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126 related items for PubMed ID: 2527849

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  • 5. Factors affecting the loss of mitochondrial function during zero-flow ischemia (autolysis) in slow and fast heart-rate hearts.
    Rouslin W.
    J Mol Cell Cardiol; 1988 Nov; 20(11):999-1007. PubMed ID: 2976846
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  • 9. Factors affecting the reactivation of the mitochondrial adenosine 5'-triphosphatase and the release of ATPase inhibitor protein during and following the reenergization of mitochondria from ischemic cardiac muscle.
    Rouslin W, Broge CW.
    Arch Biochem Biophys; 1989 Dec; 275(2):385-94. PubMed ID: 2531991
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  • 11. IF1 function in situ in uncoupler-challenged ischemic rabbit, rat, and pigeon hearts.
    Rouslin W, Broge CW.
    J Biol Chem; 1996 Sep 27; 271(39):23638-41. PubMed ID: 8798581
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  • 16. Protonic inhibition of the mitochondrial oligomycin-sensitive adenosine 5'-triphosphatase in ischemic and autolyzing cardiac muscle. Possible mechanism for the mitigation of ATP hydrolysis under nonenergizing conditions.
    Rouslin W.
    J Biol Chem; 1983 Aug 25; 258(16):9657-61. PubMed ID: 6224783
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  • 17. Effect of inhibition of the mitochondrial ATPase on net myocardial ATP in total ischemia.
    Jennings RB, Reimer KA, Steenbergen C.
    J Mol Cell Cardiol; 1991 Dec 25; 23(12):1383-95. PubMed ID: 1839801
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  • 18. Mitochondrial complexes I, II, III, IV, and V in myocardial ischemia and autolysis.
    Rouslin W.
    Am J Physiol; 1983 Jun 25; 244(6):H743-8. PubMed ID: 6305212
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  • 19. Effects of oligomycin and acidosis on rates of ATP depletion in ischemic heart muscle.
    Rouslin W, Erickson JL, Solaro RJ.
    Am J Physiol; 1986 Mar 25; 250(3 Pt 2):H503-8. PubMed ID: 2937313
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