporine (CyA) to tacrolimus (FK) may arrest the decline in forced expiratory volume in 1 second (FEV(1)) during chronic rejection after lung transplantation. Exhaled nitric oxide (eNO) has been shown to be elevated during chronic rejection. We report the concomitant stabilization of FEV(1) and decrease in eNO after changing from CyA to FK therapy in patients with chronic rejection after lung transplantation. METHODS: We used a prospective design. The study included 10 lung transplant patients (5 men and 5 women), mean age 44 +/- 14 years at time of transplantation, with a progressive decline in FEV(1) that was attributed to chronic rejection. Four patients underwent heart-lung transplantation and 3 had a sequential single and 3 a single-lung transplantation. The switch from CyA to FK occurred at 36 +/- 23 months after transplantation (Time 0). The eNO was measured using a chemiluminescence analyzer, according to standardized European Respiratory Society (ERS) criteria. RESULTS: At Time 0, there were 6 patients in bronchiolitis obliterans syndrome (BOS) Stage 0-p, with a mean decline in FEV(1) of 15 +/- 3%; 2 in BOS Stage 1; and 2 in BOS Stage 2. Compared with the best post-operative FEV(1), there was a progressive and significant decline until Time 0, from 2.56 +/- 0.9 liters to 2.03 +/- 0.94 liters (p = 0.0047). Thereafter, FEV(1) stabilized: 2.03 +/- 0.94 liters at Time 0 and 2.05 +/- 0.94 liters 6 months later (p = non-significant). Concomitantly, there was a gradual increase in eNO during the 6 months before Time 0, from 11.4 +/- 2.5 ppb at the time of best FEV(1) to 20.5 +/- 14.8 ppb at Time 0. After switching, there was a non-significant decline in eNO, from 20.5 +/- 14.8 ppb to 14.9 +/- 5.4 ppb. There was no significant difference in eNO levels between the patients in BOS Stage 0-p and patients in higher BOS stages at either timepoint in the study. CONCLUSIONS: This study illustrates that a switch from CyA to FK can stabilize pulmonary function in lung transplant patients with chronic rejection. This stabilization of FEV(1) is accompanied by a decrease in eNO, indicating that this treatment shift can reduce inflammation of airways during the course of chronic rejection. Consequently, measuring eNO may be extremely valuable in guiding the treatment of chronic rejection after lung transplantation.

Adult↗
PubMed2006

Effect of montelukast on symptoms and exhaled nitric oxide levels in 7- to 14-year-old children with seasonal allergic rhinitis.

BACKGROUND: Cysteinyl leukotrienes have been found to exert potent inflammatory effects in the upper airways and play a fundamental role in the pathogenesis of allergic rhinitis. Previous studies have reported increased levels of exhaled nitric oxide (eNO) in patients with allergic rhinitis without asthma symptoms. OBJECTIVE: To investigate the role of treatment with montelukast on symptoms, eNO levels, and peripheral eosinophil counts of children with seasonal allergic rhinitis during pollen season. METHODS: A randomized, double-blind, parallel-group study performed between April and June 2005 in 57 children aged 7 to 14 years with seasonal allergic rhinitis was performed. The study comprised a 1-week screening period, a 1-week run-in period, and a 2-week treatment period with once daily montelukast, 5 mg, or matching placebo. RESULTS: No significant difference at baseline was found in symptom scores, eNO levels, and blood eosinophil counts between the treatment and placebo groups. After 2 weeks of montelukast treatment, improvements from the baseline in the daytime nasal, composite, and daytime eye symptoms scores were significantly greater in the montelukast group compared with the placebo group (P < .001, P < .001, and P < .01, respectively). A significant decrease was also found in eosinophil counts (P < .001) in the montelukast group compared with the placebo group after treatment. Montelukast treatment did not produce a significant effect on eNO levels compared with placebo (P = .96). CONCLUSION: Montelukast treatment provided significant improvement in symptoms and peripheral eosinophil counts of school-age children with seasonal allergic rhinitis; however, it did not show a significant effect on eNO levels.

Acetates↗
PubMed2005

Effect of fluticasone propionate-salmeterol therapy on seasonal changes in airway responsiveness and exhaled nitric oxide levels in patients with pollen-induced asthma.

BACKGROUND: There has been concern that in allergic asthmatic patients there might be an interactive effect on inflammation between regular salmeterol use and exposure to allergens, resulting in increased airway responsiveness. OBJECTIVE: To determine the effects of salmeterol on allergen-induced changes in airway responsiveness and exhaled nitric oxide (ENO) levels in allergic asthmatic patients concomitantly taking inhaled corticosteroids. METHODS: Forty-two asthmatic patients sensitized to pollen allergens were randomly allocated to treatment with fluticasone propionate-salmeterol (n=21) or fluticasone propionate alone (n=21). Spirometry, the methacholine provocation concentration causing a 20% decline in forced expiratory volume in 1 second (PC20), the adenosine 5'-monophosphate (AMP) PC20, and ENO levels were measured before and at the height of the pollen season after 6 weeks of treatment. RESULTS: Changes in the methacholine PC20, the AMP PC20, and ENO levels were not significantly different between treatment groups. No significant changes in the AMP PC20 were observed among the fluticasone propionate-salmeterol and fluticasone propionate groups during natural pollen exposure. However, a significant increase in the methacholine PC20 was observed in the fluticasone propionate-salmeterol group (P = .03) and in the fluticasone propionate group (P = .04); ENO concentrations decreased significantly in both groups during natural allergen exposure (P = .009 and .005). CONCLUSIONS: In patients with pollen-induced asthma, treatment with either fluticasone propionate or fluticasone propionate-salmeterol is associated with significant reductions in methacholine responsiveness and ENO concentrations, even during natural pollen exposure. Furthermore, at least in patients with mild asthma, natural allergen exposure and the regular use of fluticasone propionate-salmeterol are not associated with a greater increase in ENO levels and airway responsiveness than natural allergen exposure and fluticasone propionate use alone.

Adenosine Monophosphate↗
PubMed2003

Relationship among pulmonary function, bronchial reactivity, and exhaled nitric oxide in a large group of asthmatic patients.

BACKGROUND: Bronchial reactivity and exhaled nitric oxide (eNO) are not often used to monitor control and severity of asthma in clinical practice. OBJECTIVE: To evaluate the relationship among different physiologic measures (pulmonary function, nonspecific bronchial reactivity, and eNO) in asthmatic patients. METHODS: Cross-sectional, hospital-based study conducted in patients with varied asthma severity. RESULTS: A total of 392 patients participated in the study. There was no difference in eNO levels between patients taking inhaled corticosteroids (ICS group) and patients not receiving inhaled corticosteroids (NICS group). However, the percentage of predicted forced expiratory volume in 1 second (FEV1) and the provocative dose of methacholine causing a 20% decrease in FEV1 were significantly lower in the ICS group compared with the NICS group (mean, 83.2%; 95% confidence interval [CI], 80.4%-86.0%; vs mean, 94.1%; 95% CI, 91.1%-97.1%; P = .001; and geometric mean, 0.32 mg; 95% CI, 0.23-0.45 mg; vs geometric mean, 0.58 mg; 95% CI, 0.42-0.81 mg; P = .01; respectively). Patients with more severe bronchial hyperresponsiveness had a lower percentage of predicted FEV1 values (P < .001) and levels of eNO were significantly increased with increasing bronchial hyperresponsiveness (P < .001). There was no relationship between the percentage of predicted FEV1 and eNO. Atopic patients had significantly higher eNO levels than nonatopic patients (geometric mean, 11.21 ppb; 95% CI, 10.07-12.49 ppb; vs geometric mean, 7.76 ppb; 95% CI, 6.11-9.85 ppb; P = .006; respectively). CONCLUSIONS: eNO values are not related to the degree of airway obstruction but are related to airway reactivity and atopic status independent of inhaled corticosteroid use. Higher values of eNO are seen with increased airway reactivity.

Adolescent↗
PubMed2001

The effect of low-dose inhaled fluticasone propionate on exhaled nitric oxide in asthmatic patients and comparison with oral zafirlukast.

BACKGROUND: Exhaled nitric oxide (ENO) is a noninvasive marker of ongoing inflammation in asthmatic patients. Comparison between inhaled and oral anti-inflammatory medications in reduction of ENO in asthmatic patients has not been performed. OBJECTIVE: We measured changes in ENO, spirometry, need for rescue medication, quality of life (QOL), and diary scores (DS) after inhaled and oral anti-inflammatory therapy in adults with moderate asthma. METHODS: A randomized, double-blind, placebo-controlled, crossover design with 4-week washout periods was used. A plateau level of ENO, measured in parts per billion (ppb), was obtained by chemiluminescence with a Sievers 280NOA as per American Thoracic Society recommendations. Eighteen asthmatic adults (15 Hispanic, with a percentage predicted forced expiratory volume in 1 second (FEV1%) of 50% to 85%) on bronchodilators (beta2) only were studied. Subjects used fluticasone propionate (FP) metered-does inhaler (44 microg), two puffs twice daily, and matching placebo (PB) for 4 weeks. Eight of the asthmatic patients (7 Hispanic, FEV1% 50% to 85%) on bronchodilators only then received blinded zafirlukast (ZK) 20 mg and matching PB twice daily for 4 weeks. RESULTS: Low-dose inhaled FP resulted in significant improvements in ENO, spirometry, QOL, DS, and beta2 use. A significant difference in mean ENO was found (P < 0.01) before and after FP from 34+/-7 ppb to 13+/-3 ppb. A significant improvement was found (P < 0.05) with FEV1% from 75+/-3 to 85+/-3 with FP treatment. The other measured parameters, percentage predicted of peak expiratory flow rate, beta2 need, DS, and QOL measurements, were improved with low-dose FP treatment. No significant reduction was found in ENO with oral ZK for 4 weeks. After oral ZK washout and the second extension arm of placebo, ENO significantly increased back to 47+/-14 ppb (P < 0.05), but spirometry measures did not worsen. Significant improvements were found with DS and beta2 use with oral ZK therapy. CONCLUSIONS: These results reveal ENO is reduced with only low-dose inhaled FP in asthmatic patients not on anti-inflammatory medication. In the smaller extension study, ENO was reduced with FP and not with oral ZK treatment, and ENO levels increased back to near prestudy levels after ZK washout and the second extension arm of placebo. As a marker of inflammation, ENO levels reveal an improvement with anti-inflammatory medication and worsening when it is discontinued.

Administration, Inhalation↗
PubMed2003

Comparisons of the complementary effect on exhaled nitric oxide of salmeterol vs montelukast in asthmatic children taking regular inhaled budesonide.

BACKGROUND: Inhaled, long-acting beta2-agonists or antileukotrienes are alternatives as add-on therapy for asthmatic children taking regular inhaled steroids. Any complementary effects would be relevant to the choice between these alternatives. Exhaled nitric oxide (FeNO) may reflect these effects. OBJECTIVE: To compare the control of FeNO provided by salmeterol or montelukast add-on therapy in asthmatic children undergoing regular maintenance treatment with a daily dose of 400 microg of budesonide. METHODS: The study included children with increased FeNO despite regular treatment with budesonide, 400 microg/d, and normal lung function. Montelukast, 5 mg/d, salmeterol, 50 microg twice daily, or placebo was compared as add-on therapy to budesonide, 400 microg, in a randomized, double-blind, double-dummy, crossover study. RESULTS: Twenty-two children completed the trial. The geometric mean FeNO level was 20 ppb (95% confidence interval [CI], 15-27 ppb) after salmeterol, which was significantly higher than after montelukast (mean, 15 ppb; 95% CI, 11-18 ppb; P = 0.002) and placebo (mean, 15 ppb; 95% CI, 10-21 ppb; P = 0.03). There was no difference in FeNO between the montelukast and placebo groups. Mean forced expiratory volume in 1 second (FEV1) was significantly increased after salmeterol (mean, 2.63 L; 95% CI, 2.34-2.91 L) compared with placebo (mean, 2.48 L; 95% CI, 2.19-2.77 L). Montelukast (mean, 2.57 L; 95% CI, 2.33-2.80 L) was no different than placebo. CONCLUSIONS: The FeNO levels were significantly higher after salmeterol add-on treatment compared with both placebo and montelukast add-on treatment. Salmeterol significantly improved lung function (FEV1) compared with placebo and nonsignificantly compared with montelukast. Montelukast failed to reduce FeNO and improve lung function compared with placebo in this group of children taking regular budesonide, 400 microg.

Acetates↗
PubMed2003

Nitrate in exhaled breath condensate of patients with different airway diseases.

There is an increasing interest in the measurement of nitric oxide (NO.) in the airways. NO. is a free radical that reacts rapidly with reactive oxygen species in aqueous solution to form peroxynitrite which can then break down to nitrite (NO(2)(-)) and nitrate (NO(3)(-)). NO(3)(-) is considered a stable oxidative end product of NO. metabolism. The aim of this study was to assay NO(3)(-) in exhaled breath condensate (EBC) of normal nonsmoking and smoking subjects, asthmatics, patients with obstructive pulmonary disease (COPD), and patients with community-acquired pneumonia (CAP). EBC was collected using a glass condenser and samples were assayed for NO(3)(-) by ion chromatography followed by conductivity measurement. NO(3)(-) was detectable in EBC of all subjects. NO(3)(-) was elevated in smokers [median (range)] [62.5 (9.6-158.0) microM] and in asthmatics [68.0 (25.8-194.6) microM] compared to controls [9.6 (2.6-119.4) microM; p=0.003 and p=0.006, respectively], whereas NO(3)(-) was not elevated in COPD patients [24.1 (1.9-337.0 microM]. The concentration of NO(3)(-) in patients with CAP [243.4 (26.1-584.5) microM] was higher than that in controls (p=0.002) and NO(3)(-) values decreased after treatment and recovery from illness [40.0 (4.1-167.0) microM, p=0.009]. This study shows that NO(3)(-) is detectable in EBC of healthy subjects and it varies in patients with inflammatory airway diseases.

Adult↗
PubMed2001

Nasal and exhaled nitric oxide in response to occupational latex exposure.

BACKGROUND: Latex sensitivity is an increasing problem among health-care workers. Allergic responses are associated with changes in nitric oxide (NO) generation and the changes secondary to latex have not been described. METHODS: A total of 22 subjects comprising equal numbers of control volunteers and subjects with self-reported latex sensitivity were recruited to undergo latex skin prick testing. Symptom scores, exhaled nitric oxide (eNO), and nasal nitric oxide (nNO) were studied 1) before and after a controlled latex challenge (n=16), and 2) at the beginning and end of the working week, during exposure to latex (n=18). RESULTS: Latex challenge caused a significant fall in nNO levels in latex-sensitive subjects, compared to normal control subjects (P=0.04). eNO levels also decreased in the latex-sensitive subjects after latex challenge, but to a lesser degree. There were no significant differences between the beginning and end of the working week in terms of eNO or nNO in either group, although symptom scores showed a nonsignificant increase in latex-sensitive subjects. CONCLUSION: Fall in nasal NO after latex challenge is associated with reported symptomatic latex sensitivity, and this corresponds to latex skin prick test positivity. Neither nNO nor eNO showed a clear relationship to routine workplace exposure.

Adult↗
PubMed2003

Similar levels of nitric oxide in exhaled air in non-asthmatic rhinitis and asthma after bronchial allergen challenge.

BACKGROUND: Nitric oxide in exhaled air (eNO) is elevated in allergic asthma compared with healthy subjects and has been proposed as a marker of bronchial inflammation. However, eNO is elevated to a lesser extent in allergic non-asthmatic rhinitis as well. Considering the distinctive clinical appearances of both allergic diseases, differences in eNO are expected to persist after allergen exposure. The aim of the study was to compare allergen-induced changes in eNO in house dust mite sensitized patients with asthma and patients with perennial rhinitis without asthma symptoms. METHODS: Bronchial allergen challenge was performed in 52 patients sensitized to house dust mite (Dermatophagoides pteronyssinus), of whom 26 had non-asthmatic rhinitis and 26 had asthma. Levels of eNO were measured before and 1 h, 1 day and 1 week after challenge. RESULTS: At baseline eNO was significantly lower in non-asthmatic rhinitis compared with asthma (geometric mean eNO (SEM): 121 (1.1) in non-asthmatic rhinitis vs 197 (1.1) nl/min in asthma, P < 0.006). However, the increase in eNO after bronchial allergen challenge in non-asthmatic rhinitis, in particular in those patients with a dual asthmatic response, significantly exceeded the increase in asthma resulting in similar levels of eNO after challenge (geometric mean eNO (SEM) at 24 h postchallenge 204 (1.1) in non-asthmatic rhinitis vs 244 (1.1)nl/min in asthma, P = 0.3). CONCLUSION: The difference in eNO between non-asthmatic rhinitis and asthma at baseline is abolished after allergen exposure due to a significantly greater increase in eNO in non-asthmatic rhinitis.

Administration, Inhalation↗
PubMed1999

Exhaled nitric oxide in patients with Wegener's granulomatosis.

In Wegener's granulomatosis (WG), a pathogenic role of infections, in particular of a chronic colonization of the nasal mucosa with Staphylococcus aureus, has been postulated. Nitric oxide (NO), which is thought to play a role in primary host defence and inflammation, is produced endogenously within the respiratory tract, mainly from the paranasal sinuses. In order to further characterize its role in WG, nasal and pulmonary NO excretion in WG patients in comparison to healthy volunteers was measured. Seventeen patients with WG were included in the study. Five patients had active disease (bloody rhinitis with ulceration and crusting) and immunosuppressive therapy (IST), and 12 were in remission (six with, and six without, IST). S. aureus was found in the swabs of all patients with active WG and in three patients in remission. NO was measured in exhaled gas using a chemiluminescence analyser. The NO excretion rate in nasally sampled gas was significantly reduced (p<0.05) in patients with active WG ((mean+/-SD)102+/-100 nL x min(-1)) compared to healthy controls (299+/-13 nL x min(-1)), and patients in remission (281+/-86 nL x min(-1) with IST, 280+/-133 nL x min(-1) without IST). Pulmonary NO excretion in active or nonactive WG patients did not significantly differ from that of healthy volunteers (48+/-21 nL x min(-1)). These results demonstrate a reduced nasal NO excretion in active Wegener's granulomatosis. This may be caused by destruction and/or functional impairment of sinus epithelium. The reduced NO concentration may well compromise host defence in the upper airways, thus contributing to colonization with Staphylococcus aureus and further promoting Wegener's granulomatosis.

Adult↗
PubMed2000

Exhaled nitric oxide in asthmatic children exposed to relevant allergens: effect of flunisolide.

Inhaled corticosteroids are capable of reducing the level of exhaled nitric oxide (expiratory nitric oxide fraction (FE,NO)) in asthmatic patients in a dose-dependent fashion. The aim of this study was to evaluate whether or not treatment with an inhaled steroid can prevent changes in FE,NO after the exposure to relevant allergens, following avoidance, in asthmatic children allergic to house dust mite. Thirty-two house dust mite-allergy asthmatic children were randomly allocated to treatment with inhaled flunisolide (500 microg b.i.d) or placebo and evaluated before and 2 weeks after a period of natural exposure to mite antigens. Lung function and FE,NO were evaluated. FE,NO was increased in the placebo-treated group after antigen exposure. Treatment with inhaled flunisolide prevented such increase in FE,NO (p<0.001). No change was observed in lung function parameters. Inhaled flunisolide is effective in preventing the increase in airway inflammation observed in allergic asthmatic children re-exposed to allergens.

Administration, Inhalation↗
PubMed2002

Effect of montelukast on exhaled NO in asthmatic children exposed to relevant allergens.

The level of exhaled nitric oxide (FENO) is increased in house dust mite (HDM)-sensitized asthmatic children after exposure to HDM antigen, and inhaled steroids can prevent this increase. The aim of this study was to evaluate whether montelukast could prevent an increase in FENO levels in allergic asthmatic children after a brief period of exposure to relevant allergens. Sixteen children were evaluated at the residential house 'Istituto Pio XII' (Misurina, Bellunio, Italy) in the Italian Alps, a dust mite-free environment. FENO levels were evaluated before (t0) and immediately after (t1) the children were exposed to HDM allergens for 2 weeks in their homes at sea level. No significant difference in FENO was observed in the fluticasone-treated group of children after 2 weeks at sea level. In the group treated with montelukast, an increase in FENO was observed between t0 and t1, which failed to reach statistical significance. These preliminary data suggest that oral montelukast could be effective in preventing the relapse in airway inflammation in allergic asthmatic children who are occasionally exposed to relevant allergens for a short period of time.

Acetates↗
PubMed2003

Nitric oxide increases dramatically in air exhaled from lung regions with occluded vessels.

BACKGROUND: We observed dramatic changes in exhaled nitric oxide concentration (DeltaNOE) during wedge measurements, and hypothesised that occlusion and redistribution of pulmonary blood flow affects NOE. METHODS: We inflated the balloon of the pulmonary artery catheter and measured NOE and central hemodynamics in closed chest anesthetised pigs (n = 11) ventilated with hyperoxic gas (fraction of inspired oxygen [FIO2] = 0.5), before and during lung injury, and in open chest anesthetised pigs (n = 17) before and during left lower lobar (LLL) hypoxia (FIO2 0.05), and during hyperoxic (FIO2 0.8) ventilation of the other lung regions (HL). RESULTS: In the closed chest pigs NOE increased from 2.0 (0.9) to 3.4 (2.0) p.p.b. (P < 0.001) during wedge, and returned to 2.0 (1.0) p.p.b. when the balloon was deflated. The increase in mean pulmonary artery pressure (MPaP) during wedge was small and insignificant (P > 0.07). When the balloon was inflated in the right pulmonary artery in the open chest pigs, the perfusion of the HL decreased from 2.57 (0.58) to 2.34 (0.55) l min(-1) (P < 0.001), and NOEHL increased from 2.5 (0.9) to 6.2 (3.2) p.p.b. (P < 0.001). The perfusion of the LLL increased from 0.33 (0.26) to 0.54 (0.34) l min(-1) (P < 0.001), and NOELLL decreased from 1.7 (0.6) to 1.5 (0.5) p.p.b. (P < 0.001). Neither lung injury nor LLL hypoxia had any influence on DeltaNOE (P > 0.07) during wedge. The correlation coefficient (R2) was 0.66 between changes in regional blood flow and DeltaNOE, and 0.37 between changes in MPaP and DeltaNOE. CONCLUSIONS: Nitric oxide concentration increases dramatically from lung regions with occluded vessels, whereas changes in MPaP have minor effects on NOE. This is an important fact to consider when comparing NOE within or between studies, and indicates a possible marker of diseases with occluded lung vessels.

Anesthesia↗
PubMed2007

Increase in exhaled nitric oxide and protective role of the nitric oxide system in experimental pulmonary embolism.

BACKGROUND AND PURPOSE: Pulmonary embolism (PE) represents a real diagnostic challenge. PE is associated with pulmonary hypertension due to pulmonary vascular obstruction and vasoconstriction. We recently reported that pulmonary gas embolism transiently increases exhaled nitric oxide (FENO), but it is not known whether solid emboli may alter FENO, and whether an intact endogenous NO synthesis has a beneficial effect in experimental solid pulmonary embolism. EXPERIMENTAL APPROACH: We used anaesthetised and ventilated rabbits in these experiments. To mimic PE, a single intravenous infusion of homogenized autologous skeletal muscle tissue (MPE) was given to rabbits with intact NO production (MPE of 60, 15, or 7.5 mg kg(-1); group 1) and to another group (group 2) with inhibited NO synthesis (L-NAME 30 mg kg(-1); MPE of 7.5, 15 or 30 mg kg(-1)). KEY RESULTS: In group 1, after MPE, FENO increased rapidly and dose-dependently and FENO was still significantly elevated after 60 min with the two highest emboli doses. All these animals survived more than 60 min after embolization. In group 2, MPE of 7.5, 15 and 30 mg kg(-1), in combination with NO synthesis inhibition, resulted in 67%, 50% and 25% survival at 60 min respectively, representing a statistically significant decrease in survival. Cardiovascular and blood-gas changes after MPE were intensified by pre-treatment with NO synthesis inhibitor. CONCLUSIONS AND IMPLICATIONS: We conclude that solid PE causes a sustained, dose-dependent increase in FENO, giving FENO a diagnostic potential in PE. Furthermore, intact NO production appears critical for tolerance to acute PE.

Anesthesia↗