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J Thorac Cardiovasc Surg 1995;110:281-282
© 1995 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Cardiac Surgery
University of Munich
Klinikum Grosshadern
Munich, Germany
To the Editor:
The recent article by Lasley and Mentzer
1 investigating the role of adenosine in enhanced myocardial preservation with University of Wisconsin (UW) solution shows the important role of the compound for the protective properties of UW solution. Functional recovery as measured by rate-pressure product was significantly improved after 18 hours of cold storage with the inclusion of adenosine in UW solution. However, no difference was observed between UW solution without adenosine and St. Thomas' Hospital cardioplegic solution. The question arising is whether the inclusion of adenosine in St. Thomas' Hospital solution would have had the same beneficial effects on functional recovery and interstitial fluid purine levels. It can be concluded from the presented data that no difference exists between UW solution without adenosine and unmodified St. Thomas' Hospital solution and that the main component leading to improved preservation is adenosine.
Therefore, the conclusion drawn by the authors that the superior preservation with UW solution is a result of its intracellular-based electrolyte composition and inclusion of lactobionate, raffinose, and hydroxyethyl starch is misleading. We have shown a dose-dependent improvement of myocardial recovery with the addition of adenosine to St. Thomas' Hospital solution No. 2 in an in vivo baboon model after 3 hours of cardioplegic arrest.
2 Our results, consistent with those of other studies, showed no beneficial effect on myocardial adenosine triphosphate content, stressing the fact that the effect of adenosine on improving postischemic refunction seems to be independent of its effects as an adenine nucleotide precursor.
The assumption that the low-sodium, high-potassium formulation of UW solution could presumably retard cell swelling by reducing the electrochemical gradients of these ions may be correct; however, the high potassium concentration is possibly the cause of postischemic endothelial dysfunction as a result of endothelial damage or disturbance. Amrani and colleagues
3 reported a marked increase in coronary vascular resistance associated with impaired myocardial protection when using UW solution in an isolated rat heart model for 60 minutes of global ischemia at a moderately hypothermic temperature (20º C). Loss of protection with UW solution at temperatures of 20º C compared with St. Thomas' Hospital solution No. 2 seems to be correlated with the high potassium concentrations. Other groups have also reported impaired endothelium-dependent coronary responses after cold potassium cardioplegia.
4
These findings show that the superior preservation with UW solution compared with other crystalloid preservation solutions is not uncontradicted. Another study from the Universities of Cape Town and Jerusalem found superior long-term preservation for 18 hours of cold storage with St. Thomas' Hospital solution No. 2 compared with UW solution in a paracorporeal porcine model.
5 Therefore, a study of a fourth group with St. Thomas' Hospital solution and inclusion of adenosine should be performed to substantiate the conclusions drawn by Lasley and Mentzer.
References
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