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Am J Physiol Lung Cell Mol Physiol 282: L693-L702, 2002. First published November 16, 2001; doi:10.1152/ajplung.00211.2001
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Vol. 282, Issue 4, L693-L702, April 2002

Carbon monoxide promotes hypoxic pulmonary vascular remodeling

Martha Sue Carraway1, Andrew J. Ghio2, Hagir B. Suliman1, Jacqueline D. Carter2, A. Richard Whorton3, and Claude A. Piantadosi1

Departments of 1 Medicine and 3 Pharmacology, Duke University Medical Center, Durham 27710; and 2 Division of Human Studies, Environmental Protection Agency, Chapel Hill, North Carolina 27514

CO is a biologically active gas that produces cellular effects by multiple mechanisms. Because cellular binding of CO by heme proteins is increased in hypoxia, we tested the hypothesis that CO interferes with hypoxic pulmonary vascular remodeling in vivo. Rats were exposed to inspired CO (50 parts/million) at sea level or 18,000 ft of altitude [hypobaric hypoxia (HH)], and changes in vessel morphometry and pulmonary pressure-flow relationships were compared with controls. Vascular cell single strand DNA (ssDNA) and proliferating cell nuclear antigen (PCNA) were assessed, and changes in gene and protein expression of smooth muscle alpha -actin (sm-alpha -actin), beta -actin, and heme oxygenase-1 (HO-1) were evaluated by Western analysis, RT-PCR, and immunohistochemistry. After 21 days of HH, vascular pressure at constant flow and vessel wall thickness increased and lumen diameter of small arteries decreased significantly. The presence of CO, however, further increased both pulmonary vascular resistance (PVR) and the number of small muscular vessels compared with HH alone. CO + HH also increased vascular PCNA and nuclear ssDNA expression compared with hypoxia, suggesting accelerated cell turnover. CO in hypoxia downregulated sm-alpha -actin and strongly upregulated beta -actin. CO also increased lung HO activity and HO-1 mRNA and protein expression in small pulmonary arteries during hypoxia. These data indicate an overall propensity of CO in HH to promote vascular remodeling and increase PVR in vivo.

pulmonary hypertension; hypoxic pulmonary vasoconstriction; actin; heme oxygenase


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