title: [Effect of hydrogen sulfide on isolated rat heart reaction under volume load and ischemia-reperfusion].
abstract: The present study was aimed to investigate the effect of H2S donor (NaHS) on heart function in conditions of functional loads and ischemia-reperfusion (I/R) injury by using Langendorf isolated heart perfusion. NaHS ("Sigma", 7,4 mg per kg) was dissolved in physiological solution and injected intraperitoneally 30 min before experiment. Rat isolated hearts were Langendorf-perfused and subjected to 20-minute non-flow ischemia followed by 40-minute reperfusion. The heart function was assessed by measuring the LVDP, dP/dt, coronary flow, heart rate. The opening of mitochondria permeability transition (MPT) pore was estimated by releasing of a stable factor with UV absorbance (lambdamax 250 nm) into the coronary outflow probes during the initial phase of reperfusion. The results showed that NaHS pretreated hearts developed greater LVDP without decreasing ofdP/dt min in response to an increase of left ventricle volume indicating greater functional reserves and effectiveness of Frank-Starling low realization. NaHS increased cardiac mitochondrial membrane potential but did not changed UCP3 gene expression. Significant post-ischemic recover of heart function in NaHS group was accompanied with tiny quantity ofmitochondrial factor releasing comparing to I/R group (p<0.001). Thus, NaHS do provides cardioprotective effect by inhibition of MPT pore opening.
authors.forename: T V
authors.initials: TV
authors.lastname: Shymans'ka
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Hoshovs'ka
authors.forename: O M
authors.initials: OM
authors.lastname: Semenikhina
authors.forename: V F
authors.initials: VF
authors.lastname: Sahach
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D009924:Organ Culture Techniques; D051381:Rats; D017208:Rats, Wistar; D013440:Sulfides / Q000378:metabolism*; D000071247:Uncoupling Protein 3
chemical_list: D002316:Cardiotonic Agents; D007473:Ion Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D024101:Mitochondrial Proteins; D013440:Sulfides; C000604394:Ucp3 protein, rat; D000071247:Uncoupling Protein 3; C025451:sodium bisulfide; D006862:Hydrogen Sulfide