The influence of CGP-40116 on bicuculline evoked seizures in mice exposed to transient episode of brain oligemia

2000 ◽  
Vol 107 (11) ◽  
pp. 1263-1272 ◽  
Author(s):  
K. Rejdak ◽  
R. Rejdak ◽  
S. J. Czuczwar ◽  
Z. Kleinrok ◽  
M. Sieklucka-Dziuba
Keyword(s):  
Cgp 40116 ◽  
Transient Episode

The effect of CGP-40116 on pilocarpine evoked seizures in mice exposed to transient episode of brain ischemia

2000 ◽  
Vol 41 (3) ◽  
pp. 213-222 ◽  
Author(s):  
Konrad Rejdak ◽  
Robert Rejdak ◽  
Zbigniew Stelmasiak ◽  
Stanislaw J Czuczwar ◽  
Zdzislaw Kleinrok ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Cgp 40116 ◽  
Transient Episode

scholarly journals The Competitive NMDA Antagonist CGP 40116 Permanently Reduces Brain Damage after Middle Cerebral Artery Occlusion in Rats

1995 ◽  
Vol 15 (4) ◽  
pp. 602-610 ◽  
Author(s):  
Dirk Sauer ◽  
Edgar Weber ◽  
Guido Lüönd ◽  
Fernando Da Silva ◽  
Peter R. Allegrini
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Brain Tissue ◽  
Brain Damage ◽  
Analysis Of Variance ◽  
Cerebral Artery ◽  
Nmda Antagonist ◽  
Histological Evaluation ◽  
Mca Occlusion ◽  
Cgp 40116

In this study we evaluated the effect of the competitive N-methyl-d-aspartate (NMDA) antagonist d-(E)-4-(3-phosphonoprop-2-enyl)piperazine-2-carboxylic acid (CGP 40116) on both early (2 days) and late (28 days) ischemic brain damage in a rodent model of focal cerebral ischemia by means of magnetic resonance imaging (MRI) and conventional histology. Immediately after occlusion of the left middle cerebral artery (MCA), rats received either CGP 40116 (20 mg/kg i.p.) or isotonic saline. Two MRI scans were performed in each animal 2 and 28 days after MCA occlusion. After the second scan, rats were perfusion fixed for histological evaluation. The volume of lesioned brain tissue as determined by MRI or histology was calculated from the damaged area in single sections and the distance between them. CGP 40116 reduced acute infarct volume as measured by MRI 2 days after MCA occlusion by 44% (p < 0.05, analysis of variance). After 28 days the lesion detected by MRI was still significantly smaller in the drug-treated animals. This finding was confirmed by the histological analysis showing a 64% reduction in the volume of brain atrophy in the CGP 40116 group (p < 0.05, analysis of variance). There was a good correlation between the MRI data and the results of the histological evaluation ( r = 0.9). Our results indicate that (a) the competitive NMDA antagonist CGP 40116 permanently protects brain tissue from the consequences of cerebral ischemia in a rat model for human stroke and (b) early and late pathological changes can be accurately measured by MRI.

scholarly journals Postischemic Blockade of AMPA but Not NMDA Receptors Mitigates Neuronal Damage in the Rat Brain following Transient Severe Cerebral Ischemia

1992 ◽  
Vol 12 (1) ◽  
pp. 2-11 ◽  
Author(s):  
B. Nellgård ◽  
T. Wieloch
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Ampa Receptor ◽  
Neuronal Damage ◽  
Transient Cerebral Ischemia ◽  
Coupled Processes ◽  
Temporal Part ◽  
Nmda Receptor Antagonists ◽  
Receptor Antagonists ◽  
Cgp 40116

Glutamatergic transmission is an important factor in the development of neuronal death following transient cerebral ischemia. In this investigation the effects of N-methyl-d-aspartate (NMDA) and non-NMDA receptor antagonists on neuronal damage were studied in rats exposed to 10 min of transient cerebral ischemia induced by bilateral common carotid occlusion combined with hypotension. The animals were treated with a blocker of the ionotropic quisqualate or α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor, 2.3-dihydroxy-6-nitro-7-sulfamoyl-benzo( F)quinoxaline (NBQX), given postischemia as an intraperitoneal bolus dose of 30 mg kg−1 followed by an intravenous infusion of 75 μg min−1 for 6 h, or with the noncompetitive NMDA receptor blocker dizocilpine(MK-801) given 1 mg kg−1 i.p. at recirculation and 3 h postischemia, or with the competitive NMDA receptor antagonist dl-( E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 40116), 5 mg kg−1, given intraperitoneally at recirculation. Treatment with NBQX provided a significant reduction of neuronal damage in the hippocampal CA1 area by 44–69%, with the largest relative decrease in the temporal part of the hippocampus. In neocortex a significant decrease in the number of necrotic neurons was also noted. No protection could be seen following postischemic treatment with dizocilpine or CGP 40116. Our data demonstrate that AMPA but not NMDA receptor antagonists decrease neuronal damage following transient severe cerebral ischemia in the rat and that the protection by NBQX may be dependent on the severity of the ischemic insult. We propose that the AMPA receptor–mediated neurotoxicity could be due to ischemia-induced changes in the control mechanisms of AMPA receptor–coupled processes or to changes of AMPA receptor characteristics.

Clinical Observations on the Pathogenesis of Peritoneal Dialysate Eosinophilia

1981 ◽  
Vol 2 (3) ◽  
pp. 118-119 ◽  
Author(s):  
Robert W. Steiner
Keyword(s):  
Peritoneal Dialysis ◽  
Peritoneal Dialysate ◽  
The Third ◽  
Clinical Observations ◽  
Transient Episode ◽  
Culture Negative

Dialysate eosinophilia was noted in three patients undergoing peritoneal dialysis. In all cases, this eosinophilia was asymptomatic, and the process resolved spontaneously after two to seven weeks. In two cases, dialysate IgE levels were measured and were not elevated. In the third case, a transient episode of antibiotic-responsive, culture-negative peritonitis resulted in temporary disappearance of eosinophils from the peritoneum. Idiopathic peritoneal dialysate eosinophilia is an apparently benign entity, which may arise via mechanisms distinct from those involved in infectious peritonitis. It does not seem that IgE, a potent eosinophilotactic agent, necessarily is involved in the development of this disorder.

Syncope and palpitation

2020 ◽  
pp. 3284-3293
Author(s):  
K. Rajappan ◽  
A.C. Rankin ◽  
A.D. McGavigan ◽  
S.M. Cobbe
Keyword(s):  
Orthostatic Hypotension ◽  
Cardiac Rhythm ◽  
Cerebral Hypoperfusion ◽  
Loss Of Consciousness ◽  
Neurocardiogenic Syncope ◽  
Cardiac Syncope ◽  
Appropriate Treatment ◽  
Heart Beating ◽  
Transient Episode ◽  
Premature Beats

Syncope is a transient episode of loss of consciousness due to cerebral hypoperfusion. Its causes can be subdivided on the basis of pathophysiology, including neurally mediated—or reflex—syncope; orthostatic hypotension; cardiac causes; and cerebrovascular or psychogenic causes. Neurocardiogenic syncope, or simple faint, is the commonest cause and is benign, but it is always important to exclude or establish the diagnosis of cardiac syncope, because this has an adverse prognosis that may be improved with appropriate treatment. Meanwhile, palpitation is the awareness of one’s heart beating—it may be due to an awareness of an abnormal cardiac rhythm, or an abnormal awareness of normal rhythm. It is most commonly due to premature beats (ectopics) and is benign. Correlation between symptoms and cardiac rhythm is the initial aim of investigations in patients presenting with palpitations.

Transient Episode of Alice in Wonderland Syndrome After Ventriculoatrial Shunt Revision

2019 ◽  
Vol 121 ◽  
pp. 149-151 ◽  
Author(s):  
Pouya Entezami ◽  
Alexandra Paul ◽  
Matthew A. Adamo ◽  
Alan S. Boulos
Keyword(s):  
Shunt Revision ◽  
Ventriculoatrial Shunt ◽  
Alice In Wonderland ◽  
Transient Episode
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