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

T V Shimanskaia, N A Strutinskaia, G L Vavilova, Iu V Goshovskaia, E N Semenikhina, V F Sagach

Index: Ross. Fiziol. Zh. Im. I. M. Sechenova 99(2) , 261-72, (2013)

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Abstract

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.