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  • Title: [Effect of hydrogen sulfide on oxidative stress in hypoxic pulmonary hypertension].
    Author: Wei HL, Du JB, Tang CS.
    Journal: Beijing Da Xue Xue Bao Yi Xue Ban; 2007 Dec 18; 39(6):565-9. PubMed ID: 18087542.
    Abstract:
    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. CONCLUSION: Hydrogen sulfide acted as antioxidant during the oxidative stress of hypoxic pulmonary hypertension, and the mechanism was partly through attenuating the content of GSSG.
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