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1 Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
* To whom correspondence should be addressed. E-mail: Jaques.Belik{at}Sickkids.ca.
Neonatal rats exposed to 60% O2 for 14 days develop lung changes compatible with human bronchopulmonary dysplasia and pulmonary hypertension. Our aim was to evaluate and compare the newborn and adult rat pulmonary vascular and airway smooth muscle force generation and relaxation potential following exposure to 60% O2 for 14 days. Vascular and airway intrapulmonary rings 100 µm in diameter were mounted on a myograph and bathed in Krebs-Henseleit solution bubbled with air/ 6% CO2 at 37 oC. Significant age-dependent changes in intrapulmonary arteries and their neighboring airways muscle properties were observed. Whereas hyperoxia enhanced force in neonatal vascular and airway muscle, the opposite was seen in adult samples. No changes in endothelium-dependent vascular relaxation were observed at either age, but the dose response to an endothelium-independent NO-donor was altered. In the newborn experimental animals the relaxation was reduced, whereas in their adult counterparts it was enhanced. Following O2 exposure, the bronchial muscle relaxation response to epithelium-dependent and -independent stimulation was not altered in either age group, whereas the epithelium-dependent response was decreased only in the adult. The antioxidant Trolox, or an endothelin A and B receptor antagonist, reversed the vascular and airway muscle's hyperoxia-induced changes. We conclude that chronic O2 exposure in the newborn rat results in enhanced lung vascular and airway muscle contraction potential via a mechanism involving reactive oxygen species and the endothelin pathway. The present findings also suggest that the newborn is more susceptible to airway hyperresponsiveness following chronic O2 exposure.
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