The Effect of the Glycine Site-Specific N-Methyl-d-Aspartate Antagonist ACEA1021 on Ischemic Brain Damage Caused by Acute Subdural Hematoma in the Rat

1995 ◽  
Vol 12 (3) ◽  
pp. 279-288 ◽  
Author(s):  
EIJI TSUCHIDA ◽  
ROSS BULLOCK
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Glycine Site ◽  
Ischemic Brain Damage ◽  
Site Specific ◽  
Ischemic Brain

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.

Ischemic brain damage in a model of acute subdural hematoma

Neurosurgery ◽  
1990 ◽  
pp. 433 ◽  
Author(s):  
J D Miller ◽  
R Bullock ◽  
D I Graham ◽  
M H Chen ◽  
G M Teasdale
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

Effect of perfluorocarbons on brain oxygenation and ischemic damage in an acute subdural hematoma model in rats

2005 ◽  
Vol 103 (4) ◽  
pp. 724-730 ◽  
Author(s):  
Taek Hyun Kwon ◽  
Dong Sun ◽  
Wilson P. Daugherty ◽  
Bruce D. Spiess ◽  
M. Ross Bullock
Keyword(s):  
Brain Tissue ◽  
Brain Damage ◽  
Subdural Hematoma ◽  
Histological Study ◽  
Acute Subdural Hematoma ◽  
Brain Oxygenation ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Content Type ◽  
Fine Print

Object. This study was conducted to determine whether perfluorocarbons (PFCs) improve brain oxygenation and reduce ischemic brain damage in an acute subdural hematoma (SDH) model in rats. Methods. Forty adult male Sprague—Dawley rats were allocated to four groups: 1) controls, acute SDH treated with saline and 30% O2; 2) 30-PFC group, acute SDH treated with PFC infusion in 30% O2; 3) 100-O2 group, acute SDH treated with 100% O2; and 4) 100-PFC group, acute SDH treated with PFC plus 100% O2. Ten minutes after the induction of acute SDH, a single dose of PFC was infused and 30% or 100% O2 was administered simultaneously. Four hours later, half of the rats were killed by perfusion for histological study to assess the extent of ischemic brain damage. The other half were used to measure brain tissue oxygen tension (PO2). The volume of ischemic brain damage was 162.4 ± 7.6 mm3 in controls, 165.3 ± 11.3 mm3 in the 30-PFC group, 153.4 ± 17.3 mm3 in the 100-O2 group, and 95.9 ± 12.8 mm3 in the 100-PFC group (41% reduction compared with controls, p = 0.002). Baseline brain tissue PO2 values were approximately 20 mm Hg, and after induction of acute SDH, PO2 rapidly decreased and remained at 1 to 2 mm Hg. Treatment with either PFC or 100% O2 improved brain tissue PO2, with final values of 5.14 and 7.02 mm Hg, respectively. Infusion of PFC with 100% O2 improved brain tissue PO2 the most, with a final value of 15.16 mm Hg. Conclusions. Data from the current study demonstrated that PFC infusion along with 100% O2 can significantly improve brain oxygenation and reduce ischemic brain damage in acute SDH.

Ischemic Brain Damage in a Model of Acute Subdural Hematoma

Neurosurgery ◽  
1990 ◽  
Vol 27 (3) ◽  
pp. 433-439 ◽  
Author(s):  
Jimmy D. Miller ◽  
Ross Bullock ◽  
David I. Graham ◽  
Graham M. Teasdale
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

Transient glucose hypermetabolism after acute subdural hematoma in the rat

1992 ◽  
Vol 76 (3) ◽  
pp. 471-477 ◽  
Author(s):  
Yasuhiro Kuroda ◽  
Fiona M. Inglis ◽  
Jimmy D. Miller ◽  
James McCulloch ◽  
David I. Graham ◽  
...  
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Excitatory Amino Acids ◽  
Glucose Utilization ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain ◽  
Content Type ◽  
Blood Injection ◽  
High Concentrations ◽  
Fine Print

✓ Ischemic brain damage occurs in most patients with acute subdural hematoma, yet many aspects of the distribution and extent of this damage remain unexplained. Previous studies in rat model, which produces a region of infarction under the hematoma, have implicated an “excitotoxic” mechanism, suggesting that high concentrations of excitatory amino acids may exacerbate ischemic damage. A study is described in which local glucose utilization is measured 2 or 4 hours after induction of acute subdural hematoma in the rat. These changes are compared to those produced by introducing the same volume of inert silicone gel into the subdural space. Massive increases (up to 142%) in glucose utilization occurred throughout both hippocampi and in a variable zone around the ischemic core, but these had normalized by 4 hours after blood injection. Hippocampal hypermetabolism was not seen after introduction of the silicone mass, suggesting that diffusible substances from the clotted blood may be responsible for these changes. This transient hypermetabolism accords with an excitotoxic process, which may amplify brain damage after acute subdural hematoma.

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