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J Thorac Cardiovasc Surg 2000;119:601-609
© 2000 Mosby, Inc.
CARDIOPULMONARY SUPPORT AND PHYSIOLOGY |
From the Research Service,a Westside Veterans Administration Medical Center, and the Departments of Physiology and Biophysicsb and Surgery,c University of Illinois College of Medicine at Chicago, Chicago, Ill.
Supported by a Veterans Administration Merit Review grant, a Living Institutes for Surgical Studies (LISS) grant, and National Institutes of Health grant GM 48219 (Dr Law). Dr Nawas was an Eleanor B. Pillsbury Fellow.
Address for reprints: William R. Law, PhD, Associate Professor, University of Illinois at Chicago, Department of Physiology and Biophysics (M/C 901), 835 S Wolcott, Chicago, IL 60612 (E-mail: wrlaw{at}uic.edu ).
Objective: Adenosine supplementation of cardioplegic solutions in cardiac operations improves postarrest myocardial recovery after cardioplegic arrest and reperfusion; however, the mechanism of the action of adenosine remains unknown. We tested the hypotheses that adenosine-supplemented cardioplegic solution improves myofibrillar protein cooperative interaction and increases myocardial anaerobic glycolysis.
Methods: The hearts of male Sprague-Dawley rats were randomized to undergo 120 minutes of cardioplegic arrest with 1 of 3 cardioplegic solutions: (1) St Thomas’ Hospital No. 2 cardioplegic solution (St Thomas group), (2) St Thomas’ Hospital No. 2 cardioplegic solution plus adenosine (100 µmol/L) (adenosine group), and (3) St Thomas’ Hospital No. 2 cardioplegic solution plus adenosine (100 µmol/L) plus the nonspecific adenosine receptor antagonist 8-p -sulfophenyltheophylline (50 µmol/L) (sulfophenyltheophylline group). A fourth group of hearts underwent no cardioplegic arrest.
Results: Systolic and diastolic functional recovery was improved in the adenosine group compared with that in the other two groups, independent of coronary flow. Adenosine supplementation of cardioplegic solution prevented the decrease in myofibrillar protein cooperative interaction seen after cardioplegic arrest and reperfusion (St Thomas and sulfophenyltheophylline groups). Adenosine-supplemented cardioplegic solution also caused significantly increased anaerobic glycolysis during cardioplegic arrest. These responses were blocked in the sulfophenyltheophylline group.
Conclusions: The changes in myocardial glycolytic activity and myofilament cooperativity coincided with functional recovery in the three cardioplegia groups and may represent mechanisms underlying protection with adenosine-supplemented cardioplegic solution.
This article has been cited by other articles:
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  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]
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T.-A. Miyamoto and K.-J. Miyamoto Are adenosine myocardial protective effects mediated through cAMP-independent effects or through cAMP inhibition/production? J. Thorac. Cardiovasc. Surg., October 1, 2000; 120(4): 829 - 830. [Full Text]
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W. R. Law Reply J. Thorac. Cardiovasc. Surg., October 1, 2000; 120(4): 830 - 830. [Full Text]
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