Biomedical subjects

Katarzyna Hildebrand

Publications and source records attributed to Katarzyna Hildebrand.

8 recordsLinked to original sources

PubMed2006

[Exhaled nitric oxide in patients with obstructive sleep apnea syndrome].

UNLABELLED: Exhaled nitric oxide has been extensively investigated as a non-invasive marker of airway inflammation. Some authors have suggested that morning FE(NO) in obstructive sleep apnea syndrome (OSAS) patients is elevated due to inflammation of upper airways, while others have not found any differences between patients and healthy subjects. The purpose of this study was to analyze concentration of exhaled nitric oxide (FE(NO)) in OSAS patients. METHODS: 119 (99 M, 20 F) consecutive patients of sleep laboratory participated in this study. Standard overnight sleep studies with polysomnography or portable screening device were carried out in the whole group: OSAS was diagnosed in 66 patients and 53 no-OSAS served as controls. FE(NO) was measured on-line with a flow rate kept at 0.045 - 0.055 l/s, according to the recommendations of ATS using a chemiluminescence analyzer twice: before the sleep study (8-10 p.m.) and after termination of data collection (6 - 8 a.m.). There were no differences in age between patients and controls. Respiratory disturbance index (RDI) was 40.3+/-24.9 in patients and 3.7+/-2.8 in controls (p<0.001). In OSAS patients both evening and morning FE(NO) was significantly higher compared to controls (23.1+/-14.8 ppb vs. 16.8+/-9.8 ppb and 22.4+/-13.2 ppb vs. 15.3+/-8.1 ppb respectively, p<0.05). Weak but statistically significant correlations for the whole group between morning FE(NO) and mean and minimum arterial oxygen saturation (SaO2) during sleep and number of study minutes with SaO2<90% were observed. Lower evening FE(NO) in OSAS patients with coexisting arterial hypertension when compared to normotensive OSAS patients was also noticed (19.1+/-10.8 ppb vs. 27.1+/-19.1 ppb; p<0.05). CONCLUSIONS: The increase in FE(NO) in OSAS patents may be caused by repetitive apneas and hypoxemia during sleep.

Adult↗

PubMed2006

[Influence of bronchoscopy on nitric oxide in exhaled air].

UNLABELLED: Nitric oxide has been extensively studied as a noninvasive marker of airway inflammation, especially in asthma. Assuming, bronchoscopy can produced not only systemic but also local inflammatory response we hypothesized that bronchofiberoscopy can be responsible for an increase in nitric oxide synthesis with resulting increase in fractional concentration of exhaled nitric oxide (FE(NO)). Seventeen subjects (10 M, 7 F), at mean age of 53.8+/-14.1 yrs undergoing diagnostic bronchoscopy participated in the study. The indications for bronchoscopy were as follows: lung cancer (n=5; 29%), interstitial lung diseases (n=3; 18%), slowly resolving pneumonia (n=3; 18%), hemoptysis (n=3; 18%), differential diagnosis of asthma/ dyspnea (n=3; 18%). During bronchoscopy bronchial washing (n=7) and bronchoalveolar lavage (BAL) (n=10) has been performed. FE(NO) has been analyzed on-line with chemiluminescence analyzer (NIOX, Aerocrine, Sweden) according to American Thoracic Society guidelines, before and at 1, 2, 3 and 24 hours after bronchoscopy. Mean FE(NO) before bronchoscopy was 19.7+/-4.5 ppb (mean +/- SEM), post - bronchoscopy a decrease with a nadir at second hour (12.1+/-1.5 ppb, p<0.05) was observed, FE(NO) 24 hours after bronchoscopy was not different than baseline (18.4+/-2.5 ppb). There were no differences in the FE(NO) profile in BAL patients when compared to those in whom only the bronchial washing has been performed. CONCLUSIONS: Bronchoscopy leads to a significant decrease in exhaled nitric oxide. The underlying mechanisms are unclear. Future studies including analysis of other inflammatory markers are needed to explain these changes.

Asthma↗

PubMed2006

[Holter ECG monitoring during research bronchofiberoscopy in patients with asthma].

UNLABELLED: Bronchoscopy is a very useful tool in asthma research studies. The study was undertaken to evaluate the effect of bronchoscopy, BAL and bronchial biopsies on heart rate and arrhytmias in patients with asthma. Twenty patients (12 M, 8 F, mean age 39,6+/-16,3 yrs) with asthma (mean FEV, 81+/-19.5% pred.; mean FEV(1)%VC 69+/-12.3%) participated in the study. Holter ECG monitoring was performed twice: before (1 or 2 days) and on the day of bronchoscopy. Heart rate and cardiac arrhythmias were compared to prebronchoscopy recording at four separate time intervals: during bronchoscopy, first postbronchoscopic hour, second postbronchoscopic hour and total 24 hours. There were no significant differences between mean heart rate at the time of bronchoscopy (88.5+/-14.1 min(-1) vs 83.7+/-11.9 min(-1)), first and second postbronchoscopic hour (80.9+/-15.8 min(-1) vs 85.7+/-13.7 min(-1) and 82.6+/-13.6 min(-1) vs 80.6+/-11.6 min(-1)) as well as total 24 hours (76.1+/-11.2 min(-1) vs 75.9+/-9.4 min(-1)) as compared to prebronchoscopic recordings. Max. heart rate during bronchoscopy was higher as compared to the corresponding time of prebronchoscopic recording (134.5+/-11.5 min(-1) vs 122.5+/-19.6 min(-1), p<0,05). No differences in the number and type of ventricular (VA) and supraventricular arrhythmias (SVA) between the pre- and peribronchoscopic monitoring were observed. Positive correlation between the age and the number of VA during bronchoscopy has been found. CONCLUSION: Bronchoscopic procedures in asthma patients do not increase the risk of cardiac arrhythmias. Some factors influencing the heart rate and number of VA during bronchoscopy can be identified.

Adult↗

PubMed2006

[Influence of nasal continuous positive airway pressure on response to exercise in patients with obstructive sleep apnea syndrome].

UNLABELLED: Obstructive sleep apnea syndrome (OSAS) patients are at risk of cardiovascular complications. The aim of this study was to assess the effect of treatment with continuous positive airway pressure (CPAP) on the response to symptom limited exercise test. METHODS: twenty nine OSAS patients (1 F, 28 M), mean age 50.7+/-9.7 yrs with body mass index of 32.6+/-4.5 kg/m2 participated in the study. OSAS was diagnosed by overnight polysomnography. Incremental cardiopulmonary exercise test (CPET) on a treadmill was performed twice: before and after 2-3 weeks of regular treatment with CPAP. RESULTS: mean apnea + hypopnea index (AHI) before therapy was 57.6+/-12 h(-1). CPAP treatment did not change peak oxygen consumption (VO2max) (38.3+/-9.0 vs. 38.9+/-6.9 mlO2/kg/min, p=ns) or peak heart rate (153.4+/-21 min- vs. 155.5+/-22 min(-1), p=ns). There were no significant changes in ventilation or gas exchange variables. However, a decrease in peak systolic blood pressure from 194.5+/-24 mmHg to 186.7+/-27.9 mmHg (p<0.05) with CPAP treatment was found. During recovery a decrease in heart rate (at 1st minute and minutes 3 - 6) and mean arterial pressure (MAP) (minutes 4-7) with CPAP treatment was observed. Significant correlations between VO2max and AHI (r=-0,38, p<0,05); MAP at peak exercise and: AHI, mean oxygen saturation (SaO2) during sleep, minutes of sleep with SaO2<90% (T90); MAP at recovery (minutes 3-8) and T90 before CPAP treatment were also noted. CONCLUSIONS: OSAS patients are not limited on exercise. Treatment with nasal CPAP attenuates circulatory response to incremental exercise on a treadmill.

Blood Pressure↗

PubMed2006

[Maximal respiratory pressures and exercise tolerance in patients with COPD].

UNLABELLED: Many authors reported respiratory muscle function impairment in patients with chronic obstructive pulmonary disease (COPD). Impaired respiratory muscle function may contribute exercise intolerance which is frequently observed in this disease. AIM OF THE STUDY: was to determine the influence of respiratory muscle function on exercise capacity in patients with COPD. METHODS: 23 patients with stable COPD aged 62.7 +/- 9.3 years (6F, 17M; mean post-bronchodilator FEV1 = 47.9 +/-12.4% value predicted) participated in the study. Exercise capacity was assessed by the six-minute walk test and the incremental cardiopulmonary exercise test (CPET) on a treadmill. Maximal respiratory pressures (PImax, PEmax) were evaluated before and directly after CPET. RESULTS: The mean peak oxygen uptake (VO max) was 27.2 +/- 6.1 mlO2/min/kg and the mean distance walked during the 6MWT was 569.4 +/- 101.7 m. Both PIMax and PE max decreased significantly after maximal exercise (71.4 +/-23.0 vs 63.6 +/- 22.2 cmH2O, p = 0.001 and 124.9 +/- 46.5 vs 112.3 +/- 46.6 cm H2O, p = 0.02 respectively). No correlation between VO2max and the 6-minute walk distance and the maximal respiratory pressures was found. We observed a negative correlation between the 6-minute walk distance and the difference between the pre- and post CPET maximal inspiratory pressure. CONCLUSIONS: respiratory muscle function is impaired in patients with COPD but this does not affect exercise performance. Exercise causes a decrease of the respiratory muscle strength.

Aged↗

PubMed2004

[The effect of asthma and COPD exacerbation on exhaled nitric oxide (FE(NO))].

UNLABELLED: Exhaled nitric oxide is a marker of airway inflammation and it is significantly decreased by glucocorticosteroid therapy, especially in patients with asthma. AIM OF THE STUDY: Evaluation of changes in FE(NO) in asthma and COPD exacerbation. MATERIALS AND METHODS: 17 patients with acute asthma and 19 patients with an exacerbation of COPD were enrolled to the study. FE(NO) (chemiluminescence, on-line, restricted breath technique measurement in accordance with the ATS recommendations) was performed for five consecutive days following admission to hospital. Results of the following additional blood investigations: peripheral white blood cell count, ESR, C-reactive protein level, arterial blood gases, spirometry or peak expiratory flow were also analyzed. RESULTS: The average value of FE(NO) on admission was 41.5+/-10.7 ppb (95% CI: 18.8-64.2 ppb) asthma patients and 28.6+/-5.4 ppb (95% CI: 17.4-40.0 ppb) in COPD patients. In asthma patients a significant decrease of FE(NO) on the third day of therapy was observed (41.5 vs 26.1 ppb, p < 0.05). We found a positive correlation between FE(NO) on admission and the peripheral blood eosinophil count. In COPD patients a significant decrease of FE(NO) on the 4th day was noted (28.6 vs 17.5 ppb, p < 0.05). FE(NO) in both groups was higher than that of 19 healthy volunteers previously studied in our laboratory (14.1+/-4.7 ppb; 95% CI: 11.8+/-16.4 ppb). CONCLUSIONS: Exacerbations of asthma and COPD are associated with an increased FE(NO). FE(NO) measurement is a useful tool in the assessment of treatment efficacy. Exhaled nitric oxide may indicate the intensity of allergic inflammation in patients with asthma.

Acute Disease↗

PubMed2004

[Reproducibility of exhaled nitric oxide (FENO) measurements in healthy subjects].

UNLABELLED: The aim of the study was to evaluate the short-term variability of FENO in healthy subjects. METHODS: 33 healthy volunteers (26 F, 7 M) aged 32.6 +/- 9.5 yrs with body mass index (BMI) of 23.3 +/- 3 kg/m2 participated in the study. Exhaled nitric oxide was analyzed on 5 consecutive days with a chemiluminescence analyzer (NIOX, Aerocrine, Sweden) according to the ATS recommendations. The exhalation flow was between 0.045 and 0.055 l/s. The measurements were performed at the same time of the day and the subjects were asked to refrain from eating and drinking for at least one hour before the analysis. RESULTS: The mean value of FENO for the whole group was 13.9 +/- 5.4 ppb, there were no correlations between FENO and age, BMI, sex or the concentration of ambient nitric oxide. Day-to-day coefficient of variation was 13.3 +/- 5.3% (range 4.6 - 23.9%), the value of pooled SD - 2.1 ppb and ICC (intraclass correlation coefficient) was 0.84. No relationship was observed between variability of FENO and intervals between measurement of exhaled nitric oxide and intake of food or beverages. CONCLUSION: Chemiluminescence analysis of FENO with NIOX is a highly reproducible method, however one has to take into account the possibility of about 13% variability of FENO within 5 days.

Adult↗

PubMed2002

[Tracheobronchopathia osteochondroplastica].

Tracheobronchopathia osteochondroplastica (TO) is a rare disease of unknown etiology affecting mainly the trachea and large bronchi. It is characterized by the presence of multiple submucosal osseus and/or cartilaginous nodules. The authors report a case of 74-year-old woman in whom fiberoptic bronchoscopy, performed because of hemoptysis, revealed typical feature of TO. Besides the typical nodules protruding into the lumen of trachea and main bronchi, a small soft nodule in the larynx was found. On histological examination it was showed to be polyp with regions of inflammation and necrosis. The direct relation between such a laryngeal polyp and TO seems to be very unlikely.

Aged↗