Savas Ustunova1, Selcuk Takir2, Nadim Yilmazer3, Huri Bulut4, Didem Altindirek5, Ozden Hatirnaz Ng6, Cihan Demirci Tansel7, B Sonmez Uydes Dogan8, Ugur Ozbek9, Elif Ilkay Armutak10, Ebru Gurel Gurevin7. 1. Department of Physiology, School of Medicine, Bezmialem Vakif University, Istanbul, Turkey sustunova@bezmialem.edu.tr. 2. Department of Medical Pharmacology, School of Medicine, Giresun University, Giresun, Turkey. 3. Department of Biology, Faculty of Arts and Sciences, Namik Kemal University, Tekirdag, Turkey. 4. Department of Medical Biochemistry, School of Medicine, Istinye University, Istanbul, Turkey. 5. Department of Genetics, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. 6. Department of Medical Biology, School of Medicine, Acibadem Mehmet Ali Aydinlar University, Istanbul, Turkey. 7. Department of Biology, Faculty of Science, Istanbul University, Istanbul, Turkey. 8. Department of Pharmacology, Faculty of Pharmacy, Istanbul University, Istanbul, Turkey. 9. Department of Medical Genetics, School of Medicine, Acibadem Mehmet Ali Aydinlar University, Istanbul, Turkey. 10. Department of Histology and Embryology, Faculty of Veterinary Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Abstract
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. Copyright
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. Copyright