scholarly journals Neuroprotective actions of immunosuppressant FK506 in transient focal cerebral ischemia in rats. Therapeutic time window for FK506 in transient focal ischemia.

Nosotchu ◽  
1998 ◽  
Vol 20 (6) ◽  
pp. 715-719
Author(s):  
Takako Arii ◽  
Tatsushi Kamiya ◽  
Kazumasa Arii ◽  
Yasuo Katayama ◽  
Akiro Terashi
Keyword(s):  
Cerebral Ischemia ◽  
Time Window ◽  
Focal Cerebral Ischemia ◽  
Focal Ischemia ◽  
Transient Focal Cerebral Ischemia ◽  
Neuroprotective Actions ◽  
Transient Focal Ischemia ◽  
Therapeutic Time Window

scholarly journals Wide therapeutic time window for nimesulide neuroprotection in a model of transient focal cerebral ischemia in the rat

2004 ◽  
Vol 1007 (1-2) ◽  
pp. 98-108 ◽  
Author(s):  
Eduardo Candelario-Jalil ◽  
Armando González-Falcón ◽  
Michel Garcı́a-Cabrera ◽  
Olga Sonia León ◽  
Bernd L Fiebich
Keyword(s):  
Cerebral Ischemia ◽  
Time Window ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia ◽  
Therapeutic Time Window

Neuroprotective effect of immunosuppressant FK506 in transient focal ischemia in rats: Therapeutic time window for FK506 in transient focal ischemia

2001 ◽  
Vol 23 (7) ◽  
pp. 755-760 ◽  
Author(s):  
Takako Arii ◽  
Tatsushi Kamiya ◽  
Kazumasa Arii ◽  
Masayuki Ueda ◽  
Chikako Nito ◽  
...  
Keyword(s):  
Time Window ◽  
Neuroprotective Effect ◽  
Focal Ischemia ◽  
Transient Focal Ischemia ◽  
Therapeutic Time Window

scholarly journals Modulation by Nitric Oxide of Cerebral Neutrophil Accumulation after Transient Focal Ischemia in Rats

2000 ◽  
Vol 20 (5) ◽  
pp. 812-819 ◽  
Author(s):  
Sophie Batteur-Parmentier ◽  
Isabelle Margaill ◽  
Michel Plotkine
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neutrophil Infiltration ◽  
Focal Ischemia ◽  
Left Middle Cerebral Artery ◽  
No Production ◽  
Myeloperoxidase Activity ◽  
Transient Focal Ischemia

A beneficial role of nitric oxide (NO) after cerebral ischemia has been previously attributed to its vascular effects. Recent data indicate a regulatory role for NO in initial leukocyte-endothelial interactions in the cerebral microcirculation under basal and ischemic conditions. In this study, the authors tested the hypothesis that endogenous NO production during and/or after transient focal cerebral ischemia can also be neuroprotective by limiting the process of neutrophil infiltration and its deleterious consequences. Male Sprague-Dawley rats were subjected to 2 hours occlusion of the left middle cerebral artery and the left common carotid artery. The effect of NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg, intraperitoneally), an NO synthase inhibitor, was examined at 48 hours after ischemia on both infarct size and myeloperoxidase activity, an index of neutrophil infiltration. L-NAME given 5 minutes after the onset of ischemia increased the cortical infarct volume by 34% and increased cortical myeloperoxidase activity by 60%, whereas administration of L-NAME at 1, 7, and 22 hours of reperfusion had no effect. Such exacerbations of infarction and myeloperoxidase activity produced when L-NAME was given 5 minutes after the onset of ischemia were not observed in rats rendered neutropenic by vinblastine. These results suggest that after transient focal ischemia, early NO production exerts a neuroprotective effect by modulating neutrophil infiltration.

scholarly journals Effects of Tissue Type Plasminogen Activator in Embolic versus Mechanical Models of Focal Cerebral Ischemia in Rats

1999 ◽  
Vol 19 (12) ◽  
pp. 1316-1321 ◽  
Author(s):  
Wei Meng ◽  
Xiaoying Wang ◽  
Minoru Asahi ◽  
Tsuneo Kano ◽  
Kazuko Asahi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Perfusion ◽  
Focal Cerebral Ischemia ◽  
Focal Ischemia ◽  
Tissue Type ◽  
Negative Effects ◽  
Tissue Type Plasminogen Activator ◽  
Rat Models ◽  
Type Plasminogen Activator ◽  
Transient Focal Ischemia

Tissue type plasminogen activator (tPA) can be effective therapy for embolic stroke by restoring cerebral perfusion. However, a recent experimental study showed that tPA increased infarct size in a mouse model of transient focal ischemia, suggesting a possible adverse effect of tPA on ischemic tissue per se. In this report, the effects of tPA in two rat models of cerebral ischemia were compared. In experiment 1, rats were subjected to focal ischemia via injection of autologous clots into the middle cerebral artery territory. Two hours after clot injection, rats were treated with 10 mg/kg tPA or normal saline. Perfusion-sensitive computed tomography scanning showed that tPA restored cerebral perfusion in this thromboembolic model. Treatment with tPA significantly reduced ischemic lesion volumes measured at 24 hours by >60%. In experiment 2, three groups of rats were subjected to focal ischemia via a mechanical approach in which a silicon-coated filament was used intraluminally to occlude the origin of the middle cerebral artery. In two groups, the filament was withdrawn after 2 hours to allow for reperfusion, and then rats were randomly treated with 10 mg/kg tPA or normal saline. In the third group, rats were not treated and the filament was not withdrawn so that permanent focal ischemia was present. In this experiment, tPA did not significantly alter lesion volumes after 2 hours of transient focal ischemia. In contrast, permanent ischemia significantly increased lesion volumes by 55% compared with transient ischemia. These results indicate that in these rat models of focal cerebral ischemia, tPA did not have detectable negative effects. Other potentially negative effects of tPA may be dependent on choice of animal species and model systems.

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