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Airway muscle in preterm infants: changes during development
S L Sward-Comunelli1, S M Mabry, W E Truog
1Department of Pediatrics, Children's Mercy Hospital, University of Missouri-Kansas City School of Medicine, USA.
Insights
Airway smooth muscle is present in premature infants from 23 weeks gestation. Infants with chronic lung disease (CLD) show increased airway muscle, suggesting bronchospasm is possible in very low birth weight infants.
Area of Science:
- Neonatal physiology
- Pulmonary development
- Pediatric pathology
Background:
- Airway smooth muscle plays a critical role in respiratory function.
- Understanding airway muscle development is crucial for managing neonatal respiratory conditions.
- Chronic lung disease (CLD) in infants can lead to significant airway abnormalities.
Purpose of the Study:
- To quantify airway muscle development in infants across a range of gestational ages.
- To compare airway muscle in healthy infants with those suffering from CLD.
- To investigate the potential for bronchospasm in premature infants.
Main Methods:
- Studied 55 human lungs from infants (23-41 weeks gestation), including 9 with CLD.
- Utilized immunohistochemistry for alpha-smooth muscle actin staining.
- Employed computerized image analysis to measure airway muscle, epithelium, and lumen size.
Main Results:
- Airway muscle is present from 23 weeks gestation in all airway levels.
- Control lungs showed consistent muscle quantity relative to airway circumference from 25 weeks gestation.
- Infants with CLD exhibited significantly more airway muscle in larger airways (>1500 microns circumference).
Conclusions:
- Airway muscle development is established early in gestation.
- Preterm infants with CLD demonstrate increased airway muscle, particularly in larger airways.
- The findings suggest the potential for bronchospasm in very low birth weight infants shortly after birth.
Objective:
To quantitate airway muscle changes in infants born at 23 to 41 weeks' gestation (control subjects) and to compare the changes with those in infants with chronic lung disease.
Methods:
Fifty-five human lungs (from infants born at 23 to 41 weeks' gestation) were studied: 46 from infants who died of various diseases within 72 hours of birth, and 9 from infants with CLD (infants born at 26.9 +/- 0.5 weeks' gestation, who lived 17 +/- 8 days). All the lungs were perfused via the trachea and pulmonary artery in a standardized protocol. Formalin-fixed tissues in paraffin blocks were cut 5 microns thick. Sections were immunohistochemically stained for alpha-smooth muscle actin. By using computerized image analysis to quantitate images digitized into the computer, we measured the area of muscle, epithelium, airway lumen, and length of basement membrane in 18 airways, from the smallest bronchioles to bronchi, in each infant.
Results:
Muscle was present at 23 weeks' gestation at all levels of the bronchial tree, and from 25 weeks to term the control lungs had a similar quantity of muscle at any given airway circumference. Relative to airway size, there was more muscle in small airways, less than 1000 microns in circumference, than in larger airways. In airways greater than 1500 microns in circumference, infants with CLD had significantly more muscle than did control lungs.
Conclusions:
Airway muscle is present at 23 weeks' gestation at all levels of the conducting airways. The 25-week gestation infants had a quantity of airway muscle relative to airway circumference similar to that of term infants. Preterm infants with CLD who were aged 9 to 29 days have increased airway muscle in airways greater than 1500 microns in circumference. Bronchospasm in very low birth weight infants is possible within the first days of life.