Skip to main content
Log in

Preconditioning: We do not need more experiments, because our current knowledge already permits us to develop pharmacological agents

  • Published:
Basic Research in Cardiology Aims and scope Submit manuscript

Conclusion

Already we know enough about preconditioning to plan our pharmacological reponses appropriately We must concentrate on activation of KATP channels in relevant clinical sitrations. More experiments, although always desirable, are not going to help as much as application of what we already know.

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.

Similar content being viewed by others

References

  1. Baines CR, Goto M, Downey JM (1997) Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium. J Mol Cell Cardiol 29: 207–216

    Google Scholar 

  2. Bolli R (1990) Mechanism of myocardial “stunning”. Circulation 82: 723–738

    Google Scholar 

  3. Cleveland JC, Meldrum DR, Rowland RT et al. (1977) Adenosine preconditioning of human myocardium is dependent upon the ATP-sensitive K+ channel. J Mol Cell Cardiol 29: 175–182

    Google Scholar 

  4. Cohen MV, Downey JM (1993) Ischaemic preconditioning: can the protection be bottled? Lancet 342: 6

    Google Scholar 

  5. Gross GJ, Auchampach JA (1992) Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs. Circ Res 70: 223–233

    Google Scholar 

  6. Headrick JP (1996) Ischemic preconditioning: bioenergic and metabolic changes and the role of endogenous adenosine. J Mol Cell Cardiol 28: 1227–1240

    Google Scholar 

  7. Ichinari K, Kakei M, Matsuoka T et al. (1996) Direct activation of the ATP-sensitive potassium channel by oxygen free radicals in guinea-pig ventricular cells: its potentiation by MgADP. J Mol Cell Cardiol 28: 1867–1877

    Google Scholar 

  8. Inagaki N, Gonoi T, Clement JP et al. (1996) A family of sulfonylurea receptors determines the pharmacological properties of ATP-sensitive K+ channels. Neurol 16: 1011–1017

    Google Scholar 

  9. Kanda A, Watanabe I, Gettes LS (1996) Pinacidil unexpectedly lessens the rise in extracellular K+ and preserves conduction during acute ischemia. Circulation 1 (Suppl I): I-306

    Google Scholar 

  10. Kantor PF, Coetzee WA, Carmeliet EE et al. (1990) Reduction of ischemic K loss and arrhythmias in rat hearts. Effect of glibenclamide, a sulfonylurea. Circ Res 66: 478–485

    Google Scholar 

  11. King LM, Opie LH (1996) Does preconditioning act by glycogen depletion in the isolated rat heart? J Mol Cell Cardiol 28: in press

  12. Kolocassides KG, Galinanes M, Hearse DJ (1996) Dichotomy of ischemic preconditioning. Improved postischemic contractile function despite intensification of ischemic contracture. Circulation 93: 1725–1733

    Google Scholar 

  13. Lawson CS, Downey JM (1993) Preconditioning: state of the art myocardial protection. Cardiovasc Res 27: 542–550

    Google Scholar 

  14. Opie LH (1989) Reperfusion injury and its pharmacologic modification. Circulation 80: 1049–1062

    Google Scholar 

  15. Speechly-Dick ME, Grover GJ, Yellon DM (1995) Does ischemic preconditioning in the human involve protein kinase C and the ATP dependent K+ channel? Studies of contractile function after simulated ischemia in an atrial in vitro model. Circ Res 77: 1030–1035

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Opie, L.H. Preconditioning: We do not need more experiments, because our current knowledge already permits us to develop pharmacological agents. Basic Res Cardiol 92 (Suppl 2), 46–47 (1997). https://doi.org/10.1007/BF00797208

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF00797208

Keywords

Navigation