Ventilation homogeneity improves with growth early in life.

Some studies have suggested that lung clearance index (LCI) is age-independent among healthy subjects early in life, which implies that ventilation distribution does not vary with growth. However, other studies of older children and adolescents suggest that ventilation becomes more homogenous with somatic growth. We describe a new technique to obtain multiple breath washout (MBWO) in sedated infants and toddlers using slow augmented inflation breaths that yields an assessment of LCI and the slope of phase III, which is another index of ventilation inhomogeneity.

Evaluation of airway reactivity and immune characteristics as risk factors for wheezing early in life.

Background: Childhood asthma is most often characterized by recurrent wheezing, airway hyperreactivity, and atopy; however, our understanding of these relationships from early in life remains unclear. Respiratory tract illnesses and atopic sensitization early in life might produce an interaction between innate and acquired immune responses, leading to airway inflammation and heightened airway reactivity.

Objective: We hypothesized that premorbid airway reactivity and immunologic characteristics of infants without prior episodes of wheezing would be associated with subsequent wheezing during a 1-year follow-up.

Lung growth in infants and toddlers assessed by multi-slice computed tomography.

Rationale And Objectives: Postnatal lung growth and development have primarily been evaluated from a very limited number of autopsied lungs, but it remains unclear whether alveolarization of the lung is complete during infancy and whether the conducting airways grow proportionately. The purpose of this study was to evaluate lung growth and development in vivo in infants and toddlers using multislice computed tomography.

Materials And Methods: Thirty-eight subjects (14 male, 24 female) aged 17 to 142 weeks underwent low-dose volumetric high-resolution computed tomographic imaging at an inflation pressure of 20 cm H(2)O during an induced respiratory pause.

Growth of lung parenchyma in infants and toddlers with chronic lung disease of infancy.

Rationale: The clinical pathology describing infants with chronic lung disease of infancy (CLDI) has been limited and obtained primarily from infants with severe lung disease, who either died or required lung biopsy. As lung tissue from clinically stable outpatients is not available, physiological measurements offer the potential to increase our understanding of the pulmonary pathophysiology of this disease.

Objectives: We hypothesized that if premature birth and the development of CLDI result in disruption of alveolar development, then infants and toddlers with CLDI would have a lower pulmonary diffusing capacity relative to their alveolar volume compared with full-term control subjects.

Growth of the lung parenchyma early in life.

Rationale: Early in life, lung growth can occur by alveolarization, an increase in the number of alveoli, as well as expansion. We hypothesized that if lung growth early in life occurred primarily by alveolarization, then the ratio of pulmonary diffusion capacity of carbon monoxide (Dl(CO)) to alveolar volume (V(A)) would remain constant; however, if lung growth occurred primarily by alveolar expansion, then Dl(CO)/V(A) would decline with increasing age, as observed in older children and adolescents.

Objectives: To evaluate the relationship between alveolar volume and pulmonary diffusion capacity early in life.

Expired nitric oxide and airway reactivity in infants at risk for asthma.

Background: Family histories of atopy, as well as histories of atopic dermatitis and food allergy, are important risk factors for an infant to have asthma. Although atopic sensitization appears to contribute to the development of asthma, it is unclear when the airways become involved with the atopic process and whether airway function relates to the atopic characteristics of the infant.

Objective: We sought to evaluate whether atopic infants without prior episodes of wheezing have increased expired nitric oxide (eNO) levels and heightened airway reactivity.