Hypoglycemia prevents increase in lactic acidosis during reperfusion after temporary cerebral ischemia in rats
✍ Scribed by Dominique Sappey-Marinier; Laureano Chileuitt; Philip R. Weinstein; Michael W. Weiner; Alan I. Faden
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 890 KB
- Volume
- 8
- Category
- Article
- ISSN
- 0952-3480
No coin nor oath required. For personal study only.
✦ Synopsis
Sequential "P and 'H MRS was used to measure cerebral phosphate metabolites, intracellular pH, and lactate in normoglycemic and hypoglycemic rats during 30 min of complete cerebral ischemia and 5.5 h of reperfusion. These results were correlated with brain levels of free fatty acids (FFAs), excitatory amino acids, cations, and water content at death. The IactatelN-acetyl aspartate ratio was not significantly different between groups before or during occlusion. During reperfusion, the ratio was higher in normoglycemic rats from 3 to 85 min (ps 0.05), and recovery time was faster in hypoglycemic rats (29 vs 45 min; p = 0.04), suggesting reduced lactate production and faster recovery of aerobic metabolism. During occlusion, significant but comparable decrease of intracellular pH occurred in each group. Intracellular pH was higher in hypoglycemic rats at 140 min and 260 min of reperfusion. Water content, Na and K+ concentrations, and FFA and excitatory amino acid levels were not significantly different between groups, but hypoglycemic rats had less depletion of levels of Mg'+ @=O.OlI). These results show that hypoglycemia has a limited but potentially beneficial effect on postischemic lactic acidosis.