Objective   To investigate the expression of heme oxygenase (HO) in pulmonary arteries of rats with hypoxic pulmonary hypertension (HPH).   Methods   A total of 60 rats were employed and equally divided into 5 groups (n=12 in each group)

i. e. control (group  Ⅰ)

HPH (group   Ⅱ)

hemin (group    Ⅲ)

tin protoporphyrin (SnPP) (group    Ⅳ)

and low concentration CO group (group Ⅴ). Of them

the rats from middle 3 groups were treated with hypoxia under normal pressure for 7 h

in every day except Sunday

consecutively for 3 weeks. Hemin and tin protoporphyrin (SnPP) were given half an hour before hypoxia while low concentration CO at 2 h after hypoxia. HO-1 activity of pulmonary arteries tissues was tested with ultraviolet spectrophotometry. The expression of HO was detected with reverse transcriptionpolymerase chain reaction (RT-PCR)

immunohistochemical staining and in situ hybridization.    Results   ① The bilirubin production increased significantly in group   [(396.28±69.62) pmol·mg

-1

·h

-1

]

group     [(668.56±189.29) pmol·mg

-1

·h

-1

]

group  [(267.38±88.59) pmol·mg

-1

·h

-1



]

and group  [(589.32±132.35) pmol·mg

-1.

h

-1

]

as compared with those in group    [(125.62±31.52) pmol·mg

-1

·h

-1

]

. ② The levels of HO-1 mRNA expression of pulmonary arteries in group    Ⅱ

group    Ⅲ

group  Ⅳ   and group  Ⅴ  were significantly higher than those in group   Ⅰ. The most significant HO-1 mRNA expression was found in group    Ⅴ (P0.01). The levels of HO-1 mRNA expression of pulmonary arteries in group  Ⅲ   and group  Ⅴ   were higher than those in group    Ⅱ

but it was lower in group    Ⅳ   than that in group    Ⅱ. ③ The strong positive granules of HO-1 were observed  in pulmonary arteries intima and media in group   Ⅱ

group   Ⅲ    and group    Ⅳ

while group    Ⅲ   and group  Ⅳ    involved more positive granules of HO-1 as compared with those in group    Ⅱ. ④ The staining was deepened in three layers of the pulmonary arteries in group    Ⅱ

while the staining was deepened more in group   Ⅲ  and group    Ⅳ. No significant change was found in staining of HO-2 in different groups.   Conclusion   CO can up-regulate the expression of HO-1

and this may play important roles in the genesis and development of pulmonary hypertension.