Date on Master's Thesis/Doctoral Dissertation


Document Type

Master's Thesis

Degree Name



Pharmacology and Toxicology

Degree Program

Pharmacology and Toxicology, MS

Committee Chair

Huang, Jiapeng

Committee Member

Cai, Lu

Committee Member

Koukam, J. Calvin

Committee Member

Young, Jamie

Committee Member

Buchanan, Robert

Author's Keywords

Cadmium; pulmonary; arterial; hypertension


We reported pulmonary artery hypertension (PAH) patients had elevated levels of Cd in both blood and urine, therefore, this study tested whether Cd directly induces PAH or facilitates PAH pathogenesis in mouse models. C57/6J mice were initially exposed to drinking water with or without 5ppm Cd for 8 weeks. Then, half the mice in both control and Cd groups were given SU5416 and hypoxia (SuHx) for 4 weeks to induce PAH, resulting in 4 subgroups: Control, Cd, PAH, and Cd+PAH. Diastolic and systolic functions of the left and right ventricles (LV, RV) were examined with echocardiography before and after PAH. Eight-week Cd exposure did not significantly change RV structure or systolic function. However, 12-week Cd exposure significantly increased RV systolic function, exacerbated PAH-associated RV dysfunction, and significantly increased structural remodeling in LV, RV, and lungs, although did not further exacerbate RV and lung remodeling in the setting of PAH.