Effect of Status Epilepticus on Hypoxic-Ischemic Brain Damage in the Immature Rat

Cataltepe, Oguz; Vannucci, Robert C.; Heitjan, Daniel F.; Towfighi, Javad

doi:10.1203/00006450-199508000-00019

Cited by 56 publications

(18 citation statements)

References 25 publications

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“…Hence, any increase in damage would be relatively more easy to detect. Second, our animals recovered for only 30 min after HI, compared with 2 h in the experimental paradigm of Cataltepe et al (17). It has been previously shown that recovery of energy reserves in the immature brain requires at least 60 min (38).…”

Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

“…Those with moderate encephalopathy have an intermediate outcome, with sequelae being seen in approximately 20%, and those with only mild encephalopathy do well. The study by Cataltepe et al (17) suggests that prevention of seizures may not be helpful in those infants with severe hypoxic-ischemic insults. However, if superimposed seizures do accentuate brain injury in those with mild to moderate hypoxic-ischemic encephalopathy, prevention of seizures would be extremely important in the large proportion of infants with less severe insults.…”

Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

“…Although these results appear contradictory to ours, several methodological differences are important. Most relevant is the fact that Cataltepe's group used a model (2 h HI) in which damage is severe (infarction) in Ͼ50% of animals (11,12,17), particularly in the area of the hippocampus. Determining an increase in damage, particularly on a background of severe infarction, under these circumstances might prove difficult and lead to falsely negative results.…”

Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

“…The degree of brain damage was graded on four sections ranging from normal to Ͼ75% damage, including infarction (Table 1), using a modification of the method described by Cataltepe et al (17). Anteriorly, sections were taken starting with a cut through the midportion of the body of the anterior commissure, and included the anterior portions of cerebral cortex and caudate nucleus.…”

Section: Neuropathologic Analysismentioning

confidence: 99%

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Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

et al. 2001

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Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

Section: Perinatal Asphyxia and Seizuresmentioning

confidence: 99%

Section: Neuropathologic Analysismentioning

confidence: 99%

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Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

et al. 2001

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“…After 3 h of HI, the animals were allowed to recover with their dams until they were killed at 72 h post HI. The brains were fixated before neurologic scoring (8). When the brain was properly fixed, two 2-mm thick coronal tissue blocks were embedded in paraffin.…”

Section: Neuropathologymentioning

confidence: 99%

Increased Plasma Beta-Hydroxybutyrate, Preserved Cerebral Energy Metabolism, and Amelioration of Brain Damage During Neonatal Hypoxia Ischemia with Dexamethasone Pretreatment

et al. 2000

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Dexamethasone (DEX) pretreatment has been shown to be neuroprotective in a neonatal rat model of hypoxia ischemia (HI). The exact mechanism of this neuroprotection is still unknown. This study used 31 P nuclear magnetic resonance spectroscopy to monitor energy metabolism during a 3-h episode of HI in 7-d-old rat pups in one of two groups. The first group was pretreated with 0.1 mL saline (i.p.) and the second group was treated with 0.1 mL of 0.1mg/kg DEX (i.p.) 22 h before HI. Animals pretreated with DEX had elevated nucleoside triphosphate and phosphocreatine levels during HI when compared with controls. Salinetreated animals had significant decreases in nucleoside triphosphate and phosphocreatine and increases in inorganic phosphate over this same period. 31 P nuclear magnetic resonance data unequivocally demonstrate preservation of energy metabolism during HI in neonatal rats pretreated with DEX. Animals pretreated with DEX had little or no brain damage following 3 h of HI when compared with matched controls, which experienced severe neuronal loss and cortical infarction. These same pretreated animals had an increase in blood beta-hydroxybutyrate levels before ischemia, suggesting an increase in ketone bodies, which is the neonate's primary energy source. Elevation of ketone bodies appears to be one of the mechanisms by which DEX pretreatment provides neuroprotection during HI in the neonatal rat. Abbreviations DEX, dexamethasone HI, hypoxia ischemia NTP, nucleoside triphosphate NMR, nuclear magnetic resonance NMRS, nuclear magnetic resonance spectroscopy BHB, beta-hydroxybutyrate D-␤-HBA, D-␤-hydroxybutyrate dehydrogenase Dexamethasone (DEX) is a synthetic glucocorticoid. A National Institutes of Health consensus committee has recommended its use for women who are believed to deliver prematurely (1). Administered antenatally (before birth), DEX can relieve or ameliorate symptoms associated with respiratory distress syndrome and intraventricular hemorrhage and thus reduce mortality. Research was recommended to guide clinical care on the "effects of antenatal corticosteroids on hypoxic-ischemic insults."The first study to document the effects of DEX on neonatal animals was performed using the modified Levine preparation in neonatal rat by Altman et al. (2). They s.c. injected rat pups with either saline, 4 mg/kg DEX, or 40 mg/kg DEX immediately before hypoxia ischemia (HI). Neither dose of DEX ameliorated brain edema, lactacidemia, or hypoglycemia. In addition, there was no preservation of high-energy metabolites and there was an increase in mortality associated with the highest dose. These negative results made other investigators reluctant to pursue DEX as an effective neuroprotective agent.Barks et al. discovered that pretreatment with DEX 3 h or more before a hypoxic-ischemic insult was neuroprotective (3). DEX at 0.5 mg/kg/d for 3 d, before the insult, prevented brain damage associated with 3 h of cerebral HI in the 7-d-old rat Received August 8, 1998; accepted November 11, 1999

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Rat model of perinatal hypoxic-ischemic brain damage

et al. 1999

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To gain insights into the pathogenesis and management of perinatal hypoxic-ischemic brain damage, the authors have used an immature rat model which they developed many years ago. The model entails ligation of one common carotid artery followed thereafter by systemic hypoxia. The insult produces permanent hypoxic-ischemic brain damage limited to the cerebral hemisphere ipsilateral to the carotid artery occlusion. The mini-review describes recently accomplished research pertaining to the use of the immature rat model, specifically, investigations involving energy metabolism, glucose transporter proteins, free radical injury, and seizures superimposed upon cerebral hypoxia-ischemia. Future research will focus on molecular mechanisms of neuronal injury with a continuing focus on therapeutic strategies to prevent or minimize hypoxic-ischemic brain damage.

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Effect of Status Epilepticus on Hypoxic-Ischemic Brain Damage in the Immature Rat

Cited by 56 publications

References 25 publications

Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

Prolonged Seizures Exacerbate Perinatal Hypoxic-Ischemic Brain Damage

Increased Plasma Beta-Hydroxybutyrate, Preserved Cerebral Energy Metabolism, and Amelioration of Brain Damage During Neonatal Hypoxia Ischemia with Dexamethasone Pretreatment

Rat model of perinatal hypoxic-ischemic brain damage

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