Lactate reduces amino acid release and fuels recovery of function in the ischemic brain.
Pre-ischemic hyperglycemia exacerbates the neuronal injury associated with cerebral ischemia/reperfusion, possibly because the accumulation of glycolytically derived lactate causes acidosis. Twenty minutes of four vessel occlusion caused significant increases in rat cerebral cortical superfusate levels of aspartate, glutamate, phosphoethanolamine, taurine, and GABA. Lactate (20 mM), applied topically, significantly reduced the ischemia/reperfusion evoked releases of glutamate and GABA, with further reductions following the higher dose (40 mM), which also significantly reduced the evoked release(s) of the other amino acids. EEG recovery was robust in the presence of 40 mM lactate. These results substantiate the ability of lactate to serve as a neuronal energy substrate but question the role of lactate accumulation in the enhancement of ischemic brain injury by hyperglycemia.
Phillis
J W
JW
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA. jphillis@med.wayne.edu
Song
D
D
Guyot
L L
LL
O'Regan
M H
MH
D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D004569:Electroencephalography / Q000187:drug effects; D007267:Injections; D019344:Lactic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D013654:Taurine / Q000378:metabolism
D000596:Amino Acids; D013654:Taurine; D019344:Lactic Acid