Abstract:Background
Bronchopulmonary dysplasia (BPD) with airway hyperreactivity is a long‐term pulmonary complication of prematurity. The endogenous nonadrenergic, noncholinergic signaling molecule, S‐nitrosoglutathione (GSNO) and its catabolism by GSNO reductase (GSNOR) modulate airway reactivity. Tracheomalacia is a major, underinvestigated complication of BPD. We studied trachealis, left main bronchus (LB), and intrapulmonary bronchiolar (IPB) relaxant responses to GSNO in a murine hyperoxic BPD model.
Methods
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