[Cyclosporin A-sensitive mitochondrial pore as a target of cardioprotective action of hydrogen sulfide donor].

: In experiments on a model of ischemia-reperfusion in Langendorff isolated rat hearts and isolated mitochondria we studied the role of hydrogen sulfide donor - sodium hydrosulfide (NaHS, 7.4 mg/kg) in modulating the sensitivity ofmitochondrial permeability transition pore opening. It was shown that NaHS increased the reserves of rat myocardium and had cardioprotective effects from ischemia-reperfusion. In experiments on isolated mitochondria NaHS in concentrations of 10(-6), 10(-5) and 5 x 10(-5) mol/L inhibited Ca(2+)-induced swelling of mitochondria. Preincubation of isolated mitochondria with K+(ATphi)-channels inhibitor 5-hydroxydecanoate (10(-4) mol/L) reduced the protective effect of NaHS (10(-5) mol/L). Thus, we consider that NaHS protective effect from reperfusion disturbances of heart function was realized via inhibition of Ca(2+)-induced mitochondrial permeability transition pore opening.