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Biomedical Engineering and Bioengineering Commons™
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Full-Text Articles in Biomedical Engineering and Bioengineering
Enhanced Na+/H+ Exchange During Ischemia And Reperfusion Impairs Mitochondrial Bioenergetics And Myocardial Function, Mohammed Aldakkak, David F. Stowe, James S. Heisner, Marisha Spence, Amadou K.S. Camara
Enhanced Na+/H+ Exchange During Ischemia And Reperfusion Impairs Mitochondrial Bioenergetics And Myocardial Function, Mohammed Aldakkak, David F. Stowe, James S. Heisner, Marisha Spence, Amadou K.S. Camara
Biomedical Engineering Faculty Research and Publications
Inhibition of Na+/H+ exchange (NHE) during ischemia reduces cardiac injury due to reduced reverse mode Na+/Ca2+ exchange. We hypothesized that activating NHE-1 at buffer pH 8 during ischemia increases mitochondrial oxidation, Ca2+ overload, and reactive O2 species (ROS) levels and worsens functional recovery in isolated hearts and that NHE inhibition reverses these effects. Guinea pig hearts were perfused with buffer at pH 7.4 (control) or pH 8 +/- NHE inhibitor eniporide for 10 minutes before and for 10 minutes after 35- minute ischemia and then for 110 minutes with pH 7.4 buffer alone. Mitochondrial NADH and FAD, [Ca2+], and superoxide …
Katp Channel Openers Have Opposite Effects On Mitochondrial Respiration Under Different Energetic Conditions, Matthias L. Riess, Amadou K.S. Camara, André Heinen, Janis T. Eells, Michele M. Henry, David F. Stowe
Katp Channel Openers Have Opposite Effects On Mitochondrial Respiration Under Different Energetic Conditions, Matthias L. Riess, Amadou K.S. Camara, André Heinen, Janis T. Eells, Michele M. Henry, David F. Stowe
Biomedical Engineering Faculty Research and Publications
Mitochondrial (m) KATP channel opening has been implicated in triggering cardiac preconditioning. Its consequence on mitochondrial respiration, however, remains unclear. We investigated the effects of two different KATP channel openers and antagonists on mitochondrial respiration under two different energetic conditions. Oxygen consumption was measured for complex I (pyruvate/malate) or complex II (succinate with rotenone) substrates in mitochondria from fresh guinea pig hearts. One of two mKATP channel openers, pinacidil or diazoxide, was given before adenosine diphosphate in the absence or presence of an mKATP channel antagonist, glibenclamide or 5-hydroxydecanoate. Without ATP synthase inhibition, both mKATP …