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 μM) 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.

中文翻译：

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硫化氢和一氧化氮协同对离体大鼠心脏缺血/再灌注损伤的心脏保护作用

背景/目的：本研究旨在为缺血/再灌注 (I/R) 损伤中硫化氢 (H2S) 和一氧化氮 (NO) 之间的相互作用提供进一步的证据。材料和方法：使用Langendorff 技术，使用H2S 供体硫氢化钠（NaHS，40 μM）和胱硫醚γ-裂解酶（CTH 或CSE）抑制剂DL-炔丙基甘氨酸（PAG，1 mM）研究大鼠心脏。在分离前给予 NO 合酶抑制剂 L-NG-硝基精氨酸甲酯 (L-NAME, 30 mg/kg, 7 天)。将心脏匀浆用于生化和分子分析。结果：NaHS 逆转了 I/R 诱导的心脏功能损害，增加了组织一氧化氮的产生并减少了心脏损伤的组织标志物，而 L-NAME 抑制了这些影响。CTH 的表达随着 PAG 的增加而增加，被L-NAME压制了。结论：H2S 和 NO 相互增加了彼此的产生，表明它们在对 I/R 损伤的心脏保护中相互作用和合作。