licostinel and Infarction--Middle-Cerebral-Artery

licostinel has been researched along with Infarction--Middle-Cerebral-Artery* in 1 studies

Other Studies

1 other study(ies) available for licostinel and Infarction--Middle-Cerebral-Artery

Article	Year
Delayed treatment with 5-nitro-6,7-dichloro-1,4-dihydro-2,3-quinoxalinedione, a glycine site N-methyl-D-aspartate antagonist, protects against permanent middle cerebral artery occlusion in male rats. Neuroscience letters, 2003, Aug-28, Volume: 347, Issue:3 The glycine site, N-methyl-D-aspartate antagonist 5-nitro-6,7-dichloro-1,4-dihydro-2,3-quinoxalinedione (ACEA1021) was previously tested only in models of transient stroke with pre-treatment paradigms. We therefore tested whether it would protect in two models of permanent stroke in two rat strains with delayed treatment. Intravenous ACEA1021 reduced cerebral infarction by 62% (15 min treatment delay) and 42% (2 h treatment delay), relative to vehicle-injected rats, when subjected to a modified Tamura and permanent intraluminal filament model of stroke, respectively. In comparison, intravenous nicotinamide (500 mg/kg), which was tested in separate animal cohorts, had no significant effect on infarction. These data show that ACEA1021 protects against permanent focal cerebral ischemia, even with a 2 h post-treatment delay. Characterization of the therapeutic window with longer outcome times including infarction and neurobehavioral endpoints is needed. Topics: Animals; Brain; Brain Infarction; Infarction, Middle Cerebral Artery; Injections, Intravenous; Male; Neuroprotective Agents; Quinoxalines; Rats; Rats, Inbred F344; Receptors, Glycine; Receptors, N-Methyl-D-Aspartate; Time Factors	2003

Article

Year

Delayed treatment with 5-nitro-6,7-dichloro-1,4-dihydro-2,3-quinoxalinedione, a glycine site N-methyl-D-aspartate antagonist, protects against permanent middle cerebral artery occlusion in male rats.

Neuroscience letters, 2003, Aug-28, Volume: 347, Issue:3

The glycine site, N-methyl-D-aspartate antagonist 5-nitro-6,7-dichloro-1,4-dihydro-2,3-quinoxalinedione (ACEA1021) was previously tested only in models of transient stroke with pre-treatment paradigms. We therefore tested whether it would protect in two models of permanent stroke in two rat strains with delayed treatment. Intravenous ACEA1021 reduced cerebral infarction by 62% (15 min treatment delay) and 42% (2 h treatment delay), relative to vehicle-injected rats, when subjected to a modified Tamura and permanent intraluminal filament model of stroke, respectively. In comparison, intravenous nicotinamide (500 mg/kg), which was tested in separate animal cohorts, had no significant effect on infarction. These data show that ACEA1021 protects against permanent focal cerebral ischemia, even with a 2 h post-treatment delay. Characterization of the therapeutic window with longer outcome times including infarction and neurobehavioral endpoints is needed.

Topics: Animals; Brain; Brain Infarction; Infarction, Middle Cerebral Artery; Injections, Intravenous; Male; Neuroprotective Agents; Quinoxalines; Rats; Rats, Inbred F344; Receptors, Glycine; Receptors, N-Methyl-D-Aspartate; Time Factors

2003