THE INFLUENCE OF PREISCHEMIC HYPERGLYCEMIA ON ACUTE CHANGES IN BRAIN WATER ADC FOLLOWING FOCAL ISCHEMIA IN RATS

Citation
Nc. Huang et al., THE INFLUENCE OF PREISCHEMIC HYPERGLYCEMIA ON ACUTE CHANGES IN BRAIN WATER ADC FOLLOWING FOCAL ISCHEMIA IN RATS, Brain research, 788(1-2), 1998, pp. 137-143
Citations number
22
Categorie Soggetti
Neurosciences
Journal title
Volume
788
Issue
1-2
Year of publication
1998
Pages
137 - 143
Database
ISI
SICI code
Abstract
The effect of preischemic hyperglycemia on the acute decline of brain apparent diffusion coefficient of water (ADCw) following cerebral isch emia was studied in a rat model of middle cerebral artery occlusion (M CAO). ADCw was measured by NMR with a newly developed spin-echo line-s can protocol that provides for an ADCw calculation every 15 s at a spa tial resolution of 3.4 mu l/pixel. A remote controlled occluding devic e was used to initiate ischemia from outside the magnet, allowing for continuous monitoring of ADCw before, during and after MCAO. Preischem ic hyperglycemia (25-30 mM) was achieved via i.v. infusion of 50% gluc ose. The decline in ADCw following ischemia was analyzed to obtain thr ee-time constants: the time from onset of ischemia to initial signific ant ADCw decline below baseline level (i.e., 20% of maximal decline, T -0.20), the time to decline by 50% (T-0.50), and the time to decline b y 95% (T-0.95). Mean (+/-S.D.) values for T-0.20, T-0.50, T-0.95 were: 39.6 +/- 7.2, 54.0 +/- 7.8, 105.0 +/- 15.0 s for the normoglycemic gr oup (n = 7), and 49.2 +/- 33.0, 116.4 +/- 2.4, 351.0 +/- 189.0 s for t he hyperglycemic group (n = 6), respectively. Hyperglycemia significan tly prolongs T-0.50 and T-0.95 but does not affect T-0.20. The tempora l profiles of ADCw decline following ischemia under normo- and hypergl ycemia are distinctively different from the known time course of membr ane depolarization under similar experimental conditions, suggesting t hat mechanisms other than membrane depolarization and cell swelling ma y contribute to changes in ADCw in cerebral ischemia. (C) 1998 Elsevie r Science B.V.