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- W2267768504 abstract "We reported that alkaline buffer activated Na+/H+ exchanger (NHE) in isolated hearts and increased mitochondrial Ca2+ (mCa2+) and ROS production, which were abated by inhibiting NHE. We tested if blocking mCa2+ uniporter with ruthenium red (RuR, 2.5 μM) before and after ischemia, would reduce mCa2+ overload and ROS, and restore NADH and cardiac function during activated NHE. Guinea pig isolated hearts were perfused (HEPES buffer) with or without RuR at pH 7.4 (control), pH 8 to activate, or pH 6.5 to inhibit, NHE for 10 min before, after, and during 35 min ischemia. NADH, mCa2+, and ROS were assessed at the LV wall by fluorescence. We found that mCa2+ increased less during ischemia in all groups in the presence of RuR. NADH was higher with pH 8+RuR vs pH 8 alone, but RuR had no added effect in other pH groups. ROS was higher after pH 8 alone than in other groups, but adding RuR did not decrease ROS. pH 8+RuR did not protect LVP function or restore coronary flow better than pH 8, but pH 7.4+RuR was better than pH 7.4, pH 7.4 was better than pH 8±RuR, and pH 6.5 was most protective. Results indicate that RuR reduced mCa2+ loading (all pHs) and improved redox state (pH 8), did not reduce ROS (all pHs), and improved function (pH 7.4). These data show that blocking the mCa2+ uniporter reduces mCa2+ loading at all NHE activities but suggest that reducing mCa2+ may be less important than reducing ROS production for improving cardiac function after ischemia." @default.
- W2267768504 created "2016-06-24" @default.
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- W2267768504 date "2008-03-01" @default.
- W2267768504 modified "2023-09-25" @default.
- W2267768504 title "Blocking mitochondrial Ca 2+ uniport activity during activated Na + /H + exchange reduces mCa 2+ loading but does little to better protect function on reperfusion" @default.
- W2267768504 doi "https://doi.org/10.1096/fasebj.22.1_supplement.730.24" @default.
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