Release of the excitotoxic amino acids, glutamate and aspartate, from the isolated ischemic/anoxic rat heart.
An isolated rat Langendorff heart preparation has been developed as a model in which to study the release of glutamate, aspartate and other amino acids during ischemia, anoxia and hypoglycemia. 15 min periods of ischemia resulted in large increases in perfusate levels of glutamate, aspartate, glycine, phosphoethanolamine, serine, alanine, taurine and glutamine. Amino acid levels returned towards pre-ischemic levels in subsequent perfusate collections. Anoxia (15 min duration) increased perfusate levels of most of the measured amino acids, with glutamate and aspartate being particularly affected. In contrast to ischemia, glutamate and aspartate levels declined slowly following reoxygenation. Hypoglycemia (15 min) resulted in small but significantly elevated levels of glutamate and glycine in heart perfusates. As the effects of ischemia or anoxia on glutamate and aspartate release from the heart appear to be comparable to those observed in the brain, it is proposed that the heart preparation may be a suitable model in which to study the ischemia-evoked release of these amino acids in the absence of complications arising from their depolarizing and excitotoxic actions on central neurons.
Song
D
D
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
O'Regan
M H
MH
Phillis
J W
JW
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D001921:Brain / Q000378:metabolism; D018846:Excitatory Amino Acids / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism*; D007003:Hypoglycemia / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism*; D051381:Rats
D018846:Excitatory Amino Acids; D001224:Aspartic Acid; D018698:Glutamic Acid