Skip to main content

Advertisement

Log in

Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion

  • Published:
Heart Failure Reviews Aims and scope Submit manuscript

Abstract

Infarct size is determined not only by the duration and severity of ischemia, but also by pathological processes initiated at reperfusion (reperfusion injury). Numerous pharmacological strategies have been reported which administer drugs at or just before the onset of reperfusion, with subsequent salubrious effects, notably a reduction in infarct size. However, few if any of these strategies have become standard of care in the catheterization laboratory setting. Postconditioning, defined as repeated brief cycles of reperfusion interrupted by ischemia (or hypoxia) applied at the onset of reperfusion, was recently introduced as a mechanical strategy to attenuate reperfusion injury. Postconditioning intervenes only during the first few minutes of reperfusion. However, it reduces endothelial activation and dysfunction, the inflammatory response to reperfusion, necrosis, and apoptosis both acutely and long-term. Cardioprotection has been demonstrated by multiple independent laboratories and in multiple species. Postconditioning stimulates G-protein coupled receptors by their cognate endogenously released ligands and surprisingly activates survival kinases that may converge on mitochondrial KATP channels and the permeability transition pore. Postconditioning has been shown in two clinical studies to reduce infarct size in patients undergoing percutaneous coronary intervention in the catheterization laboratory, and at least five other studies are in some phase of implementation. This significant reduction in infarct size has implications for reduction in heart failure as a consequence of myocardial infarction, but this link has yet to be demonstrated. The salubrious effects of postconditioning are an indirect validation of the experimental and clinical importance of reperfusion injury in the setting of coronary artery occlusion.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1

Similar content being viewed by others

References

  1. Gheorghiade M, Bonow RO (1998) Chronic heart failure in the United States. A manifestation of coronary artery disease. Circulation 97:282–289

    PubMed  CAS  Google Scholar 

  2. Massie BM, Shah NB (1997) Evolving trends in the epidemiologic factors of heart failure: rational for preventive strategies and comprehensive disease management. Am Heart J 133:703–712

    Article  PubMed  CAS  Google Scholar 

  3. Sharpe N, Doughty R (1998) Epidemiology of heart failure and ventricular dysfunction. Lancet 352:3–7

    Article  Google Scholar 

  4. Ho KK, Anderson KM, Kannel WB, Grossman W, Levy D (1993) Survival after the onset of congestive heart failure in Framingham heart study subjects. Circulation 88:107–115

    PubMed  CAS  Google Scholar 

  5. Pfeffer MA, Braunwald E (1990) Ventricular remodeling after myocardial infarction. Experimental observation and clinical implications. Circulation 81:1161–1172

    PubMed  CAS  Google Scholar 

  6. Gaballa MA, Goldman S (2002) Ventricular remodeling in heart failure. J Card Fail 8:S476–S485

    Article  PubMed  Google Scholar 

  7. Bolognese L, Neskovic AN, Parodi G, Cerisano G, Buonamici P, Santoro GM, Antoniucci D (2002) Left ventricular remodeling after primary coronary angioplasty: patterns of left ventricular dilation and long-term prognostic implications. Circulation 106:2351–2357

    Article  PubMed  Google Scholar 

  8. Yang F, Liu YH, Yang XP, Xu J, Kaplan A, Carretero OA (2002) Myocardial infarction and cardiac remodelling in mice. Exp Physiol 87:547–555

    Article  PubMed  CAS  Google Scholar 

  9. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, Vinten-Johansen J (2003) Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol 285:H579–H588

    CAS  Google Scholar 

  10. Staat P, Rioufol G, Piot C, Cottin Y, Cung TT, L’Huillier I, Aupetit J-F, Bonnefoy E, Finet G, Andre-Fouet X, Ovize MM (2005) Postconditioning the human heart. Circulation 112:2143–2148

    Article  PubMed  Google Scholar 

  11. Darling CE, Solari PB, Smith CS, Furman MI, Przyklenk K (2007) ‘Postconditioning’ the human heart: multiple balloon inflations during primary angioplasty may confer cardioprotection. Basic Res Cardiol 102:274–278

    Article  PubMed  CAS  Google Scholar 

  12. Yang X-C, Liu Y, Wang L-F, Cui L, Ge Y-G, Wang H-S, Li W-M, Xu L, Ni Z-H, Liu H-S, Zhang L, Wang T, Jia H-M, Vinten-Johansen J, Zhao Z-Q (2006) Permanent reduction in myocardial infarct size by postconditioning in patients after primary coronary angioplasty. Circulation 114(18):II–812(3795)

    Google Scholar 

  13. Heusch G (2004) Postconditioning: old wine in a new bottle? J Am Coll Cardiol 44:1111–1112

    Article  PubMed  Google Scholar 

  14. Vinten-Johansen J, Lefer DJ, Nakanishi K, Johnston WE, Brian CA, Cordell AR (1992) Controlled coronary hydrodynamics at the time of reperfusion reduces postischemic injury. Cor Art Dis 3:1081–1093

    Article  Google Scholar 

  15. Sato H, Jordan JE, Zhao Z-Q, Sarvotham SS, Vinten-Johansen J (1997) Gradual reperfusion reduces infarct size and endothelial injury but augments neutrophil accumulation. Ann Thorac Surg 64:1099–1107

    Article  PubMed  CAS  Google Scholar 

  16. Kin H, Zhao ZQ, Sun H-Y, Wang NP, Corvera JS, Halkos ME, Kerendi F, Guyton RA, Vinten-Johansen J (2004) Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res 62:74–85

    Article  PubMed  CAS  Google Scholar 

  17. Piper HM, Garcia-Dorado D, Ovize M (1998) A fresh look at reperfusion injury. Cardiovasc Res 38:291–300

    Article  PubMed  CAS  Google Scholar 

  18. Piper HM, Schafer AC (2004) The first minutes of reperfusion: a window of opportunity for cardioprotection. Cardiovasc Res 61:365–371

    Article  PubMed  CAS  Google Scholar 

  19. Tsao PS, Aoki N, Lefer DJ, Johnson G, III Lefer AM (1990) Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation 82:1402–1412

    PubMed  CAS  Google Scholar 

  20. Kin H, Zatta AJ, Lofye MT, Amerson BS, Halkos ME, Kerendi F, Zhao ZQ, Guyton RA, Headrick JP, Vinten-Johansen J (2005) Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine. Cardiovasc Res 67:124–133

    Article  PubMed  CAS  Google Scholar 

  21. Heusch G, Buchert A, Feldhaus S, Schulz R (2006) No loss of cardioprotection by postconditioning in connexin 43-deficient mice. Basic Res Cardiol 101:354–356

    Article  PubMed  CAS  Google Scholar 

  22. Kerendi F, Kin H, Halkos ME, Jiang R, Zatta AJ, Zhao Z-Q, Guyton RA, Vinten-Johansen J (2005) Remote postconditioning: brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous activation of adenosine receptors. Basic Res Cardiol 100:404–412

    Article  PubMed  CAS  Google Scholar 

  23. Tsang A, Hausenloy DJ, Macanu MM, Yellon DM (2004) Postconditioning-A form of “modified reperfusion” protects the myocardium by activating the P13K-Akt pathway. Circulation 110:III167

    Google Scholar 

  24. Zhu M, Feng J, Lucchinetti E, Fischer G, Xu L, Pedrazzini T, Schaub MC, Zaugg M (2006) Ischemic postconditioning protects remodeled myocardium via the PI3K-PKB/Akt reperfusion injury salvage kinase pathway. Cardiovasc Res 72:152–162

    Article  PubMed  CAS  Google Scholar 

  25. Yang XM, Philipp S, Downey JM, Cohen MV (2005) Postconditioning’s protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. Basic Res Cardiol 100:57–63

    Article  PubMed  CAS  Google Scholar 

  26. Philipp S, Yang X-M, Cui L, Davis AM, Downey JM, Cohen MV (2006) Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade. Cardiovasc Res 70:308–314

    Article  PubMed  CAS  Google Scholar 

  27. Yang X-M, Proctor JB, Cui L, Krieg T, Downey JM, Cohen MV (2004) Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol 44:1103–1110

    Article  PubMed  Google Scholar 

  28. Halkos ME, Kerendi F, Corvera JS, Wang NP, Kin H, Payne CS, Sun H-Y, Guyton RA, Vinten-Johansen J, Zhao ZQ (2004) Myocardial protection with postconditioning is not enhanced by ischemic preconditioning. Ann Thorac Surg 78:961–969

    Article  PubMed  Google Scholar 

  29. Iliodromitis EK, Georgiadis M, Cohen MV, Downey JM, Bofilis E, Kremastinos DT (2006) Protection from postconditioning depends on the number of short ischemic insults in anesthetized pigs. Basic Res Cardiol 101:502–507

    Article  PubMed  Google Scholar 

  30. Schwartz LM, Lagranha CJ (2006) Ischemic postconditioning during reperfusion activates Akt and ERK without protecting against lethal myocardial ischemia-reperfusion injury in pigs. Am J Physiol 290:H1011–H1018

    CAS  Google Scholar 

  31. Wang HC, Zhang HF, Guo WY, Su H, Zhang KR, Li QX, Yan W, Ma XL, Lopez BL, Christopher TA, Gao F (2006) Hypoxic postconditioning enhances the survival and inhibits apoptosis of cardiomyocytes following reoxygenation: role of peroxynitrite formation. Apoptosis 11:1453–1460

    Article  PubMed  CAS  Google Scholar 

  32. Sun H-Y, Wang NP, Halkos M, Kerendi F, Kin H, Guyton RA, Vinten-Johansen J, Zhao ZQ (2006) Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Apoptosis 11:1583–1593

    Article  PubMed  CAS  Google Scholar 

  33. Entman ML, Michael L, Rossen RD, Dreyer WJ, Anderson DC, Taylor AA, Smith CW (1991) Inflammation in the course of early myocardial ischemia. FASEB J 5:2529–2537

    PubMed  CAS  Google Scholar 

  34. Vinten-Johansen J, Jiang R, Reeves JG, Mykytenko J, Deneve J, Jobe LJ (2007) Inflammation, proinflammatory mediators and myocardial ischemia-reperfusion injury. Hematol Oncol Clin N Am 21:123–145

    Article  Google Scholar 

  35. Lucchesi BR (2001) Myocardial reperfusion injury-role of free radicals and mediators of inflammation. In: Sperelakis N, Kurachi Y, Terzic A, Cohen MV (eds) Heart Physiology and Pathophysiology, 4th edn. pp 1181–1210

  36. Lefer AM, Tsao PS, Lefer DJ, Ma X-L (1991) Role of endothelial dysfunction in the pathogenesis of reperfusion injury after myocardial ischemia. FASEB J 5:2029–2034

    PubMed  CAS  Google Scholar 

  37. Cohen MV, Yang X-M, Downey JM (2007) The pH hypothesis of postconditioning: Staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosis. Circulation

  38. Jordan JE, Zhao ZQ, Vinten-Johansen J (1999) The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res 43:860–878

    Article  PubMed  CAS  Google Scholar 

  39. Kennedy TP, Vinten-Johansen J (2006) A review of the clinical use of anti-inflammatory therapies for reperfusion injury in myocardial infarction and stroke: where do we go from here? Curr Opinion Investigation Drugs 7:229–242

    CAS  Google Scholar 

  40. Vinten-Johansen J (2004) Involvement of neutrophils in the pathogenesis of lethal myocardial reperfusion injury. Cardiovasc Res 61:481–497

    Article  PubMed  CAS  Google Scholar 

  41. Meldrum DR (1998) Tumor necrosis factor in the heart. Am J Physiol 274:R577–R595

    PubMed  CAS  Google Scholar 

  42. Lefer AM, Ma X-L, Weyrich A, Lefer DJ (1993) Endothelial dysfunction and neutrophil adherence as critical events in the development of reperfusion injury. Agents Actions 41:127–135

    CAS  Google Scholar 

  43. Baxter GF (2002) The neutrophil as a mediator of myocardial ischemia-reperfusion injury: time to move on. Basic Res Cardiol 97:268–275

    Article  PubMed  Google Scholar 

  44. Olafsson B, Forman MB, Puett DW, Pou A, Cates CU, Friesinger GC, Virmani R (1987) Reduction of reperfusion injury in the canine preparation by intracoronary adenosine: importance of the endothelium and the no-reflow phenomenon. Circulation 76:1135–1145

    PubMed  CAS  Google Scholar 

  45. Pitarys CJ, Virmani R, Vildibill HD Jr, Jackson EK, Forman MB (1991) Reduction of myocardial reperfusion injury by intravenous adenosine administered during the early reperfusion period. Circulation 83:237–247

    PubMed  Google Scholar 

  46. Jordan JE, Zhao ZQ, Sato H, Taft S, Vinten-Johansen J (1997) Adenosine A2 receptor activation attenuates reperfusion injury by inhibiting neutrophil accumulation, superoxide generation and coronary endothelial adherence. J Pharmacol Exp Ther 280:301–309

    PubMed  CAS  Google Scholar 

  47. Bell RM, Yellon DM (2003) Bradykinin limits infarction when adminstered as an adjunct to reperfusion in mouse heart: the role of P18K, Akt and eNOS. J Mol Cell Cardiol 35:185–193

    Article  PubMed  CAS  Google Scholar 

  48. Yang XM, Krieg T, Cui L, Downey JM, Cohen MV (2004) NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NO. J Mol Cell Cardiol 36:411–421

    Article  PubMed  CAS  Google Scholar 

  49. Peart JN, Gross GJ (2003) Adenosine and opioid receptor-mediated cardioprotection in the rat: evidence for cross-talk between receptors. Am J Physiol 285:H81–H89

    CAS  Google Scholar 

  50. Jordan JE, Thourani VH, Auchampach JA, Robinson JA, Wang NP, Vinten-Johansen J (1999) A(3) adenosine receptor activation attenuates neutrophil function and neutrophil-mediated reperfusion injury. Am J Physiol 277:H1895–H1905

    PubMed  CAS  Google Scholar 

  51. Yang Z, Day YJ, Toufektsian MC, Ramos SI, Marshall M, Wang XQ, French BA, Linden J (2005) Infarct-sparing effect of A2A-adenosine receptor activation is due primarily to its action on lymphocytes. Circulation 111:2190–2197

    Article  PubMed  CAS  Google Scholar 

  52. Gross GJ (2003) Role of opioids in acute and delayed preconditioning. J Mol Cell Cardiol 35:709–718

    Article  PubMed  CAS  Google Scholar 

  53. Gross ER, Hsu AK, Gross GJ (2004) Opioid-induced cardioprotection occurs via glycogen synthase kinase β inhibition during reperfusion in intact rat hearts. Circ Res 94:960–966

    Article  PubMed  CAS  Google Scholar 

  54. Chang WL, Lee SS, Su MJ (2005) Attenuation of post-ischemia reperfusion injury by thaliporphine and morphine in rat hearts. J Biomed Sci 12:611–619

    Article  PubMed  CAS  Google Scholar 

  55. Kin H, Zatta AJ, Jiang R, Reeves JG, Mykytenko J, Sorescu G, Zhao Z-Q, Wang N-P, Guyton RA, Vinten-Johansen J (2005) Activation of opioid receptors mediates the infarct size reduction by Postconditioning. J Mol Cell Cardiol 38:827

    Google Scholar 

  56. Hausenloy DJ, Yellon DM (2006) Survival kinases in ischemic preconditioning and postconditioning. Cardiovasc Res 70:240–253

    Article  PubMed  CAS  Google Scholar 

  57. Hausenloy DJ, Tsang A, Yellon DM (2005) The reperfusion injury salvage kinase pathway: a common target for both ischemic preconditioning and postconditioning. TCM 15:69–75

    PubMed  CAS  Google Scholar 

  58. Mykytenko J, Reeves JG, Kin H, Zatta AJ, Jiang R, Guyton RA, Vinten-Johansen J, Zhao Z-Q (2005) Postconditioning reduces infarct size via mitochondrial KATP channel activation during 24 hours of reperfusion. J Mol Cell Cardiol 38:830

    Google Scholar 

  59. Argaud L, Gateau-Roesch O, Raisky O, Loufouat J, Robert D, Ovize M (2005) Post-conditioning inhibits mitochondrial permeability transition. Circulation 111:194–197

    Article  PubMed  CAS  Google Scholar 

  60. Darling CE, Jiang R, Maynard M, Whittaker P, Vinten-Johansen J, Przyklenk K (2005) Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2. Am J Physiol 289:H1618–H1626

    CAS  Google Scholar 

  61. Ytrehus K, Liu Y, Downey J (1994) Preconditioning protects ischemic rabbit heart by protein kinase C activation. Am J Physiol 266:H1145–H1152

    PubMed  CAS  Google Scholar 

  62. Inagaki K, Churchill E, Mochly-Rosen D (2006) Epsilon protein kinase C as a potential therapeutic target for the ischemic heart. Cardiovasc Res 70:222–230

    Article  PubMed  CAS  Google Scholar 

  63. Schulz R, Gres P, Skyschally A, Duschin A, Belosjorow S, Konietzka I, Heusch G (2003) Ischemic preconditioning preserves connexin 43 phosphorylation during sustained ischemia in pig hearts in vivo. FASEB J 17:1355–1357

    PubMed  CAS  Google Scholar 

  64. Inagaki K, Hahn HS, Dorn II GW, Mochly-Rosen D (2003) Additive protection of the ischemic heart ex vivo by combined treatment with ð-Protein kinase C inhibitor and ε-Protein kinase C activator. Circulation 108:869–875

    Article  PubMed  CAS  Google Scholar 

  65. Inagaki K, Chen L, Ikeno F, Lee FH, Imahashi K, Bouley DM, Rezaee M, Yock PG, Murphy E, Mochly-Rosen D (2003) Inhibition of delta-protein kinase C protects against reperfusion injury of the ischemic heart in vivo. Circulation 108:2304–2307

    Article  PubMed  CAS  Google Scholar 

  66. Churchill EN, Szweda LI (2005) Translocation of deltaPKC to mitochondria during cardiac reperfusion enhances superoxide anion production and induces loss in mitochondrial function. Arch Biochem Biophys 439:194–199

    Article  PubMed  CAS  Google Scholar 

  67. Murriel CL, Churchill E, Inagaki K, Szweda LI, Mochly-Rosen D (2004) Protein kinase Cdelta activation induces apoptosis in response to cardiac ischemia and reperfusion damage: a mechanism involving BAD and the mitochondria. J Biol Chem 279:47985–47991

    Article  PubMed  CAS  Google Scholar 

  68. Toma O, Weber NC, Wolter JI, Obal D, Preckel B (2004) Desflurane preconditioning induces time-dependent activation of protein kinase C epsilon and extracellular signal-regulated kinase 1 and 2 in the rat heart in vivo. Anesthesiology 101:1372–1380

    Article  PubMed  CAS  Google Scholar 

  69. Kostyak JC, Hunter JC, Korzick DH (2006) Acute PKCdelta inhibition limits ischaemia-reperfusion injury in the aged rat heart: role of GSK-3beta. Cardiovasc Res 70:325–334

    Article  PubMed  CAS  Google Scholar 

  70. Baines CP, Song C-X, Zheng Y-T, Wang G-W, Zhang J, Wang O-L, Guo Y, Bolli R, Cardwell EM, Ping P (2003) Protein kinase C[epsilon] interacts with and inhibits the permeability transition pore in cardiac mitochondria. Circ Res 92:873–880

    Article  PubMed  CAS  Google Scholar 

  71. Zatta AJ, Kin H, Lee G, Wang N, Jiang R, Lust R, Reeves JG, Mykytenko J, Guyton RA, Zhao ZQ, Vinten-Johansen J (2006) Infarct-sparing effect of myocardial postconditioning is dependent on protein kinase C signalling. Cardiovasc Res 70:315–324

    Article  PubMed  CAS  Google Scholar 

  72. Penna C, Rastaldo R, Mancardi D, Raimondo S, Cappello S, Gattullo D, Losano G, Pagliaro P (2006) Post-conditioning induced cardioprotection requires signaling through a redox-sensitive mechanism, mitochondrial ATP-sensitive K+ channel and protein kinase C activation. Basic Res Cardiol 101:180–189

    Article  PubMed  CAS  Google Scholar 

  73. Hearse DJ, Humphrey SM, Chain EB (1973) Abrupt reoxygenation of the anoxic potassium-arrested perfused rat heart: a study of myocardial enzyme release. J Mol Cell Cardiol 5:395–407

    Article  PubMed  CAS  Google Scholar 

  74. Duilio C, Ambrosio G, Kuppusamy P, DiPaula A, Becker LC, Zweier JL (2001) Neutrophils are primary source of 02 radicals during reperfusion after prolonged myocardial ischemia. Am J Physiol 280:H2649–H2657

    CAS  Google Scholar 

  75. Zweier JL, Flaherty JT, Weisfeldt ML (1987) Direct measurement of free radicals generated following reperfusion of ischemic myocardium. Proc Natl Acad Sci 84:1404–1407

    Article  PubMed  CAS  Google Scholar 

  76. Serviddio G, Di Venosa N, Federici A, D’Agostino D, Rollo T, Prigigallo F, Altomare E, Fiore T, Vendemiale G (2005) Brief hypoxia before normoxic reperfusion (postconditioning) protects the heart against ischemia-reperfusion injury by preventing mitochondria peroxyde production and glutathione depletion. FASEB J 19:354–361

    Article  PubMed  CAS  Google Scholar 

  77. Ytrehus K, Myklebust R, Mjos OD (1986) Influence of oxygen radicals generated by xanthine oxidase in the isolated perfused rat heart. Cardiovasc Res 20:597–603

    Article  PubMed  CAS  Google Scholar 

  78. Sun H-Y, Wang NP, Kerendi F, Halkos M, Kin H, Guyton RA, Vinten-Johansen J, Zhao ZQ (2005) Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload. Am J Physiol 288:H1900–H1908

    CAS  Google Scholar 

  79. Mykytenko J, Kerendi F, Reeves JG, Kin H, Zatta AJ, Jiang R, Guyton RA, Vinten-Johansen J, Zhao ZQ (2007) Long-term inhibition of myocardial infarction by postconditioning during reperfusion. Basic Res Cardiol 102:90–100

    Article  PubMed  CAS  Google Scholar 

  80. Di Lisa F, Menabo R, Canton M, Barile M, Bernardi P (2001) 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 276:2571–2575

    Article  PubMed  CAS  Google Scholar 

  81. Griffiths EJ, Halestrap AP (1995) Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion. Biochem J 307:93–98

    PubMed  CAS  Google Scholar 

  82. Bopassa JC, Ferrera R, Gateau-Roesch O, Couture-Lepetit E, Ovize M (2006) PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning. Cardiovas Res 69:178–185

    Article  CAS  Google Scholar 

  83. Donato M, D’Annunzio V, Saban M, Flor L, Gelpi RJ (2004) Ischemic postconditioning reduced infarct size in normal and hypercholesterolemic rabbit hearts. J Mol Cell Cardiol 37:179

    Google Scholar 

  84. Iliodromitis EK, Zoga A, Vrettou A, Andreadou I, Paraskevaidis IA, Kaklamanis L, Kremastinos DT (2006) The effectiveness of postconditioning and preconditioning on infarct size in hypercholesterolemic and normal anesthetized rabbits. Atherosclerosis 188:356–362

    Article  PubMed  CAS  Google Scholar 

  85. Vinten-Johansen J, Johnston WE, Mills SA, Faust KB, Geisinger KR, DeMasi RJ, Cordell AR (1988) Reperfusion injury after temporary coronary occlusion. J Thorac Cardiovasc Surg 95:960–968

    PubMed  CAS  Google Scholar 

  86. Jolly SR, Kane WJ, Bailie MB, Abrams GD, Lucchesi BR (1984) Canine myocardial reperfusion injury: its reduction by the combined administration of superoxide dismutase and catalase. Circ Res 54:277–285

    PubMed  CAS  Google Scholar 

  87. Bolli R, Becker L, Gross G, Mentzer RM, Balshaw D Jr, Lathrop DA (2004) Myocardial protection at a crossroads: the need for translation into clinical therapy. Circ Res 95:125–134

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Jakob Vinten-Johansen.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Vinten-Johansen, J. Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion. Heart Fail Rev 12, 235–244 (2007). https://doi.org/10.1007/s10741-007-9024-3

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10741-007-9024-3

Keywords

Navigation