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

BACKGROUND/AIMThis 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 METHODSRat hearts were studied with the Langendorff technique using the H2S donor sodium hydrosulfide (NaHS,...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:In vivo (Athens) 2020-09, Vol.34 (5), p.2507-2516
Hauptverfasser: USTUNOVA, SAVAS, TAKIR, SELCUK, YILMAZER, NADIM, BULUT, HURI, ALTINDIREK, DIDEM, NG, OZDEN HATIRNAZ, TANSEL, CIHAN DEMIRCI, DOGAN, B. SONMEZ UYDES, OZBEK, UGUR, ARMUTAK, ELIF ILKAY, GUREVIN, EBRU GUREL
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:BACKGROUND/AIMThis 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 METHODSRat 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. RESULTSNaHS 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. CONCLUSIONH2S and NO increase each other's production suggesting their interaction and cooperation in cardioprotection against I/R injury.
ISSN:0258-851X
1791-7549
DOI:10.21873/invivo.12067