Profound, reversible energy loss in the hypoxic immature rat brain

Jensen, Frances E.; Tsuji, Miles; Offutt, Martin; Firkusny, Igor R.; Holtzman, David

doi:10.1016/0165-3806(93)90051-b

Cited by 27 publications

(9 citation statements)

References 35 publications

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“…Owens et al (61) 452 reported on the morphologic and electrophysiologic consequences of hypoxia-induced seizures. In their groups of immature animals (postnatal d 8 -10), 3% oxygen, causing bradycardia (47), near complete energy depletion (62), and seizures, resulted in neuronal injury detected acutely in the dentate and hilar regions of the hippocampus, but not when the animals were examined at 60 -80 d of recovery. Similarly, Toth et al (63) found that in their model of febrile seizures in the immature rat, hyperthermic seizures resulted in the appearance of cell damage in the limbic system within 24 h, but by 4 wk of recovery no significant neuronal dropout was evident.…”

Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

et al. 2001

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Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

et al. 2001

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“…During a seizure, the brain of a normoglycemic neonate would run out of ATP in 2.51 min. Profound ATP depletion during hypoxic seizures has been observed [19]. Since cerebral metabolic rate increases 5.3% per degree [22], hyperthermia to 39°C would be expected to raise energy use rate during seizures in our animals to 10.09 mmole ~P/kg/min.…”

Section: Discussionmentioning

confidence: 92%

Brain Energy Metabolism During Experimental Neonatal Seizures

et al. 2010

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During flurothyl seizures in 4-day-old rats, cortical concentration of ATP, phosphocreatine and glucose fell while lactate rose. Cortical energy use rate more than doubled, while glycolytic rate increased fivefold. Calculation of the cerebral metabolic balance during sustained seizures suggests that energy balance could be maintained in hyperglycemic animals, and would decline slowly in normoglycemia, but would be compromised by concurrent hypoglycemia, hyperthermia or hypoxia. These results suggest that the metabolic challenge imposed on the brain by this model of experimental neonatal seizures is milder than that seen at older ages, but can become critical when associated with other types of metabolic stress.

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“…Even by 21 days, the absence of increases in Lac or Pi suggest that global tissue ischemia is not a major factor, although the existence of some local areas of anaerobic metabolism cannot be excluded, as discussed previously Chumas et al, 1994). It is interesting to note there appears to be a window of susceptibility to hypoxia/ischemia in rat pups at 9-13 days of age (Jensen et al, 1993;Suzuki et al, 1992). This age coincides with the period of rapid cortical growth (Eayrs and Goodhead, 1959) and the increased capacity for Lac production and anaerobic glycolysis (Holtzman et al, 1982).…”

Section: Reversibility Of Changesmentioning

confidence: 91%

Progressive Changes in Cortical Metabolites at Three Stages of Infantile Hydrocephalus Studied byIn VitroNMR Spectroscopy

Jones

Harris²,

Rocca³

et al. 1997

Journal of Neurotrauma

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Infantile hydrocephalus is most often caused by an obstruction in the cerebrospinal fluid flow pathway and results in ventricular dilatation and chronic trauma to the surrounding brain. Surgical treatment alleviates the condition but does not cure or prevent neurological deficits. The H-Tx rat has severe hydrocephalus due to a spontaneous aqueduct obstruction in late gestation. In order to determine how hydrocephalus affects brain metabolism in tissue adjacent to the expanded ventricles, cortical extracts have been made from groups of hydrocephalic and control littermates with early, intermediate, and advanced hydrocephalus at 4, 11, and 21 days after birth. Extracts were analyzed with 1H and 31P NMR spectroscopy and metabolite peaks were quantified using an external standard. Metabolite concentrations were calculated relative to tissue wet weight and subsequently expressed relative to tissue dry weight, using values for water content obtained from additional groups of rats. In early hydrocephalus there was a significant decrease in the phosphomonoester phosphorylcholine, and there were small, nonsignificant changes in other compounds. By 11 days, in addition to phosphomonoesters, there were significant decreases in ATP, phosphocreatine, and in inorganic phosphate, but with no change in lactate. By 21 days there were also substantial decreases in cholines, inositol, creatine, glutamate, glutamine, aspartate, N-acetylaspartate, alanine, and taurine. It is concluded that the sequence of pathological events starts with changes in membrane lipids. This is followed by reductions in energy metabolite which leads to cell swelling with loss of intracellular osmolytes and neurotransmitters. These changes are discussed in relation to hydrocephalus pathophysiology and to prevention and reversibility with shunt treatment.

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Profound, reversible energy loss in the hypoxic immature rat brain

Cited by 27 publications

References 35 publications

Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

Brain Energy Metabolism During Experimental Neonatal Seizures

Progressive Changes in Cortical Metabolites at Three Stages of Infantile Hydrocephalus Studied byIn VitroNMR Spectroscopy

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