Effects of dexamethasone on brain edema induced by kainic acid seizures

Sztriha, L.; Joó, Ferenc; Szerdahelyi, P.; Eck, Erna; Koltai, M.

doi:10.1016/0306-4522(86)90229-0

Cited by 47 publications

(22 citation statements)

References 38 publications

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“…A 3-h recovery period with the dam was followed by 3 h in 8% oxygen wit11 92% nitrogen in a plastic chamber inside a neonatal incubator with an air temperature of 37°C. This well-established model of pelinatal cerebral hypoxiaischemia reliably produces ipsilateral infarction of the striatum, thalamus, hippocampus, and overlying cortex (1 [8][9][10][11][12][13][14][15][16][17][18][19][20]. The experimental protocol was approved by the Animal Care Committee of The Hospital for Sick Children.…”

Section: Methodsmentioning

confidence: 99%

“…Treatment with veIy high doses of glucocorticoids (3-6 n~g/kg dexamethasone or 15-30 mg/kg methylprednisolone) have both reduced pathologic damage induced by experimental spinal cord trauma (5,6) and improved neurologic outcome after human spinal cord injury (7). Reductions in cerebral edema caused by tumors, infarction, pneumothorax, or convulsions with glucocorticoid therapy have also been reported (8)(9)(10)(11)(12). However, until the present study, glucocorticoid therapy did not appear to be effective in reducing brain damage due to cerebral hypoxia-ischemia.…”

mentioning

confidence: 97%

“…In our study, we investigated the effect of glucocorticoid administration on the extent of brain damage produced in a perinatal model of cerebral hypoxia-ischemia in the rat (1 [8][9][10][11][12][13][14][15][16][17][18][19][20]. The results demonstrate that in the neonate, rather than exacerbating neuronal damage, glucocorticoid administration before an episode of hypoxia-ischemia actually protects the brain from injury.…”

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confidence: 99%

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Dexamethasone Prevents Hypoxic-Ischemic Brain Damage in the Neonatal Rat

1991

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ABSTRACT. Glucocorticoid therapy is frequently used in perinatology and neonatology for its beneficial pulmonary effects. We investigated the influence of neonatal glucocorticoid administration on brain damage caused by a concurrent episode of cerebral hypoxia-ischemia. Various doses of dexamethasone in several treatment schedules were administered to 7-d-old rats that were also subjected to unilateral cerebral hypoxia-ischemia. In 79% of control rats, a large unilateral cerebral infarction occurred, whereas all rats pretreated with dexamethasone in doses At present, glucocorticoids are frequently used in perinatal medicine, both antenatally to prevent respiratory distress syndrome by inducing fetal production of pulmonary surfactant and postnatally to improve lung function in infants with bronchopulmonary dysplasia after mechanical ventilation (1-4). Both groups of infants are at risk of experiencing episodes of cerebral hypoxia-ischemia either during or after glucocorticoid administration, due to con~plications of prematurity and neonatal intensive care.Glucocorticoids have long been used for the treatment of various neurologic disorders in the adult. Several beneficial effects of steroid therapy have been demonstrated. Treatment with veIy high doses of glucocorticoids (3-6 n~g/kg dexamethasone or 15-30 mg/kg methylprednisolone) have both reduced pathologic damage induced by experimental spinal cord trauma (5, 6) and improved neurologic outcome after human spinal cord injury (7). Reductions in cerebral edema caused by tumors, Received August 28, 1990; accepted January 28, 1991 infarction, pneumothorax, or convulsions with glucocorticoid therapy have also been reported (8-12). However, until the present study, glucocorticoid therapy did not appear to be effective in reducing brain damage due to cerebral hypoxia-ischemia. Clinical (1 3-15) and experimental (1 6, 17) studies indicated that, in the adult, glucocorticoids are of no benefit or are detrimental (16,17) for the treatment of a focal ischemic stroke or global cerebral ischemia.In our study, we investigated the effect of glucocorticoid administration on the extent of brain damage produced in a perinatal model of cerebral hypoxia-ischemia in the rat (1 8-20). The results demonstrate that in the neonate, rather than exacerbating neuronal damage, glucocorticoid administration before an episode of hypoxia-ischemia actually protects the brain from injury. MATERIALS AND METHODSProduction of cerebral hypoxia-ischemia. Seven-d-old rats (Wistar or Sprague-Dawley) were anesthetized with halothane (4% for induction, 0.5-1% for maintenance) and the incision site was infiltrated with 2% lidocaine. The right carotid artery was isolated and ligated. A 3-h recovery period with the dam was followed by 3 h in 8% oxygen wit11 92% nitrogen in a plastic chamber inside a neonatal incubator with an air temperature of 37°C. This well-established model of pelinatal cerebral hypoxiaischemia reliably produces ipsilateral infarction of the striatum, thalamus, hippocampus, and overly...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 97%

mentioning

confidence: 99%

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Dexamethasone Prevents Hypoxic-Ischemic Brain Damage in the Neonatal Rat

1991

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“…BBB disruption has been reported in experimental and human epilepsy (Nitsch et al, 1985;Cornford and Oldendorf, 1986;Deli et al, 2005;Sztriha et al, 1986;Seiffert et al, 2004). Leakage of serum-derived components into the brain parenchyma results in neuronal hyperexcitability and seizure onset ( Therefore, dysfunction of the BBB leads to epileptogenesis and contributes to progression of epilepsy (Nitsch et al, 1985;Cornford and Oldendorf, 1986;Deli et al, 2005;Sztriha et al, 1986;Seiffert et al, 2004).…”

Section: Discussionmentioning

confidence: 96%

“…Nitsch et al, 1985;Cornford and Oldendorf, 1986;Deli et al, 2005;Sztriha et al, 1986;Seiffert et al, 2004).…”

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Endothelial NOS activation induces the blood–brain barrier disruption via ER stress following status epilepticus

Kim

Hyun

2015

Brain Research

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Testosterone up‐regulates aquaporin‐4 expression in cultured astrocytes

Hata

Toku

et al. 2003

J of Neuroscience Research

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Aquaporin-4 (AQP4) is located on astrocyte endfeet that face blood vessels in the brain and in the pia. It is thought to play a crucial role in the development of brain edema. To confirm the notion that sex steroids and dexamethasone influence brain edema through AQP4 regulation, we investigated the effects of 17beta-estradiol, testosterone, and dexamethasone on the expression of AQP4 in cultured astrocytes. Testosterone significantly up-regulated AQP4 at the level of both protein and mRNA. At a concentration of 100 nM, testosterone significantly increased AQP4 protein levels and ameliorated the osmotic fragility of astrocytes from hypoosmotic stress, suggesting that the increased levels of AQP4 facilitated the testosterone function. Moreover, this effect was attenuated by the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate, which can rapidly decrease AQP4 mRNA expression, indicating that the response was specific. These results indicate that AQP4 can alter the osmotic fragility of astrocytes and that testosterone can influence brain edema through AQP4 regulation, whereas 17beta-estradiol and dexamethasone cannot.

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Effects of dexamethasone on brain edema induced by kainic acid seizures

Cited by 47 publications

References 38 publications

Dexamethasone Prevents Hypoxic-Ischemic Brain Damage in the Neonatal Rat

Dexamethasone Prevents Hypoxic-Ischemic Brain Damage in the Neonatal Rat

Endothelial NOS activation induces the blood–brain barrier disruption via ER stress following status epilepticus

Testosterone up‐regulates aquaporin‐4 expression in cultured astrocytes

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