Üstünova, SavaşTakır, SelçukYılmazer, NadimBulut, HuriAltındirek, DidemHatırnaz, ÖzdenGürel Gürevin, Ebru2022-05-112022-05-1120200258-851X1791-7549https://doi.org/10.21873/invivo.12067https://hdl.handle.net/20.500.11776/6910Background/Aim: This study was designed to provide further evidence for the interactions between hydrogen sulfide (H2S) and nitric oxide (NO) in ischemia/reperfiision (I/R) injury. Materials and Methods: Rat hearts were studied with the Langendorff technique using the H2S donor sodium hydrosulfide (NaHS, 40 mu 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.en10.21873/invivo.12067info:eu-repo/semantics/openAccessHydrogen sulfidenitric oxideisolated heartischemia/reperfusion injuryoxidative damageIschemia-Reperfusion InjuryH2s ProtectsSynthaseExpressionInhibitionFailureHypertensionMiceArticle34525072516Q4WOS:0005749790000072-s2.0-8509018231532871779Q2