Changes in cerebral energy metabolism and calcium levels in relation to delayed neuronal death after ischemia.
Using a brief transient ischemic model, we examined changes in regional tissue calcium content and energy metabolism in the hippocampus. In the CA1 region, tissue calcium ions began to increase 24 h after reperfusion, accompanied by changes in tissue pH and ATP. In the CA3 region, energy metabolism remained unchanged for 72 h after reperfusion, and the calcium pool was first noted 24 h after reperfusion, while tissue calcium ions began to increase 48 h after reperfusion. These results suggest that the neurons in the CA3 region seem to survive because of the well-preserved metabolic function to cope with excessive calcium ions.
Hashimoto
K
K
Department of Neurosurgery, Faculty of Medicine, Kyoto University, Japan.
Kikuchi
H
H
Ishikawa
M
M
Kobayashi
S
S
D000255:Adenosine Triphosphate / Q000378:metabolism; D000471:Alkalosis / Q000503:physiopathology; D000818:Animals; D001921:Brain / Q000503:physiopathology*; D001923:Brain Chemistry / Q000502:physiology; D002118:Calcium / Q000032:analysis / Q000502:physiology*; D016923:Cell Death / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D004800:Enzymes, Immobilized; D005849:Gerbillinae; D006863:Hydrogen-Ion Concentration; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D015424:Reperfusion
D004800:Enzymes, Immobilized; D000255:Adenosine Triphosphate; D002118:Calcium