Endogenous hydrogen sulfide contributes to the cardioprotection by metabolic inhibition preconditioning in the rat ventricular myocytes.

摘要: Abstract The possible role of hydrogen sulfide (H 2 S) in cardioprotection was investigated isolated rat ventricular myocytes exposed to severe metabolic inhibition (MI) glucose-free buffer containing 2-deoxy-D-glucose (2-DOG), an inhibitor glycolysis. Pretreatment (30 min) with NaHS (a H S donor) at concentrations 10 −5 −4 mol/L caused a concentration related increase cell viability and the ratio rod-shaped cells. A time course study showed that NaHS-induced occurred windows (~1 h 16-28 h). To observe whether endogenous may be involved delayed response IP, DL-propargylglycine (PAG) β-cyano-L-alanine (BCA; two inhibitors biosynthesis) were used. Both drugs significantly attenuated produced by MI using viability, cellular injury index, electrically-induced [Ca 2+ ] i transients as end-points. These data suggest plays important following preconditioning. In attempt determine mechanism cardioprotective effect S, we examined blocking K ATP channels glibenclamide non-selective channel blocker), 5-hydroxydecanoic acid (5-HD, mitochondrial HMR-1098 sarcolemmal blocker). effects treatment but not 5-HD. Inhibition NO production L-NG nitroarginine methyl ester (L-NAME) also NaHS. conclusion, our findings provide first evidence protect heart most probably activating and/or provoking release ischemic preconditioning is, least partially, mediated S.