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Am J Physiol Lung Cell Mol Physiol (July 7, 2006). doi:10.1152/ajplung.00480.2005
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Submitted on November 10, 2005
Accepted on July 5, 2006

Therapeutic Hypercapnia Prevents Chronic Hypoxia-Induced Pulmonary Hypertension in the Newborn Rat

Crystal Kantores1, Patrick J McNamara1, Lilian Teixeira1, Doreen Engelberts1, Prashanth Murthy1, Brian P Kavanagh1, and Robert P Jankov1*

1 Clinical Integrative Biology, Sunnybrook & Womens Research Institute, Toronto, Canada; Lung Biology Programme, Hospital for Sick Children Research Institute, Toronto, Canada; Paediatrics, University of Toronto, Toronto, Canada; Anaesthesia, University of Toronto, Toronto, Canada; Physiology, University of Toronto, Toronto, Canada

* To whom correspondence should be addressed. E-mail: robert.jankov{at}sw.ca.

Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO2) may have beneficial effects upon the pulmonary circulation. We tested the hypothesis that exposure to CO2 would protect against chronic pulmonary hypertension in newborn rats. Atmospheric CO2 was maintained at < 0.5% (normocapnia), 5.5% or 10% during exposure from birth for 14 d to normoxia (21% O2) or moderate hypoxia (13% O2). Pulmonary vascular and hemodynamic abnormalities in animals exposed to chronic hypoxia included increased pulmonary arterial resistance, right ventricular hypertrophy and dysfunction, medial thickening of pulmonary resistance arteries and distal arterial muscularization. Exposure to 10% CO2 (but not to 5.5% CO2) significantly attenuated pulmonary vascular remodeling and increased pulmonary arterial resistance in hypoxia-exposed animals (p < 0.05), whereas both concentrations of CO2 normalized right ventricular performance. Exposure to 10% CO2 attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented up-regulation of endothelin-1, a critical mediator of pulmonary vascular remodeling. We conclude that hypercapnic acidosis has beneficial effects on pulmonary hypertension and vascular remodeling induced by chronic hypoxia, which we speculate derives from antioxidant properties of CO2 on the lung and consequent modulating effects upon the endothelin pathway.




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