Key result
Glutamate and aspartate-rich cardioplegic solutions may enhance myocardial preservation and left ventricular function during ischemia and reperfusion through various biochemical mechanisms.
Why the study?
Do cardioplegic solutions rich in glutamate and aspartate improve myocardial preservation and left ventricular function during ischemia?
Do cardioplegic solutions rich in glutamate and aspartate improve myocardial preservation and left ventricular function during ischemia?
Amino acid-rich cardioplegic solutions, particularly those containing glutamate and aspartate, offer a safe and inexpensive biochemical mechanism to enhance myocardial preservation during ischemia and reperfusion.
Cardioplegic solutions rich in the hydrophilic, basic amino acids, glutamate and aspartate, have enhanced myocardial preservation and left ventricular function. This has been demonstrated in assorted animal preparations involving ischemia with and without reperfusion. Published clinical data, though limited, strongly support the contention that these amino acids have myocardial protective properties. Several biochemical mechanisms exist by which certain amino acids may attenuate ischemic or reperfusion injury. Glutamate and aspartate may become preferred myocardial fuels in the setting of ischemia. They may also reduce myocardial ammonia production and reduce cytoplasmic lactate levels, thereby deinhibiting glycolysis. Some amino acids may become substrate for the citric acid cycle. Glutamate and aspartate also move reducing equivalents from cytoplasm to mitochondria where they are necessary for oxidative phosphorylation and energy generation. A rationale exists for the use of an amino acid-rich cardioplegia-like solution in myocardial infarction. These solutions are safe and inexpensive.
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Michael A. Arsenian (1998) conducted a review in Myocardial ischemia and infarction. Glutamate, aspartate, and other amino acids was evaluated. Glutamate and aspartate-rich cardioplegic solutions may enhance myocardial preservation and left ventricular function during ischemia and reperfusion through various biochemical mechanisms.
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