Does long-term glucose infusion reduce brain damage after transient cerebral ischemia?

Li, Ping An; He, Qing; Csiszár, Katalin; Siesjö, Bo K.

doi:10.1016/s0006-8993(01)02724-x

Cited by 19 publications

(9 citation statements)

References 7 publications

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“…The mechanism(s) by which the hyperglycemia intensifies brain damage is the subject of much controversy (15)(16)(17)(18)(19)(20). The role of hyperglycemia in perinatal hypoxic-ischemic CNS insults has not been completely elucidated.…”

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confidence: 99%

Effects of Exogenous Glucose on Brain Ischemia in Ovine Fetuses

et al. 2004

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confidence: 99%

Effects of Exogenous Glucose on Brain Ischemia in Ovine Fetuses

et al. 2004

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“…[1][2][3] This is in contrast with juvenile diabetic patients in whom the episodes of severe hypoglycemia frequently are associated with alterations of mental state, such as confusion or loss of orientation, 4 and eventually seizures and coma may occur. [5][6][7] Hyperglycemia also is known to aggravate ischemic brain damage 8 -10 (although there may be differential effects of long-term and short-term hyperglycemia [11][12][13] ), whereas fasting-induced hypoglycemia has protective effects in ischemia and neurotoxic neuronal damage. 14 -17 Similarly, fasting-induced hypoglycemia is associated with decreases in susceptibility to hyperbaric oxygen-induced seizures.…”

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confidence: 99%

Correlation between extracellular glucose and seizure susceptibility in adult rats

Schwechter

Velı́šková

Velı́šek

2002

Annals of Neurology

107

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In adult diabetic patients, periods of hyperglycemia may be associated with exacerbation of focal seizures. Our objective was to determine in the adult rats the correlation between seizure susceptibility and extracellular glucose concentration in two models of seizures. Male rats were injected with two doses of streptozocin (40 mg/kg IP) on 2 consecutive days to induce diabetic hyperglycemia. Controls either received vehicle or were not injected. After 2 weeks, blood glucose concentration was measured, and the rats were subjected to flurothyl seizure test. Another group of rats received glucose solution (20%, 5 ml IP) 30 minutes before testing to induce nondiabetic hyperglycemia. Thresholds for flurothyl-induced clonic and tonic-clonic seizures were determined. Finally, in vitro epileptiform activity was induced in the entorhinal cortex-hippocampal slices from naive rats by perfusing with magnesium-free medium with various glucose concentrations. In additional slices, paired-pulse paradigm was determined in the perforant path. Susceptibility to clonic and tonic-clonic flurothyl-induced seizures positively correlated with blood glucose concentrations as the increased glucose concentration was associated with proconvulsant effects. Similarly, in the in vitro experiments, epileptiform activity was promoted by increased and suppressed by decreased glucose concentrations. Data indicate that, in the adult rats, high glucose concentrations are associated with proconvulsant effects.

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“…66,82 What is not well publicized is that the ATP decline appears to be significantly slower in white matter than in gray matter. 86,87 It is not known whether this observation is also true for white matter. The implication is that white matter may retain sufficient ATP to prolong the time it can endure ischemia without sustaining irreversible injury.…”

Section: Derangement Of Transmembrane Ion Gradientsmentioning

confidence: 99%