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Articles in PresS, published online ahead of print November 16, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00211.2001
Submitted on June 8, 2001
Accepted on December 31, 1969
1 Medicine, Duke University Medical Center, Durham, NC, USA
2 Environmental Protection Agency, Chapel Hill, NC, USA
3 Pharmacology, Duke University Medical Center, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: piant001{at}mc.duke.edu.
Carbon monoxide (CO) is a biologically active gas, which produces cellular effects by multiple mechanisms. Because cellular binding of CO by heme proteins is increased by hypoxia, we tested the hypothesis that CO interferes with hypoxic pulmonary vascular remodeling in vivo. Rats were exposed to inspired CO (50ppm) at sea level or at high altitude (18,000 feet), and changes in vessel morphometry and pulmonary vascular resistance (PVR) were compared to controls. Vascular cell ssDNA and proliferating cell nuclear antigen (PCNA) were assessed, and changes in gene and protein expression of smooth muscle 
-actin (sm--actin), ß-actin and heme oxygenase-1 (HO-1) were evaluated by Western analysis, rtPCR, and immunohistochemistry. Over 21 days of hypoxia, PVR and vessel wall thickness increased and lumen diameter of small arteries decreased significantly. The presence of CO, however, further increased both PVR and the number of small muscular vessels compared to hypoxia alone. CO in hypoxia also increased vascular PCNA and nuclear ssDNA expression compared to hypoxia, suggesting cell turnover had been accelerated. The sm--actin was down regulated and ß-actin up regulated strongly by CO in hypoxia. 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 hypoxia to promote vascular remodeling and increase PVR in vivo.
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