[Effect of hydrogen sulfide on oxidative stress in hypoxic pulmonary hypertension].
OBJECTIVE
To study the modulatory effect of hydrogen sulfide (H(2)S) on oxidative stress in the development of pulmonary hypertension induced by hypoxia.


METHODS
Twenty male Wistar rats were randomly divided into control group (n=6), hypoxic group (n=6) and hypoxia+NaHS group (n=8). Hypoxic challenge was performed everyday for 21 days. NaHS solution was injected intra-peritoneally everyday before hypoxic challenge for rats in the hypoxia+NaHS group. After 21 days of hypoxia, the mean pulmonary artery pressure(mPAP) was measured by cardiac catheterization. The weight ratio of right ventricle to left ventricle+septum [RV/(LV+SP)] was also measured. The lung homogenates were assayed for total antioxidant capacity(T-AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione (GSH), malondialdehyde(MDA) and hydroxy radical(*OH), and the SOD mRNA levels were assayed by real time polymerase chain reaction.


RESULTS
After three weeks of hypoxic disposure, hypoxic hypertension and vascular remodeling developed. Compared with the control group, the mPAP[(23.7+/-2.2) mm Hg vs (16.3+/-3.7) mm Hg,P<0.01] and the weight ratio of RV/(LV+SP) increased (P<0.01), but lung tissue T-AOC was decreased by 21.4% (P<0.01).But GSSG was increased by 68.5% (P<0.01) as compared with those of the control rats. However, compared with those of the hypoxic group, the mPAP in rats of hypoxia+NaHS group was decreased [(16.3+/-2.8) mm Hg vs (23.7 +/-2.2) mm Hg]. Administration of NaHS increased T-AOC by 18.8% (P<0.05) but eliminated GSSG by 23.2% (P<0.05) in rats of hypoxia+NaHS group as compared with the hypoxic group. There were no significant changes in lung tissue SOD mRNA level and its capacity among the three groups.


CONCLUSIONS
Hydrogen sulfide acted as antioxidant during the oxidative stress of hypoxic pulmonary hypertension, and the mechanism was partly through attenuating the content of GSSG.
Wei
Hong Ling
HL
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Du
Jun Bao
JB
Tang
Chao Shu
CS
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D006976:Hypertension, Pulmonary / Q000378:metabolism*; D000860:Hypoxia / Q000503:physiopathology*; D008168:Lung / Q000378:metabolism*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D013482:Superoxide Dismutase; D005978:Glutathione; D006862:Hydrogen Sulfide