Tidal fractional exhaled nitric oxide (FE(NO)) changes were investigated in healthy, unsedated infants with or without prenatal tobacco exposure. Tidal flow (V), FE(NO), and CO(2) were measured in 20 healthy, unsedated infants [age: 25-58 days, length: 56.5 +/- 2.5 (SE) cm]. NO output (VNO) was calculated (VNO = FE(NO) x V). Two approaches were used to investigate within-breath changes of FE(NO) and VNO. First, we identified phases II and III from the expiratory capnogram. Second, we divided expiration into time-based quartiles. Tidal FE(NO) (range: 14.5 +/- 1.6 to 17.6 +/- 2.1 parts/billion: quartile 4 and phase II, respectively) was not different between portions and exhibited significant negative V dependence. VNO was significantly dependent on the expiratory portion, with quartile 4 being significantly lower than the remaining expiratory portions. Infants exposed to prenatal cigarette smoke (n = 7) exhibited significantly lower FE(NO) and VNO compared with nonexposed (n = 13) infants. We conclude that tidal FE(NO) is V dependent and that VNO may be a more suitable outcome parameter in variable V conditions. Prenatal tobacco exposure resulted in a decreased FE(NO) and VNO in infants.
Small airway disease in infants is characterised by abnormal lung volume and uneven ventilation distribution. An inert tracer gas washin/washout technique using a pulsed ultrasonic flow meter is presented to measure functional residual capacity (FRC) and ventilation distribution in spontaneously breathing and unsedated infants. With a pulsed ultrasound sent through the main stream of the flow meter, flow, volume and MM of the breathing gas can be calculated. Sulphur hexafluoride was used as a tracer gas. In a mechanical lung model (volume range 53-188 mL) and in 12 healthy infants (aged 38.3+/-9.2 days; mean+/-SD) accuracy and reproducibility of the technique was assessed. Indices of ventilation distribution such as alveolar-based mean dilution number (AMDN) and pulmonary clearance delay (PCD) were calculated. Mean error of volume measurement in the lung model was 0.58% (coefficient of variance (CV) 1.3%). FRC was in the low predicted range for normal infants (18.0+/-2.0 mL x kg(-1)) and highly reproducible (5.5+/-1.7% intra-subject CV). AMDN was 1.63+/-0.15 and PCD was 52.9+/-11.1%. Measurement of functional residual capacity and ventilation distribution using a sulphur hexafluoride washin/washout and an ultrasonic flow meter proved to be highly accurate and reproducible in a lung model and in healthy, spontaneously breathing and unsedated infants.
In a prospective healthy birth cohort, we determined whether levels of exhaled nitric oxide (eNO) in healthy unselected infants at the age of 1 month were associated with maternal atopic disease and prenatal and early postnatal environmental exposures. Tidal eNO was measured in 98 healthy, unsedated infants (35 from mothers with atopy) (mean age +/- SD, 36.0 +/- 6.2 days) and was compared with histories taken in standardized interviews. eNO was higher in males compared with females (17.7 vs. 14.6 ppb, p = 0.042) and infants exposed to postnatal maternal smoking (+4.4 ppb, p = 0.027), adjusting for weight and tidal breathing parameters. Prenatal tobacco exposure was associated with higher eNO (+12.0 ppb, p = 0.01) in infants of mothers with asthma and lower eNO (-5.7 ppb) in infants of mothers without asthma (p for interaction < 0.0001). Coffee consumption in pregnancy decreased eNO (-6.0 ppb, p = 0.008) only in children of mothers with atopy (p for interaction = 0.015). Paternal atopy had no influence. In the early phase of immunologic development, before the onset of infections and allergic disease, the effect of prenatal or early postnatal environmental factors on eNO was modified by the presence of maternal atopic disease. This underlines the complex interaction of maternal and environmental factors in the development of airway disease.
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