Ventilator-dependent infants are thought to have airway bronchospasm causing desaturation. Preterminal bronchiolar acinar muscle spasm may also be a source of desaturation. The development of acinar muscle throughout gestation and with BPD has not been reported. Using a library of formalin-fixed lungs, we assessed acinar muscle at the alveolar-alveolar duct(AA) and respiratory bronchiole (RB) levels. Infants who died <48 hrs postnatally were categorized by gestational age: 21-22 (n=5), 23-24(n=7), 25-26 (n=6), 27-30 (n=6), 31-34(n=4), 35-36 (n=5), and 37-42 (n=5) wks. We analyzed lungs from thirteen infants born at 23-28 wks gestation who died 2-4 wks later with either minimal ventilator support (n=6) without BPD(MV), or greater support (n=7) with findings of BPD at postmortem. Lungs were expanded and fixed at 24 cm H2O pressure for 5 days with 10% formalin. The tissue was stained using a monoclonal antibody to α-smooth muscle actin (Sigma).

Using computerized image analysis, AA muscle was semiquantitated as actin area per length of AA wall length and RB muscle as muscle area per length of RB wall. Six measurements per lung were obtained for both sites by observers blinded to clinical history. Individual values were standardized by dividing by the crown-heel length. For both AA and RB, the 23-24 wk infants tended to have more muscle than all other age groups, and significantly more than at 21-22, 35-36, and 37-42 wks. Infants with BPD, whose chronological age was 27-30 wks, had significantly more muscle than 27-30 wk control infants. The MV group was not different from the 27-30 wk controls. We conclude that acinar muscle per wall length reaches a maximum at 23-24 wks and decreases relative to gestational age and that infants with findings of BPD have increased acinar muscle--a potential source of ventilation-perfusion abnormalities.