| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 2002;73:569-574
© 2002 The Society of Thoracic Surgeons
a Department of Surgery, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA
b Department of Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA
c Department of Biostatistics, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA
Accepted for publication September 9, 2001.
* Address reprint requests to Dr Holman, Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35294-0007, USA
e-mail: wholman{at}its.uab.edu
Background. Intramyocyte sodium (Na+) increases during ischemia and reperfusion, which causes myocardial calcium (Ca2+) uptake and leads to myocyte injury or death. This study determines if ischemic preconditioning and myocyte sodium-hydrogen ion (Na+-H+) exchange (NHE) inhibition decreases Na+ gain that otherwise occurs with cardioplegic arrest and reperfusion.
Methods. Pigs had 1 hour of cardioplegic arrest followed by reperfusion. Group 1 had no intervention (controls). Group 2 received dimethyl amiloride (DMA, an NHE inhibitor), and group 3 had ischemic preconditioning before cardioplegic arrest. Precardioplegia to postreperfusion change in intramyocyte ion content was measured with atomic absorption spectrometry. The time to initial electrical activity and number of defibrillations needed to establish an organized rhythm postreperfusion were used as electrophysiologic variables to measure ischemia-reperfusion injury.
Results. Intramyocyte Na+ content for group 1 increased from 45.9 ± 6.7 to 61.9 ± 22.5 µmol/g (p = 0.02). Group 2 had an insignificant decrease in intramyocyte Na+ of 27.7 ± 19.58 µmol/g (p = 0.06), and group 3 had an insignificant decrease of 10.8 ± 46.33 µmol/g (p = 0.48). Interstitial water increased significantly in all groups, but there were no significant increases in intramyocyte water content. Electrophysiologic recovery was similar for all three groups.
Conclusions. The NHE inhibition and ischemic preconditioning each eliminated the increase in intramyocyte Na+ content that otherwise occurred with cardioplegic arrest and reperfusion in this porcine model. Because their mechanisms are distinct, it is possible that an additive beneficial effect against ischemia-reperfusion injury can be achieved by using NHE inhibition together with a preconditioning stimulus as prereperfusion therapy.
This article has been cited by other articles:
|
|
 |
|
  S. Wang, J. Radhakrishnan, I. M. Ayoub, J. D. Kolarova, D. M. Taglieri, and R. J. Gazmuri Limiting sarcolemmal Na+ entry during resuscitation from ventricular fibrillation prevents excess mitochondrial Ca2+ accumulation and attenuates myocardial injury J Appl Physiol, July 1, 2007; 103(1): 55 - 65. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. E. Davies, S. B. Digerness, C. R. Killingsworth, C. Zaragoza, C. R. Katholi, R. K. Justice, S. P. Goldberg, and W. L. Holman Multiple Treatment Approach to Limit Cardiac Ischemia-Reperfusion Injury Ann. Thorac. Surg., October 1, 2005; 80(4): 1408 - 1416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Nicolini, C. Beghi, C. Muscari, A. Agostinelli, A. M. Budillon, I. Spaggiari, and T. Gherli Myocardial protection in adult cardiac surgery: current options and future challenges Eur. J. Cardiothorac. Surg., December 1, 2003; 24(6): 986 - 993. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
