Abstract
The possibility was examined that it is the slow rate of cardiac adenine nucleotide biosynthesis that may be responsible for the retarded metabolic recovery of the myocardium during the reperfusion period following a brief ischemic insult. The approach that was used is based on the fact that ribose expands the available pool of 5-phosphoribosyl-l-pyrophosphate and thus leads to the stimulation of the biosynthesis of adenine nucleotides in heart and skeletal muscle. The effect of this stimulation on the cardiac ATP pool was then studied. Two experimental models of myocardial ischemia and reperfusion were examined in rats: recovery from multiple asphyxie periods and recovery from temporary regional ischemia. The spontaneous increase in adenine nucleotide biosynthesis that occurred in the myocardium during the reperfusion period in both models was further stimulated with ribose. During the recovery from a 15-minutes’ period of regional ischemia, the restoration of the ATP pool was achieved much earlier when ribose had been applied It can therefore be concluded that the slow adenine nucleotide biosynthesis determines the speed of ATP repletion, and that ribose accelerates this metabolic recovery process. It is shown that ribose fulfills the essential criteria that should be met by a suitable cardioprotective agent.KeywordsAdenine NucleotideStun MyocardiumReperfusion PeriodOxidative Pentose Phosphate PathwayRegional Myocardial IschemiaThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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