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Mechanisms of Heme Oxygenase-1-Mediated Cardiac and Pulmonary Vascular Protection in Chronic Hypoxia*: Roles of Carbon Monoxide and Bilirubin

Sally H. Vitali, MD; S.A. Mitsialis; Helen Christou, MD; Angeles Fernandez-Gonzalez;; Xianlan Liu; Stella Kourembanas, MD
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*From the Children’s Hospital Boston, Boston, MA.

Correspondence to: Sally H. Vitali, MD, MSICU Office, FA517, Children’s Hospital Boston, 300 Longwood Ave, Boston, MA 02115; e-mail: sally.vitali@tch.harvard.edu



Chest. 2005;128(6_suppl):578S-579S. doi:10.1378/chest.128.6_suppl.578S
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Heme oxygenase (HO)-1 null mice have a maladaptive right ventricular (RV) response to chronic hypoxia-induced pulmonary hypertension. After 7 weeks of exposure to 8 to 10% fraction of inspired oxygen, the majority of HO-1 null mice develop evidence of RV oxidative stress, apoptosis, and infarction, while wild-type mice do not. The cytoprotective effects of HO-1 are thought to result from its enzymatic products carbon monoxide (CO), a vasodilator with antiinflammatory effects, and bilirubin, an antioxidant.

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