Reduction of cerebral infarct size by non-competitive AMPA antagonists in rats subjected to permanent and transient focal ischemia

2004 ◽  
Vol 1019 (1-2) ◽  
pp. 210-216 ◽  
Author(s):  
Éva Matucz ◽  
Krisztina Móricz ◽  
Gábor Gigler ◽  
Annamária Simó ◽  
József Barkóczy ◽  
...  
Keyword(s):  
Infarct Size ◽  
Focal Ischemia ◽  
Cerebral Infarct ◽  
Ampa Antagonists ◽  
Transient Focal Ischemia

Comparison of the Effects of Propofol and Pentobarbital on Neurologic Outcome and Cerebral Infarct Size after Temporary Focal Ischemia in the Rat 

1997 ◽  
Vol 87 (5) ◽  
pp. 1139-1144 ◽  
Author(s):  
Janet E. Pittman ◽  
Huaxin Sheng ◽  
Robert Pearlstein ◽  
Ann Brinkhouse ◽  
Franklin Dexter ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Wistar Rats ◽  
Focal Cerebral Ischemia ◽  
Focal Ischemia ◽  
Cerebral Infarct ◽  
Early Reperfusion ◽  
Recovery Interval ◽  
Neurologic Function ◽  
Cerebral Physiology

Background Although propofol is known to have effects on cerebral physiology similar to the barbiturates, a direct comparison of the relative effects of these drugs on outcome from cerebral ischemia has not been performed. The authors postulated that pentobarbital or propofol would yield similar effects on neurologic and histologic outcome from temporary focal ischemia in the rat. Methods Wistar rats were anesthetized with sufficient doses of pentobarbital (n = 20) or propofol (n = 20) to cause electroencephalographic burst suppression. The middle cerebral artery was then occluded for 75 min. Animals were awakened 4-6 h after onset of reperfusion and allowed to recover for 1 week. Neurologic function and infarct size were then assessed. Results Relevant physiologic values were similar between groups during ischemia and early reperfusion. No difference between groups was observed for severity of hemiparesis (P = 0.10). Total cerebral infarct volumes (median +/- quartile deviation) were similar for the two groups (pentobarbital = 190 +/- 36 mm3; propofol = 200 +/- 24 mm3, P = 0.35). Conclusion Neurologic and histologic outcome were similar in pentobarbital or propofol anesthetized rats undergoing temporary focal cerebral ischemia and a 1-week recovery interval.

Khat affects apoptosis and related gene XIAP and Smac expression following transient focal ischemia in rats

2010 ◽  
Vol 34 (8) ◽  
pp. S16-S16
Author(s):  
Fang‑fang Bi ◽  
Hadi M. Mujlli ◽  
Yue‑qiang Hu ◽  
Fa‑fa Tian ◽  
Zhi‑guo Wu ◽  
...  
Keyword(s):  
Focal Ischemia ◽  
Related Gene ◽  
Transient Focal Ischemia

Aggravation of brain injury after transient focal ischemia in p53-deficient mice

2001 ◽  
Vol 88 (1-2) ◽  
pp. 54-61 ◽  
Author(s):  
Keiichiro Maeda ◽  
Ryuji Hata ◽  
Frank Gillardon ◽  
Konstantin-Alexander Hossmann
Keyword(s):  
Brain Injury ◽  
Focal Ischemia ◽  
Transient Focal Ischemia ◽  
Deficient Mice

scholarly journals Protective Role for Type 4 Metabotropic Glutamate Receptors against Ischemic Brain Damage

2010 ◽  
Vol 31 (4) ◽  
pp. 1107-1118 ◽  
Author(s):  
Slavianka G Moyanova ◽  
Federica Mastroiacovo ◽  
Lidia V Kortenska ◽  
Rumiana G Mitreva ◽  
Erminia Fardone ◽  
...  
Keyword(s):  
Brain Damage ◽  
Metabotropic Glutamate Receptors ◽  
Infarct Volume ◽  
Focal Ischemia ◽  
Protective Role ◽  
Ischemic Brain Damage ◽  
Systemic Injection ◽  
Ischemic Brain ◽  
Metabotropic Glutamate ◽  
Transient Focal Ischemia

We examined the influence of type 4 metabotropic glutamate (mGlu4) receptors on ischemic brain damage using the permanent middle cerebral artery occlusion (MCAO) model in mice and the endothelin-1 (Et-1) model of transient focal ischemia in rats. Mice lacking mGlu4 receptors showed a 25% to 30% increase in infarct volume after MCAO as compared with wild-type littermates. In normal mice, systemic injection of the selective mGlu4 receptor enhancer, N-phenyl-7-(hydroxyimino)cyclopropa[b]chromen-1a-caboxamide (PHCCC; 10 mg/kg, subcutaneous, administered once 30 minutes before MCAO), reduced the extent of ischemic brain damage by 35% to 45%. The drug was inactive in mGlu4 receptor knockout mice. In the Et-1 model, PHCCC administered only once 20 minutes after ischemia reduced the infarct volume to a larger extent in the caudate/putamen than in the cerebral cortex. Ischemic rats treated with PHCCC showed a faster recovery of neuronal function, as shown by electrocorticographic recording and by a battery of specific tests, which assess sensorimotor deficits. These data indicate that activation of mGlu4 receptors limit the development of brain damage after permanent or transient focal ischemia. These findings are promising because selective mGlu4 receptor enhancers are under clinical development for the treatment of Parkinson's disease and other central nervous system disorders.

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