Effect of hypoglycemia on changes of brain lactic acid and intracellular pH produced by ischemia.
Previous investigators have attributed the fall of brain intracellular pH (pHi) produced by ischemia to accumulation of lactic acid. The goal of the present experiments was to examine the hypothesis that the acidosis produced by cerebral ischemia is due to accumulation of lactic acid. The present experiments inhibited lactic acid production by lowering glucose availability using insulin-induced hypoglycemia. The adverse effects of hypoglycemia were prevented by the prior elevation of beta-hydroxybutyric acid and acetoacetic acid induced by a high lipid diet. Brain pHi and lactic acid were measured by 31P and 1H NMR. The results showed that insulin-induced hypoglycemia markedly inhibits production of lactic acid, but has no effect on brain pHi during ischemia. These findings suggest that, at least under some conditions, the acidosis produced by cerebral ischemia is not due to accumulation of lactic acid.
Nagai
Y
Y
Department of Medicine, Veterans Administration Medical Center, San Francisco, California 94121.
Naruse
S
S
Weiner
M W
MW
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007003:Hypoglycemia / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D007328:Insulin; D007424:Intracellular Fluid / Q000378:metabolism; D007773:Lactates / Q000096:biosynthesis*; D019344:Lactic Acid; D008297:Male; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000031:analogs & derivatives / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000494:pharmacology
D007328:Insulin; D007773:Lactates; D010710:Phosphates; D014280:Triglycerides; D010725:Phosphocreatine; D019344:Lactic Acid; C025403:phosphocreatinine; D000255:Adenosine Triphosphate