Effect of U74006F on Neurologic Function and Brain Edema After Fluid Percussion Injury in Rats

Sanada, Takahiro; Nakamura, Toshio; Nishimura, Merry; Isayama, Kazuo; Pitts, Lawrence H.

doi:10.1089/neu.1993.10.65

Cited by 39 publications

(12 citation statements)

References 29 publications

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“…The doses of TM, MP and vitamin E were selected on the basis of previous studies. 13,47,48 Our experimental study demonstrated that all three treatment regimens decreased the level of LP following spinal cord trauma in rats. Vitamin E was less e ective than TM and MP.…”

Section: Discussionmentioning

confidence: 67%

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

et al. 1999

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E ect of methylprednisolone (MP), tirilazad mesylate (TM) and vitamin E on lipid peroxidation (LP) was evaluated in an experimental model of spinal cord compression injury in anesthetized rats. Forty rats, divided randomly into four groups, were injured by compressing on the spinal cord at Th 3 for 1 min. Bolus injections of saline solution, MP (30 mg/kg bolus and 5.4 mg/kg/h), TM (10 mg/kg four times per day), or vitamin E (30 mg/ kg four times per day) were begun 1 h after the spinal cord injury (SCI). Twenty-four hours after treatment, the rats were killed, and malondialdehyde (MDA), a LP product, was measured in the spinal cord tissues. Rats treated with MP, TM and vitamin E had signi®cantly decreased MDA levels (P50.01) than rats in the control group. The lowest MDA levels were found in the TM group. These results suggest that MP, TM and vitamin E may have a protective e ect against SCI in rats by its antioxidant e ect.

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Section: Discussionmentioning

confidence: 67%

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

et al. 1999

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“…FPI adversely affects global cerebral blood flow for up to 1 hr (Yuan et al, 1988), and there is a local metabolic dysfunction reflected by decreased glucose utilization that lasts at least 5 days postinjury (Yoshino et al, 1991). Recently, free radical scavengers, such as the 21-aminosteroids (Sanada et al, 1993) and superoxide dismutase (Levasseur et al, 1989), were noted to reduce the metabolic and functional consequences of FPI. FPI also causes a marked increase in extracellular glutamate that is associated with cellular injury and death (Katayama et al, 1990a).…”

Section: Discussionmentioning

confidence: 99%

Fluid Percussion Injury Causes Loss of Forebrain Choline Acetyltransferase and Nerve Growth Factor Receptor Immunoreactive Cells in the Rat

Leonard

Maris²,

Grady³

1994

Journal of Neurotrauma

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Memory dysfunction is a common sequela of human traumatic brain injury (TBI). Cholinergic forebrain neurons are recognized for their role in memory. We tested the hypothesis that forebrain cholinergic neurons are vulnerable to fluid percussion injury (FPI), a model of human TBI. Rodents were subjected to a moderate parasagittal FPI, sham injury, or fimbria/fornix axotomy and then killed 10 days after the procedure. Additional animals underwent FPI or sham injury and were killed 7, 14, and 28 days after the procedure. Neurons in the medial septal nucleus and vertical limb of the nucleus of the diagonal band of Broca were identified and quantitated using choline acetyltransferase (ChAT) and low affinity nerve growth factor receptor (NGF-R) immunohistochemistry. Our results showed a significant decrease in ChAT (17% +/- 5%) and NGF-R (24% +/- 8%) immunoreactive cells in FPI animals killed after 10 days when compared to sham-injured animals. Animals undergoing fimbria/fornix axotomy showed a greater reduction in ChAT (53% +/- 13%) and NGF-R (55% +/- 5%) immunoreactive cells 10 days postaxotomy. The number of ChAT and NGF-R immunoreactive neurons was reduced at all time points. However, statistical significance was present 10 and 14 days postinjury for ChAT immunoreactive neurons and 10 days only for NGF-R immunoreactive neurons. These studies have shown that FPI produces transient loss of ChAT and NGF-R immunoreactive neurons.

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“…15 min and 3 h after fluid percussion head injury induced a decrease in brain oedema, contralateral to the injury side, 48 h after injury [30]. Sonada et al [33] suggested that TM did not significantly reduce brain water content at 1, 3, 10 or 30 mg/kg doses, but that rats treated with TM at a dose of 10 mg/kg had significantly better motor function scores than rats in the control group. The results of our study have not confirmed the decrease in oedema determined by Petty et al [32] and McIntosh et al [30] following trauma.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, TM has been shown to result in significant reductions in brain water, potassium loss, and sodium accumulation [30,33].…”

Section: Introductionmentioning

confidence: 99%

Lipid peroxidation and oedema in experimental brain injury: comparison of treatment with methylprednisolone, tirilazad mesylate and vitamin E

et al. 1999

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Trauma-induced lipid peroxidation (LP) is one of the most important factors that produces tissue damage in head trauma. In the present study, the protective effects of free radical suppression with methylprednisolone (MP), tirilazad mesylate (TM) and vitamin E on the development of cerebral LP and oedema resulting from head trauma have been investigated. Rats were divided randomly into four groups. Bolus injections of physiological saline, MP (initial 30 mg/kg for 1 h, continuing administration of 5.4 mg/kg per hour until 24 h), TM (10 mg/kg), or vitamin E (30 mg/kg) were given 1 h after the head trauma. The animals were killed 24 h after the weight-drop injury for removal of the brain, and the malondialdehyde (MDA) level and water content of the brain were determined. Rats treated with TM had MDA levels which decreased significantly in comparison with the control group (P<0.03), and none of the drugs had an effect on LP and water content of the brain (P>0.05) that was statistically different. These findings demonstrated the beneficial effect of TM in this model of experimental brain injury.

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Effect of U74006F on Neurologic Function and Brain Edema After Fluid Percussion Injury in Rats

Cited by 39 publications

References 29 publications

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

Fluid Percussion Injury Causes Loss of Forebrain Choline Acetyltransferase and Nerve Growth Factor Receptor Immunoreactive Cells in the Rat

Lipid peroxidation and oedema in experimental brain injury: comparison of treatment with methylprednisolone, tirilazad mesylate and vitamin E

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