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Department of Pediatrics, University of Utah, Salt Lake City, Utah 84132
Nitric oxide (NO), produced in lung
vascular endothelium and airway epithelium, has an important role in
regulating smooth muscle cell growth and tone. Chronic lung disease, a
frequent complication of premature birth, is characterized by excess
abundance, tone, and reactivity of smooth muscle in the pulmonary
circulation and conducting airways, leading to increased lung vascular
and airway resistance. Whether these structural and functional changes are associated with diminished pulmonary expression of endothelial nitric oxide synthase (eNOS) protein is unknown. Both quantitative immunoblot analysis and semiquantitative immunohistochemistry showed
that there was less eNOS protein in the endothelium of small
intrapulmonary arteries and epithelium of small airways of preterm
lambs that were mechanically ventilated for 3 wk compared with control
lambs born at term. No significant differences were detected for other
proteins (inducible NOS, 
-smooth muscle actin, and pancytokeratin).
Lung vascular and respiratory tract resistances were greater in the
chronically ventilated preterm lambs compared with control term lambs.
These results support the notion that decreased eNOS in the pulmonary
circulation and respiratory tract of preterm lambs may contribute to
the pathophysiology of chronic lung disease.
chronic lung disease of prematurity; bronchopulmonary dysplasia; pulmonary vascular resistance; airway resistance; pulmonary circulation; respiratory failure; immunohistochemistry
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