1140 CEREBROSPINAL FLUID/BLOOD GLUCOSE RATIOS In PREMATURE AND FULL-TERM INFANTS

Monaco, Michele; Kopen, Pamela; Bloom, Emily C.; Carter, Arthur; Vannucci, Robert C.

doi:10.1203/00006450-197804001-01146

Cited by 3 publications

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“…Since ventricular fluid glucose reflects, at least in part, blood glucose concentrations, a more meaningful expression of hypoglycorrhachia is the ventricular fluid/ blood glucose ratio. The mean cerebrospinal fluid/blood glucose ratio in 83 normoglycemic (blood glucose 40-80mg/dl) preterm and full-term infants without IVH or meningitis was 0.81 fO.23 (sD) (Monaco et al 1978). In the present investigation, ventricular fluid/blood glucose ratios below 0.35 (-2 sD) occurred in all six patients when the two fluids were analysed simultaneously.…”

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confidence: 39%

Cerebral Oxidative Metabolism in Perinatal Post‐hemorrhagic Hydrocephalus

Vannucci

Hellmann

Dubynsky

et al. 1980

Develop Med Child Neuro

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SUMMARY Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome characterized by hydrocephalus and biochemical abnormalities in cerebrospinal fluid. The authors investigated six neonates with post‐hemorrhagic obstructive hydro‐cephalus in order to identify cerebral metabolic disturbances responsible for the hypo‐glycorrhachia observed in this disorder. Lactic acid concentrations and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post‐hemorrhagic hydrocephalus compared with the values in five with congenital (non‐hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the two groups. There is evidence that neither residual cellular elements in ventricular fluid nor a disrupted blood‐CSF barrier can fully explain the observed alterations in ventricular‐fluid glucose, lactate or lactate/pyruvate ratios. It is suggested that when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting in hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction. RÉSUMÉ Metabolisme oxidatif cerebral dans I'hydrocéphalic péri‐natale post‐háemorragique Les survivants d'hémorragie intra‐ventriculaire périnatale développent souvent un syndrome clinique particulier caracterise par une hydrocephalie et des anomalies biochimiques du liquide cephalo‐rachidien. Les auteurs ont etudie six nouveaux‐nes, porteurs d'une hydrocephalie non communicante post‐h6morragique en vue d'identifier les troubles du metabolisme cerebral responsable de l'hypoglycarachie observee dans cette affection. Les concentrations d'acide lactique et les rapports lactate‐pyruvate dans le liquide ventriculaire etaient significativement eleves chez les nourrissons avec hydrocephalie post‐hemorragique par comparaison avec les valeurs observees chez cinq nourrissons avec hydrocephalie congenitale non communicante (non hemorragique). La dilatation ventriculaire et l'hypertension intra‐cranienne etaient presentes et de valeur comparable dans les deux groupes. II semble bien que ni les elements cellulaires residuels dans le liquide ventriculaire, ni la rupture de la barriere cerebro‐meningee ne peut expliquer pleinement les alterations observees du glucose, du lactate, du rapport lactate‐pyruvate dans le liquide ventriculaire. Les auteurs suggerent qu'en cas d'hemorragie peri‐ventriculaire, l'ischemie cerebrale associee provoque localement une glycolyse anaerobie et accroit les exigences en glucose. L'apport de glucose cerebral a partir du sang n'etant pas adequat, le glucose diffuse dans le cerveau a partir du liquide ventriculaire et il en resulte une hypoglycorachie. La production d'acide lactique cerebral est renforcee et ce corps...

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Section: Resultssupporting

confidence: 39%

Cerebral Oxidative Metabolism in Perinatal Post‐hemorrhagic Hydrocephalus

Vannucci

Hellmann

Dubynsky

et al. 1980

Develop Med Child Neuro

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Glucose, lactic acid, and perinatal hypoxic-ischemic brain damage

Vannucci

Yager²

1992

Pediatric Neurology

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Cerebral Metabolic Responses of Hyperglycemic Immature Rats to Hypoxia-Ischemia

1987

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ABSTRACT. Unlike adult rats, glucose supplementation of immature rats does not lead to accentuated hypoxicischemic brain damage. To explore the reason for this agespecific paradox, we subjected 7-day postnatal rats to unilateral common carotid artery occlusion followed by a subcutaneous injection of either 0.1 ml 50% glucose or normal saline. They were then exposed to hypoxia with 8% oxygen, during which they received 2.5 wCi 2-[I4Cj-glucose or were quick-frozen for brain metabolite analysis. During hypoxia-ischemia, glucose transport into the ipsilateral cerebral hemisphere of the hyperglycemic rats was greater (+loo-150%) than in normoglycemic animals. However, glucose consumption was similar in the two groups. Glucose concentrations in brain were lower during hypoxia-ischemia in the normoglycemic animals, whereas lactate increased to similar levels in the two groups. The high-energy phosphate reserves, ATP and phosphocreatine, were depleted to a similar extent. Thus, hyperglycemia combined with hypoxia-ischemia, although associated with increased glucose transport into brain, does not lead to enhanced glucose utilization or lactate accumulation by brain over that of hypoxia-ischemia alone. (Pediatr Res 21: 524-529,1987) Abbreviation PCA, perchloric acidIt is unclear whether elevated blood glucose concentrations are protective or damaging to the human brain during perinatal hypoxia-ischemia. This is an important question, since glucose infusions ranging in concentrations from 5 to 25% are administered frequently to premature and distressed full-term newborn infants. Furthermore, blood glucose concentrations can be quite variable in newborn infants, with levels occasionally exceeding 500 mg/dl (1, 2). Based on data in experimental animals, many physicians believe that even modestly high blood glucose concentrations are beneficial to the newborn infant undergoing hypoxic stress (3). In this regard, Himwich et al. (4) found that immature rats pretreated with glucose and then rendered anoxic survive twice as long as untreated controls (see also Refs. 5-8). The mechanism of this glucose protection presumably relates to increased endogenous carbohydrate stores (glucose and glycogen) Received September 15, 1986; accepted December 24, 1986. All correspondence and reprint requests to Robert C. Vannucci, M.D., Department of Pediatrics, The Milton S. Hershey Medical Center, P.O. Box 850, Hershey, PA 17033.Supported by Grant 15738 from The National Institute of Child Health and Human Development and by a grant from the American Diabetes Association. 5 in brain and heart sufficient to maintain blood and tissue glucose levels for an extended interval during a hypoxic or anoxic insult (6, 7, 9, 10).Despite the heightened hypoxic resistance of glucose supplemented perinatal animals, recent experiments have shown that glucose can be damaging to the brain during hypoxia-ischemia. Myers and Yamaguchi (1 1) found that food-deprived juvenile monkeys recover relatively undamaged after a 10-to 14-min cardiorespiratory arrest, w...

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1140 CEREBROSPINAL FLUID/BLOOD GLUCOSE RATIOS In PREMATURE AND FULL-TERM INFANTS

Cited by 3 publications

References 0 publications

Cerebral Oxidative Metabolism in Perinatal Post‐hemorrhagic Hydrocephalus

Cerebral Oxidative Metabolism in Perinatal Post‐hemorrhagic Hydrocephalus

Glucose, lactic acid, and perinatal hypoxic-ischemic brain damage

Cerebral Metabolic Responses of Hyperglycemic Immature Rats to Hypoxia-Ischemia

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