Autoimmune Mechanisms of Trophic Dysfunction and Ischemic Brain Damage

2003 ◽  
pp. 147-182
Author(s):  
Eugene Gusev ◽  
Veronica I. Skvortsova
Keyword(s):  
Brain Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

Blockade of central histaminergic H2 receptors facilitates catecholaminergic metabolism and aggravates ischemic brain damage in the rat telencephalon

2003 ◽  
Vol 974 (1-2) ◽  
pp. 117-126 ◽  
Author(s):  
Ryu Otsuka ◽  
Naoto Adachi ◽  
Gen Hamami ◽  
Keyue Liu ◽  
Toshihiro Yorozuya ◽  
...  
Keyword(s):  
Brain Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
H2 Receptors

Ischemic neuronal damage after acute subdural hematoma in the rat: effects of pretreatment with a glutamate antagonist

1991 ◽  
Vol 74 (6) ◽  
pp. 944-950 ◽  
Author(s):  
Min-Hsiung Chen ◽  
Ross Bullock ◽  
David I. Graham ◽  
Jimmy D. Miller ◽  
James McCulloch
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Nmda Receptor Antagonist ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Content Type ◽  
Irreversible Brain Damage ◽  
Slow Injection

✓ The ability of a competitive N-methyl-D-aspartate (NMDA) receptor antagonist (D-CPP-ene) to reduce irreversible brain damage has been examined in a rodent model of acute subdural hematoma. Acute subdural hematoma was produced by the slow injection of 400 µl homologous blood into the subdural space overlying the parietal cortex in halothane-anesthetized rats. Brain damage was assessed histologically in sections at multiple coronal planes in animals sacrificed 4 hours after induction of the subdural hematoma. Pretreatment with D-CPP-ene (15 mg/kg) significantly reduced the volume of ischemic brain damage produced by the subdural hematoma from 62 ± 8 cu mm (mean ± standard error of the mean) in vehicle-treated control rats to 29 ± 7 cu mm in drug-treated animals. These data demonstrate the anti-ischemic efficacy of NMDA antagonists in an animal model of intracranial hemorrhage in which intracranial pressure is elevated, and suggest that excitotoxic mechanisms (which are susceptible to antagonism by D-CPP-ene) may play a role in the ischemic brain damage which is observed in patients who die after acute subdural hematoma.

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