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Am J Physiol Lung Cell Mol Physiol 291: L912-L922, 2006. First published July 7, 2006; doi:10.1152/ajplung.00480.2005
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Therapeutic hypercapnia prevents chronic hypoxia-induced pulmonary hypertension in the newborn rat

Crystal Kantores,1,* Patrick J. McNamara,3,5,* Lilian Teixeira,3 Doreen Engelberts,2 Prashanth Murthy,1 Brian P. Kavanagh,2,4,6 and Robert P. Jankov1,5

1Clinical Integrative Biology, Sunnybrook Research Institute; 2Lung Biology and 3Cardiovascular Programs, The Hospital for Sick Children Research Institute; and the Departments of 4Critical Care, 5Pediatrics, and 6Physiology, University of Toronto, Toronto, Ontario, Canada

Submitted 10 November 2005 ; accepted in final form 5 July 2006

Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO2) may have beneficial effects on 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 days 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 upregulation 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 on the endothelin pathway.

carbon dioxide; endothelin; oxidant stress; 8-isoprostane; echocardiography


Address for reprint requests and other correspondence: R. P. Jankov, Dept. of Newborn and Developmental Paediatrics, Sunnybrook Health Sciences Centre, 76 Grenville St., Toronto, Ontario, Canada M5S 1B2 (e-mail: robert.jankov{at}sunnybrook.ca)




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