Effect of Ascorbic Acid on Infarct Size in Experimental Focal Cerebral Ischaemia and Reperfusion in a Primate Model

1998 ◽  
Vol 140 (9) ◽  
pp. 977-980 ◽  
Author(s):  
P. T. Henry ◽  
M. J. Chandy
Keyword(s):  
Ascorbic Acid ◽  
Infarct Size ◽  
Cerebral Ischaemia ◽  
Focal Cerebral Ischaemia ◽  
Primate Model ◽  
Ischaemia And Reperfusion

Ascorbic acid and focal cerebral ischaemia in a primate model

1993 ◽  
Vol 123 (1-2) ◽  
pp. 87-91 ◽  
Author(s):  
A. Ranjan ◽  
D. Theodore ◽  
R. P. Haran ◽  
M. J. Chandy
Keyword(s):  
Ascorbic Acid ◽  
Cerebral Ischaemia ◽  
Focal Cerebral Ischaemia ◽  
Primate Model

Changes of superoxide dismutase activity and ascorbic acid in focal cerebral ischaemia in rats

1992 ◽  
Vol 14 (1) ◽  
pp. 26-30 ◽  
Author(s):  
Kiyoshi Takagi ◽  
Hideaki Kanemitsu ◽  
Noriko Tomukai ◽  
Hidemune Oka ◽  
Akira Tamura ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Cerebral Ischaemia ◽  
Superoxide Dismutase Activity ◽  
Focal Cerebral Ischaemia

Reduction of Edema and Infarction by Memantine and MK-801 After Focal Cerebral Ischaemia and Reperfusion in Rat

2000 ◽  
Vol 142 (11) ◽  
pp. 1287-1292 ◽  
Author(s):  
A. Görgülü ◽  
T. Kınş ◽  
S. Çobanoğlu ◽  
F. U¨nal ◽  
N. İ zgi ◽  
...  
Keyword(s):  
Cerebral Ischaemia ◽  
Focal Cerebral Ischaemia ◽  
Mk 801 ◽  
Ischaemia And Reperfusion

Effects of an analogue of thyrotrophin-releasing hormone, RX77368, on infarct size and cerebral blood flow in focal cerebral ischaemia in the rat

1989 ◽  
Vol 67 (10) ◽  
pp. 1345-1350 ◽  
Author(s):  
C. T. O'Shaughnessy ◽  
N. J. Rothwell ◽  
J. Shrewsbury-Gee
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Infarct Size ◽  
Middle Cerebral Artery ◽  
Cerebral Ischaemia ◽  
Lesion Size ◽  
Focal Cerebral Ischaemia ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulation Of

Effects of a stable analogue of thyrotrophin-releasing hormone, RX77368, on cerebral blood flow and infarct size have been studied in an acute model of cerebral ischaemia in the rat. Two hours after electrocoagulation of the left middle cerebral artery (MCA), the mean area of ischaemia (± SEM), determined histochemically, was 11.5 ± 2.2% of a single hemisphere and blood flow, determined using radiolabeled microspheres, was reduced by 40% in the left forebrain (p < 0.001 compared with sham-operated animals). Administration of RX77368 (50 μg/kg, intracerebroventricularly) within 10 min of arterial occlusion caused a significant (p < 0.01) reduction in mean lesion size to 3.7 ± 1.8% and stimulation of blood flow to the left ischaemic forebrain (60% above saline treated). Peripheral administration of RX77368 (1 mg/kg intraperitoneally) also significantly stimulated blood flow to the ischaemic forebrain and caused an apparent decrease in frequency of large infarcted areas of brain tissue, although mean lesion size was not significantly affected. These findings indicate that RX77368 ameliorates tissue damage in acute focal cerebral ischaemia. Such effects may be related to stimulation of cerebral blood flow.Key words: middle cerebral artery, focal cerebral ischaemia, cerebral blood flow, thyrotrophin-releasing hormone analogue.

scholarly journals GlyT1 Inhibitor NFPS Exerts Neuroprotection via GlyR Alpha1 Subunit in the Rat Model of Transient Focal Cerebral Ischaemia and Reperfusion

2016 ◽  
Vol 38 (5) ◽  
pp. 1952-1962 ◽  
Author(s):  
Baosheng Huang ◽  
Qingsong Xie ◽  
Xiaocheng Lu ◽  
Tengda Qian ◽  
Shuai Li ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Rat Model ◽  
Cerebral Ischaemia ◽  
Artery Occlusion ◽  
High Dose ◽  
Focal Cerebral Ischaemia ◽  
Ischaemia And Reperfusion ◽  
Cerebral Artery Occlusion

Background/Aims: Glycine is a strychnine-sensitive inhibitory neurotransmitter in the central nervous system (CNS), especially in the spinal cord, brainstem, and retina. The objective of the present study was to investigate the potential neuroprotective effects of GlyT1 inhibitor N [3-(4'-fluorophenyl)-3-(4'-phenylphenoxy) propyl] sarcosine (NFPS) in the rat model of experimental stroke. Methods: In vivo ischaemia was induced by transient middle cerebral artery occlusion (tMCAO). The methods of Western Blotting, Nissl Staining and Morris water maze methods were applied to analyze the anti-ischaemia mechanism. Results: The results showed that high dose of NFPS (H-NFPS) significantly reduced infarct volume, neuronal injury and the expression of cleaved caspase-3, enhanced Bcl-2/Bax, and improved spatial learning deficits which were administered three hours after transient middle cerebral artery occlusion (tMCAO) induction in rats, while, low dose of NFPS (L-NFPS) exacerbated the injury of ischaemia. These findings suggested that low and high dose of NFPS produced opposite effects. Importantly, it was demonstrated that H-NFPS-dependent neuronal protection was inverted by salicylate (Sal), a specific GlyR ɑ1 antagonist. Such effects could probably be attributed to the enhanced glycine level in both synaptic and extrasynaptic clefts and the subsequently altered extrasynaptic GlyRs and their subtypes. Conclusions: These data imply that GlyT1 inhibitor NFPS may be a novel target for clinical treatment of transient focal cerebral ischaemia and reperfusion which are associated with altered GlyR alpha 1 subunits.

Intravenous phosphocreatine improves neurological outcome in focal cerebral ischaemia and reperfusion

2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
T Pfefferkorn ◽  
A Bender ◽  
A Trinkl ◽  
GF Hamann ◽  
M Dichgans ◽  
...  
Keyword(s):  
Cerebral Ischaemia ◽  
Neurological Outcome ◽  
Focal Cerebral Ischaemia ◽  
Ischaemia And Reperfusion
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