Stojanovic, M. (56403464200)M. (56403464200)StojanovicZivkovic, V. (55352337400)V. (55352337400)ZivkovicSrejovic, I. (55754581700)I. (55754581700)SrejovicJakovljevic, V. (56425747600)V. (56425747600)JakovljevicJeremic, N. (56609154900)N. (56609154900)JeremicDjuric, D. (36016317400)D. (36016317400)Djuric2025-06-122025-06-122016https://doi.org/10.1556/2060.103.2016.4.3https://www.scopus.com/inward/record.uri?eid=2-s2.0-85015824779&doi=10.1556%2f2060.103.2016.4.3&partnerID=40&md5=3ef348c0567b9ec4fc21108b29e30560https://remedy.med.bg.ac.rs/handle/123456789/7420This study aimed to assess the role of H2S in homocysteine-induced cardiodynamic effects in the isolated rat heart. The hearts were retrogradely perfused according to the Langendorff technique. The maximum and minimum rates of pressure in the left ventricle (dp/dt max, dp/dt min), systolic and diastolic left ventricular pressures (SLVP, DLVP), heart rate (HR), and coronary flow (CF) were measured. A spectrophotometrical method was used to measure the following oxidative stress markers: index of lipid peroxidation (thiobarbituric acid reactive substances, TBARS), nitrite level (NO2-), superoxide anion radicals (O2•-), and hydrogen peroxide (H2O2) concentrations. The administration of 10 μmol/l DL-homocysteine (DL-Hcy) alone decreased dp/dt max, SLVP, and CF but did not change any oxidative stress parameters. The administration of 10 μmol/l DL-propargylglycine (DL-PAG) decreased all cardiodynamic parameters and increased the concentration of O2•-. The co-administration of DL-Hcy and DL-PAG induced a significant decrease in all estimated cardiodynamic parameters and decreased the concentration of NO2- and O2 •- but increased the levels of TBARS and H2O2. Homocysteine shows a lower pro-oxidative effect in the presence of hydrogen sulfide (H2S), which indicates a potential anti-oxidative capacity of H2S. © 2016 Akadémiai Kiadó, Budapest.CardiodynamicsH<sub>2</sub>SHomocysteineLangendorff techniqueOxidative stressThe role of hydrogen sulfide in homocysteine-induced cardiodynamic effects and oxidative stress markers in the isolated rat heart