This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tyson, R. L. Articles by Peeling, J. Search for Related Content PubMed PubMed Citation Articles by Tyson, R. L. Articles by Peeling, J. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CARBON DIOXIDE OXYGEN SODIUM Medline Plus Health Information Hypoglycemia Transient Ischemic Attack

(Stroke. 1996;27:957-964.)
© 1996 American Heart Association, Inc.

Articles

²³Na Nuclear Magnetic Resonance Spectral Changes During and After Forebrain Ischemia in Hypoglycemic, Normoglycemic, and Hyperglycemic Rats

Randy L. Tyson, MSc; Garnette R. Sutherland, MD James Peeling, PhD

From the Departments of Chemistry (R.L.T., J.P.), Pharmacology and Therapeutics (J.P.), and Radiology (J.P.), University of Manitoba; the Department of Chemistry, University of Winnipeg (Manitoba) (J.P.); and the Department of Neurosurgery, Foothills Hospital, Calgary, Alberta (G.R.S.), Canada.

Background and Purpose The severity of brain injury in animal models of forebrain ischemia increases with blood glucose level. During ischemia, energy failure is slower and maintenance of ion gradients is prolonged as the level of glycemia increases. It is not clear how the level of glycemia influences recovery of ion homeostasis on reperfusion. It has been shown that changes in the intensity of the multiple-quantum ²³Na nuclear magnetic resonance (NMR) signals reflect changes in intracellular Na⁺ levels. We have used ²³Na NMR spectroscopy to evaluate the influence of the level of glycemia on changes in Na⁺ concentration during and after forebrain ischemia in rats.

Methods Single-quantum (SQ) and double-quantum (DQ) ²³Na NMR spectra were measured before and during 10-minute forebrain ischemia and during reperfusion in hypoglycemic, normoglycemic, and hyperglycemic rats.

Results The DQ ²³Na NMR signal increased to 210% of preischemia intensity in all rats, but a delay in this increase was observed in normoglycemic and hyperglycemic animals. The rate of the DQ ²³Na NMR signal increase was fastest in hypoglycemic (apparent first-order rate constant 0.673±0.046 min^-1, P<.002 compared with normoglycemic animals) and slowest in hyperglycemic (0.285±0.024 min^-1, P<.03) rats. During reperfusion, the signal intensity recovered rapidly in hypoglycemic (0.385±0.050 min^-1) and normoglycemic (0.464±0.047 min^-1) rats, whereas in hyperglycemic animals recovery was slow (0.108±0.044 min^-1, P<.0001 compared with normoglycemic animals). The SQ ²³Na NMR signal intensity increased to 117% of preischemia level in hypoglycemic (P<.05 compared with normoglycemic animals) and to 107% in normoglycemic and hyperglycemic animals during reperfusion.

Conclusions The slower increase in the ²³Na DQ NMR signal intensity during forebrain ischemia in rats with higher blood glucose levels suggests that Na⁺ homeostasis is maintained longer in these animals. On reperfusion, the slower recovery of the DQ ²³Na NMR signal intensity in hyperglycemic animals likely indicates a slower recovery of Na⁺ homeostasis, perhaps contributing to the increased neuronal injury after cerebral ischemia in hyperglycemic animals.

Key Words: cerebral ischemia, transient • glucose • sodium • spectroscopy, nuclear magnetic resonance • rats