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Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart

机译:硫化氢和一氧化氮中的心脏保护免受缺血/再灌注损伤在孤立的大鼠心脏

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Background/Aim: This study was designed to provide further evidence for the interactions between hydrogen sulfide (H2S) and nitric oxide (NO) in ischemia/reperfusion (I/R) injury. Materials and Methods: Rat hearts were studied with the Langendorff technique using the H2S donor sodium hydrosulfide (NaHS, 40 M) and the cystathionine gamma-lyase (CTH or CSE) inhibitor DL-propargylglycine (PAG, 1 mM). NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 30 mg/kg, 7 days) was administered before the isolation. The hearts were homogenized for biochemical and molecular analysis. Results: NaHS reversed I/R-induced cardiac performance impairment, increased tissue nitric oxide production and decreased tissue markers for cardiac injury, while L-NAME inhibited these effects. The expression of CTH was increased with PAG, which was suppressed by L-NAME. Conclusion: H2S and NO increase each other's production suggesting their interaction and cooperation in cardioprotection against I/R injury.
机译:背景/目的:本研究旨在提供进一步的证据,用于在缺血/再灌注(I / R)损伤中硫化氢(H2S)和一氧化氮(NO)之间的相互作用。材料和方法:使用H2S供体硫化钠(NaH,40M)和胱硫脲γ-裂解酶(CTH或CSE)抑制剂D1-丙基甘氨酸(PAG,1mM)用Langendorff技术研究了大鼠心脏。在分离前施用不施用合酶抑制剂L-NG-NITRORAARINE甲酯(L-NAME,30mg / kg,7天)。心脏均质化以进行生化和分子分析。结果:NAHS逆转I / R诱导的心脏性能损伤,增加组织一氧化氮产生和心损伤的组织标志物,而L-NAME抑制了这些效果。用PAG增加CTH的表达,由L-name抑制。结论:H2S且彼此的生产不增加,暗示其对I / R损伤的心脏保护互动和合作。

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