Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral ischemia was produced in the Mongolian gerbil by bilateral occlusion of the carotid arteries. Although the cerebral ischemia so produced was not total, a mortality rate of 100% was obtained if the occlusion was maintained for 60 min in gerbils weighing 45--55 gm. Few deaths were observed after 50 min of bilateral carotid arterial occlusion. Test drugs were administered, after the removal of the arterial clips, to groups of gerbils to determine the mortality rate associated with each drug. Isoproterenol 50 mg/kg, amphetamine 5.0 mg/kg, and methylprednisolone 35 mg/kg improved survival after cerebral ischemia. Atropine 1 mg/kg, thiosemicarbazide 4 mg/kg, aminooxyacetic acid 100 mg/kg, theophylline 100 mg/kg, and phenytoin 50 mg/kg were associated with a reduced survival after cerebral ischemia. The known tendency of the gerbil to exhibit spontaneous seizures and the frequency and severity of the observed post-ischemic seizures suggest that the lethality of prolonged cerebral ischemia may be, in part, related to seizures triggered by the cerebral ischemia.
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PMID:A gerbil model of cerebral ischemia suitable for drug evaluation. 698 34

1. Cerebral ischemia of 5 min duration was induced in unanesthetized gerbils by bilateral occlusion of the carotid arteries. 2. The extent of cerebral damage was assessed by the elevation of motor activity in comparison with control animals and by a histological assessment of the extent of neuronal degeneration in the CA1 area of the hippocampus. 3. Atropine, an antagonist of ACh, at either a low (1 mg/kg) or a high (10 mg/kg) dose administered 15 min prior to the ischemic episode, did not confer protection against cerebral ischemic damage. 4. This finding suggests that ACh does not play a critical role in the generation of ischemia reperfusion injury.
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PMID:Atropine and cerebral ischemic injury in the Mongolian gerbil. 795 34

Temporal changes in cholinergic functions following transient cerebral ischemia (10 min) were studied in the hippocampus of awake unrestrained gerbils using in vivo microdialysis. These data were compared with the results for temporal change in the area of each CA1 cell soma, measured with a microcomputer imaging device. KCl-induced release of acetylcholine (ACh) tended to be lower within 1 day after recirculation, and was significantly lower on the 4th, 7th and 14th days. Atropine-induced release of ACh gradually decreased over the test period. In histological estimation, no differences were observed within the 1st day, but a significant decrease of the area of CA1 cell soma was observed from the 4th to 14th days. Moreover, ischemia over 2 min decreased KCl- and atropine-induced ACh release on the 14th day without significant changes of hippocampal CA1 pyramidal cell. From these results, it is clear that ischemia produced dysfunction of hippocampal cholinergic neurons, and that dysfunction of the hippocampal cholinergic system following transient ischemia precedes pyramidal cell damage in the hippocampal CA1 subfield.
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PMID:Temporal changes in extracellular acetylcholine and CA1 pyramidal cells in gerbil hippocampus following transient cerebral ischemia. 818 Aug 40