HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Andre Terzic Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jovanovic, A. Articles by Terzic, A. Search for Related Content PubMed PubMed Citation Articles by Jovanovic, A. Articles by Terzic, A.

Ann Thorac Surg 1998;65:586
© 1998 The Society of Thoracic Surgeons

---

Current Reviews

Adenosine Prevents K-Induced Ca² Loading: Insight Into Cardioprotection During Cardioplegia

Aleksandar Jovanovi, MD, Jose R. Lopez, MD, Alexey E. Alekseev, PhD, Win K. Shen, MD, Andre Terzic, MD

Division of Cardiovascular Diseases, Department of Medicine, and Clinical Pharmacology Unit, Department of Pharmacology, Mayo Clinic, Mayo Foundation, Rochester, Minnesota, USA

Dr Terzic, Mayo Clinic, G-7, Rochester, MN 55905 (e-mail: terzic.andre@mayo.edu).

In clinical practice, hyperkalemic cardioplegia induces sarcolemmic depolarization, and therefore is used to arrest the heart during open heart operations. However, the elevated concentration of K⁺ that is present in cardioplegic solutions promotes intracellular Ca²⁺ loading, which could aggravate ventricular dysfunction after cardiac operations. This review highlights recent findings that have established, at the single cell level, the protective action of adenosine against hyperkalemia-induced Ca²⁺ loading. When it was added to hyperkalemic cardioplegic solutions, adenosine, at millimolar concentrations and through a direct action on ventricular cardiomyocytes, prevented K⁺-induced Ca²⁺ loading. This action of adenosine required the activation of protein kinase C, and it was effective only in cardiomyocytes with low diastolic Ca²⁺ levels. Of importance, adenosine did not diminish the magnitude of K⁺-induced membrane depolarization, allowing unimpeded cardiac arrest. Taken together, these findings provide direct support for the idea that adenosine is valuable when used as an adjunct to hyperkalemic cardioplegia. This idea has emerged from previous clinical studies that have shown improvement of the clinical outcome after cardiac operations when adenosine or related substances were used to supplement cardioplegic solutions. Further studies are required to define more precisely the mechanism of action of adenosine, and the conditions that may determine the efficacy of adenosine as a cytoprotective supplement to cardioplegia.

This article has been cited by other articles:

				S. Hyun Lim, S. Lee, K. Noda, T. Kawamura, Y. Tanaka, N. Shigemura, A. Nakao, and Y. Toyoda Adenosine injection prior to cardioplegia enhances preservation of senescent hearts in rat heterotopic heart transplantation Eur J Cardiothorac Surg, June 1, 2013; 43(6): 1202 - 1208. [Abstract] [Full Text] [PDF]

				R. Mukherjee, W. M. Yarbrough, E. S. Reese, J. S. Leiser, J. A. Sample, J. T. Mingoia, A. E. Hardin, R. E. Stroud, J. E. McLean, J. W. Hendrick, et al. Myocyte contractility with caspase inhibition and simulated hyperkalemic cardioplegic arrest Ann. Thorac. Surg., May 1, 2004; 77(5): 1684 - 1689. [Abstract] [Full Text] [PDF]

				G. P. Dobson and M. W. Jones Adenosine and lidocaine: a new concept in nondepolarizing surgical myocardial arrest, protection, and preservation J. Thorac. Cardiovasc. Surg., March 1, 2004; 127(3): 794 - 805. [Abstract] [Full Text] [PDF]

				Z. S. Jonjev, D. W. Schwertz, J. M. Beck, J. D. Ross, and W. R. Law Subcellular distribution of protein kinase C isozymes during cardioplegic arrest J. Thorac. Cardiovasc. Surg., December 1, 2003; 126(6): 1880 - 1885. [Abstract] [Full Text] [PDF]

				M. Scorsin, A. Mebazaa, N. A. Attar, B. Medini, J. Callebert, R. Raffoul, R. Ramadan, J. M. Maillet, A. Ruffenach, F. Simoneau, et al. Efficacy of esmolol as a myocardial protective agent during continuous retrograde blood cardioplegia J. Thorac. Cardiovasc. Surg., May 1, 2003; 125(5): 1022 - 1029. [Abstract] [Full Text] [PDF]

				G. Vassort Adenosine 5'-Triphosphate: a P2-Purinergic Agonist in the Myocardium Physiol Rev, April 1, 2001; 81(2): 767 - 806. [Abstract] [Full Text] [PDF]

				C. Ozcan, E. L. Holmuhamedov, A. Jahangir, and A. Terzic Diazoxide protects mitochondria from anoxic injury: Implications for myopreservation J. Thorac. Cardiovasc. Surg., February 1, 2001; 121(2): 0298 - 306. [Abstract] [Full Text] [PDF]

				S. Jovanovic, A. Jovanovic, W. K. Shen, and A. Terzic Protective action of 17{beta}-estradiol in cardiac cells: implications for hyperkalemic cardioplegia Ann. Thorac. Surg., November 1, 1998; 66(5): 1658 - 1661. [Abstract] [Full Text] [PDF]

				E. L. Holmuhamedov, S. Jovanovic, P. P. Dzeja, A. Jovanovic, and A. Terzic Mitochondrial ATP-sensitive K+ channels modulate cardiac mitochondrial function Am J Physiol Heart Circ Physiol, November 1, 1998; 275(5): H1567 - H1576. [Abstract] [Full Text] [PDF]

				A. Jovanovic, S. Jovanovic, E. Lorenz, and A. Terzic Recombinant Cardiac ATP-Sensitive K+ Channel Subunits Confer Resistance To Chemical Hypoxia-Reoxygenation Injury Circulation, October 13, 1998; 98(15): 1548 - 1555. [Abstract] [Full Text] [PDF]

				D. Pucar, E. Janssen, P. P. Dzeja, N. Juranic, S. Macura, B. Wieringa, and A. Terzic Compromised Energetics in the Adenylate Kinase AK1 Gene Knockout Heart under Metabolic Stress J. Biol. Chem., December 22, 2000; 275(52): 41424 - 41429. [Abstract] [Full Text] [PDF]