Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart.
In vivo (Athens, Greece), vol.34, no.5, pp.2507-2516, 2020 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 34 Issue: 5
- Publication Date: 2020
- Doi Number: 10.21873/invivo.12067
- Journal Name: In vivo (Athens, Greece)
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE
- Page Numbers: pp.2507-2516
- Keywords: Hydrogen sulfide, nitric oxide, isolated heart, ischemia/reperfusion injury, oxidative damage, ISCHEMIA-REPERFUSION INJURY, H2S PROTECTS, SYNTHASE, EXPRESSION, INHIBITION, FAILURE, HYPERTENSION, MICE
- Open Archive Collection: AVESIS Open Access Collection
- Acibadem Mehmet Ali Aydinlar University Affiliated: Yes
Abstract
Background/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.