Enhanced Na +/H + exchange during ischemia and reperfusion impairs mitochondrial bioenergetics and myocardial function

Journal of Cardiovascular Pharmacology

Volumn 52, Issue 3, 2008, Pages 236-244

  Aldakkak, Mohammed ^a   Stowe, David F ^a,b,c   Heisner, James S ^a   Spence, Marisha ^d   Camara, Amadou K S ^a  

^a MEDICAL COLLEGE OF WISCONSIN   (United States)

^b CLEMENT J ZABLOCKI VETERANS AFFAIRS MEDICAL CENTER   (United States)

^c Medical College of Wisconsin and Marquette University   (United States)

^d UNIVERSITY OF WISCONSIN MILWAUKEE   (United States)

Author keywords

Energy metabolism; Free radicals; Ischemia; Mitochondria; Na + H + exchange; Reperfusion

Indexed keywords

CALCIUM; ENIPORIDE; FLAVINE ADENINE NUCLEOTIDE; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE; SODIUM PROTON EXCHANGE PROTEIN 1; SUPEROXIDE; GUANIDINE DERIVATIVE; NICOTINAMIDE ADENINE DINUCLEOTIDE; SODIUM PROTON EXCHANGE PROTEIN; SULFONE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL ENERGY; CELL FUNCTION; CONTROLLED STUDY; DRUG ACTIVITY; GUINEA PIG; HEART FUNCTION; HEART MITOCHONDRION; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; HEART PERFORMANCE; ISOLATED HEART; MITOCHONDRIAL RESPIRATION; NONHUMAN; OXIDATION REDUCTION STATE; PH; PRIORITY JOURNAL; SPECTROFLUOROMETRY; ANIMAL; DRUG ANTAGONISM; METABOLISM; OXIDATION REDUCTION REACTION; REPERFUSION INJURY;

ANIMALS; CALCIUM; FLAVIN-ADENINE DINUCLEOTIDE; GUANIDINES; GUINEA PIGS; HYDROGEN-ION CONCENTRATION; MITOCHONDRIA, HEART; MYOCARDIAL REPERFUSION INJURY; NAD; OXIDATION-REDUCTION; REACTIVE OXYGEN SPECIES; SODIUM-HYDROGEN ANTIPORTER; SPECTROMETRY, FLUORESCENCE; SULFONES; SUPEROXIDES;

EID: 58149269445     PISSN: 01602446     EISSN: None     Source Type: Journal    
DOI: 10.1097/FJC.0b013e3181831337     Document Type: Article

References (66)

1. Brookes PS, Yoon Y, Robotham JL, et al. Calcium, ATP, and ROS: a mitochondrial love-hate triangle. Am J Physiol Cell Physiol. 2004;287: C817-833.
2. m overload in rat hearts. Am J Physiol. 1996;271:H2145-2153.
3. Vaughan-Jones RD, Wu ML, Bountra C. Sodium-hydrogen exchange and its role in controlling contractility during acidosis in cardiac muscle. Mol Cell Biochem. 1989;89:157-162.
4. Karmazyn M. The role of the myocardial sodium-hydrogen exchanger in mediating ischemic and reperfusion injury. From amiloride to cariporide. Ann N Y Acad Sci. 1999;874:326-334.
5. Pike MM, Kitakaze M, Marban E. 23Na-NMR measurements of intracellular sodium in intact perfused ferret hearts during ischemia and reperfusion. Am J Physiol. 1990;259:H1767-1773.
6. 2+ overload in reperfused ischemic myocardium. Annu Rev Physiol. 1990;52:543-559.
7. Gursahani HI, Schaefer S. Acidification reduces mitochondrial calcium uptake in rat cardiac mitochondria. Am J Physiol Heart Circ Physiol. 2004;287:H2659-2665.
8. Ruiz-Meana M, Garcia-Dorado D, Pina P, et al. Cariporide preserves mitochondrial proton gradient and delays ATP depletion in cardiomyo-cytes during ischemic conditions. Am J Physiol Heart Circ Physiol. 2003; 285:H999-1006.
9. + isoform-1 exchange protects hearts perfused after 6-hour cardioplegic cold storage. J Heart Lung Transplant. 2002;21:374-382.
10. 2+] and myocardial damage after cold ischemia. J Cardiovasc Pharmacol. 2003;41:686-698.
11. i load after ischemia and improves function in intact hearts. Am J Physiol Heart Circ Physiol. 2001;281:H2398-2409.
12. + exchanger virtually prevents ischemic Na+ overload in rat hearts. Mol Cell Biochem. 2007;297:101-110.
13. + exchange blockers EIPA, cariporide and eniporide. Mol Cell Biochem. 2003;250:47-54.
14. +-overload in ischemia and is cardioprotective. J Mol Cell Cardiol. 1999;31:1985-1995.
15. + exchanger are resistant to cardiac ischemia-reperfusion injury. Circ Res. 2003;93:776-782.
16. 2 radicals in intact hearts with ischemia and reperfusion. Am J Physiol Heart Circ Physiol. 2003;284:H566-574.
17. Riess ML, Camara AK, Chen Q, et al. Altered NADH and improved function by anesthetic and ischemic preconditioning in guinea pig intact hearts. Am J Physiol Heart Circ Physiol. 2002;283:H53-H60.
18. 2+ overload and ROS release. Cardiovasc Res. 2008;77:406-415.
19. 2+ activity during pH changes in vitro. J Electrocardiol. 1986;19:143-154.
20. Brandes R, Bers DM. Increased work in cardiac trabeculae causes decreased mitochondrial NADH fluorescence followed by slow recovery. Biophys J. 1996;71:1024-1035.
21. Chance B, Williamson JR, Jamieson D, et al. Properties and kinetics of reduced pyridine nucleotide fluorescence of the isolated and in vivo rat heart. Biochem Z. 1965;341:357-377.
22. Nuutinen EM. Subcellular origin of the surface fluorescence of reduced nicotinamide nucleotides in the isolated perfused rat heart. Basic Res Cardiol. 1984;79:49-58.
23. Barth E, Stammler G, Speiser B, et al. Ultrastructural quantitation of mitochondria and myofilaments in cardiac muscle from 10 different animal species including man. J Mol Cell Cardiol. 1992;24:669-681.
24. Vinnakota KC, Bassingthwaighte JB. Myocardial density and composition: a basis for calculating intracellular metabolite concentrations. Am J Physiol Heart Circ Physiol. 2004;286:H1742-1749.
25. Camara AK, Riess ML, Kevin LG, et al. Hypothermia augments reactive oxygen species detected in the guinea pig isolated perfused heart. Am J Physiol Heart Circ Physiol. 2004;286:H1289-1299.
26. 2+ overload, and changes in redox state. Am J Physiol Cell Physiol. 2007;292:C2021- 2031.
27. 2+] to contractility relationships in intact hearts. J Cardiovasc Pharmacol. 2003;42: 539-553.
28. Vanden Hoek TL, Li C, Shao Z, et al. Significant levels of oxidants are generated by isolated cardiomyocytes during ischemia prior to reperfu-sion. J Mol Cell Cardiol. 1997;29:2571-2583.
29. Zhao H, Joseph J, Fales HM, et al. Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence. Proc Natl Acad Sci U S A. 2005;102:5727-5732.
30. Zhao H, Kalivendi S, Zhang H, et al. Superoxide reacts with hydroethidine but forms a fluorescent product that is distinctly different from ethidium: potential implications in intracellular fluorescence detection of superoxide. Free Radic Biol Med. 2003;34:1359-1368.
31. 2+ concentration in living single rat cardiac myocytes. Am J Physiol. 1991;261:H1123-1134.
32. 2+] sensitivity by moderate hypothermia in guinea pig isolated hearts. Am J Physiol. 1999;277:H2321-2332.
33. + exchange inhibitor, inhibits the mitochondrial death pathway. Circulation. 2003;108:2275-2281.
34. Lazdunski M, Frelin C, Vigne P. The sodium/hydrogen exchange system in cardiac cells: its biochemical and pharmacological properties and its role in regulating internal concentrations of sodium and internal pH. J Mol Cell Cardiol. 1985;17:1029-1042.
35. + exchange. Am J Physiol. 1983;244: C422-428.
36. Vaughan-Jones RD. Regulation of intracellular pH in cardiac muscle. Ciba Found Symp. 1988;139:23-46.
37. + exchange in cardiac sarcolemmal vesicles. Biochim Biophys Acta. 1985;818:109-116.
38. Meng HP, Lonsberry BB, Pierce GN. Influence of perfusate pH on the postischemic recovery of cardiac contractile function: involvement of sodium-hydrogen exchange. J Pharmacol Exp Ther. 1991;258:772-777.
39. Javadov S, Choi A, Rajapurohitam V, et al. NHE-1 inhibition-induced cardioprotection against ischaemia/reperfusion is associated with attenuation of the mitochondrial permeability transition. Cardiovasc Res. 2007.
40. 2+ overload in ischemic/reperfused rat hearts. J Cardiovasc Pharmacol. 2002;39:569-575.
41. Crompton M. The mitochondrial permeability transition pore and its role in cell death. Biochem J. 1999;341:233-249.
42. Halestrap AP, Clarke SJ, Javadov SA. Mitochondrial permeability transition pore opening during myocardial reperfusion-a target for cardioprotection. Cardiovasc Res. 2004;61:372-385.
43. Regula KM, Ens K, Kirshenbaum LA. Mitochondria-assisted cell suicide: a license to kill. J Mol Cell Cardiol. 2003;35:559-567.
44. Weiss JN, Korge P, Honda HM, et al. Role of the mitochondrial permeability transition in myocardial disease. Circ Res. 2003;93:292-301.
45. Bagchi D, Wetscher GJ, Bagchi M, et al. Interrelationship between cellular calcium homeostasis and free radical generation in myocardial reperfusion injury. Chem Biol Interact. 1997;104:65-85.
46. Flitter WD. Free radicals and myocardial reperfusion injury. Br Med Bull. 1993;49:545-555.
47. Becker LB, vanden Hoek TL, Shao ZH, et al. Generation of superoxide in cardiomyocytes during ischemia before reperfusion. Am J Physiol. 1999; 277:H2240-2246.
48. Wikstrom M, Saari H. A spectral shift in cytochrome a induced by calcium ions. Biochim Biophys Acta. 1975;408:170-179.
49. Brookes PS, Darley-Usmar VM. Role of calcium and superoxide dismutase in sensitizing mitochondria to peroxynitrite-induced permeability transition. Am J Physiol Heart Circ Physiol. 2004;286:H39-46.
50. 2+ release channel from skeletal muscle sarcoplasmic reticulum. J Biol Chem. 1995;270:25557-25563.
51. 2+ overload in NRVM involves ERK1/2 MAP kinases: role for an NHE-1-dependent pathway. Am J Physiol Heart Circ Physiol. 2002;283:H598-605.
52. + exchange in neonatal rat cardiac myocytes. Circ Res. 1998;82:1053-1062.
53. Goldhaber JI, Qayyum MS. Oxygen free radicals and excitation-contraction coupling. Antioxid Redox Signal. 2000;2:55-64.
54. Cairns CB, Ferroggiaro AA, Walther JM, et al. Postischemic administration of succinate reverses the impairment of oxidative phosphorylation after cardiac ischemia and reperfusion injury. Circulation. 1997;96: II-260-265.
55. Ferrari R. The role of mitochondria in ischemic heart disease. J Cardiovasc Pharmacol. 1996;28 (Suppl 1):S1-10.
56. ATP channel in preservation of mitochondrial function. Am J Physiol Heart Circ Physiol. 2000;278:H305-H312.
57. Di Lisa F, Menabo R, Canton M, et al. Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart. J Biol Chem. 2001;276: 2571-2575.
58. Akao M, O'Rourke B, Teshima Y, et al. Mechanistically distinct steps in the mitochondrial death pathway triggered by oxidative stress in cardiac myocytes. Circ Res. 2003;92:186-194.
59. + exchanger. J Biol Chem. 1998;273:6951-6959.
60. Javadov S, Purdham DM, Zeidan A, et al. NHE-1 inhibition improves cardiac mitochondrial function through regulation of mitochondrial biogenesis during postinfarction remodeling. Am J Physiol Heart Circ Physiol. 2006;291:H1722-1730.
61. 2+ exchange in ferret heart mitochondria. Biochem Biophys Res Commun. 1990;166:1352- 1357.
62. + and pH flux in cardiac mitochondria using in vitro spectrofluorometry [Abstract]. FASEB J. 2007;21:946.3.
63. 2+ flux in isolated mitochondria; Novel spectrofluorometric measurements [Abstract]. Bio Med Eng Soc J 2007;454:P2.14.
64. 2+ overload in isolated perfused rabbit heart. Circulation. 1994;89:2787-2798.
65. + exchange inhibition in ischemic, reperfused porcine hearts. Circulation. 1995;92:912-917.
66. + exchange inhibitor eniporide on cardiac performance and myocardial high energy phosphates in pigs subjected to cardioplegic arrest. Ann Thorac Surg. 2004;77:658-663.