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

The present study was undertaken to elucidate the pathological and pathophysiological characteristics of experimental cerebral ischemia in rats. The purpose of this study was also to clarify whether this animal model is useful for the research of multiple cerebral infarction. In order to create a cerebral ischemia model, arterioles were embolized by injecting 2000 carbon-microspheres (50 microns in diameter) into the right internal carotid artery of ketamine anesthetized rats. Pathological studies and pathophysiological evaluations were performed by electrocorticography (ECoG) and by measuring regional cortical blood flow (CBF) in embolized rats. An attempt was also made to examine learning ability: embolized rats were subjected to the passive avoidance test. Pathophysiological studies revealed most microspheres to be located in the ipsilateral hemisphere with a few in the contralateral hemisphere. Most foci of cerebral infarction were distributed in the area fed by the ipsilateral middle cerebral artery and the anterior cerebral artery, while a few of them were found in the area fed by the contralateral anterior cerebral artery. Regions of cerebral infarction consisted of microcerebral infarctions, some of which were fused to each other. The pathological characteristics of this experimentally induced cerebral ischemia were those of multifocal cerebral infarction. Both ECoG and CBF decreased after injection of carbon-microspheres, and these two parameters did not recover for more than 60 min in both hemispheres. Seven days after cerebral embolization, the shortened response latency in the passive avoidance test, possibly indicating memory impairment, was observed. Our findings suggest that cerebral ischemia of the rat produced by carbon-microspheres (50 microns in diameter) is useful in the pathophysiological investigation of multiple cerebral infarction.
 ...
PMID:[Pathological and pathophysiological studies on central nervous system in experimental cerebral ischemia of the rat]. 155 55

Patient RB became amnesic following an episode of global ischemia that resulted in a bilateral lesion of the CA1 field of the hippocampus. This finding suggested that damage restricted to the hippocampus is sufficient to produce clinically significant memory impairment. To evaluate further the effect of ischemic brain damage on memory, we have developed an animal model of cerebral ischemia in the monkey. Monkeys were subjected to 15 min of reversible ischemia, using a noninvasive technique involving carotid occlusion and pharmacologically induced hypotension. These monkeys sustained significant loss of pyramidal cells in the CA1 and CA2 fields of the hippocampus, as well as loss of somatostatin-immunoreactive cells in the hilar region of the dentate gyrus. Cell loss occurred bilaterally throughout the rostrocaudal extent of the hippocampus but was greater in the caudal portion. Except for patchy loss of cerebellar Purkinje cells, significant damage was not detected in areas outside the hippocampus, including adjacent cortical regions, that is, entorhinal, perirhinal, and parahippocampal cortex, and other regions that have been implicated in memory function. On behavioral tests, the ischemic monkeys exhibited significant and enduring memory impairment. On the delayed nonmatching to sample task, the ischemic monkeys were as impaired as monkeys with lesions of the hippocampal formation and adjacent parahippocampal cortex (the H+ lesion). On two other memory tasks, the ischemic monkeys were less impaired than monkeys with the H+ lesion. In neuropathological evaluations, it has always been difficult to rule out the possibility that significant areas of neuronal dysfunction have gone undetected. The finding that ischemic lesions produced overall less memory impairment than H+ lesions indicates that the ischemic monkeys (and by extension, patient RB) are unlikely to have widespread neuronal dysfunction affecting memory that was undetected by histological examination. These results provide additional evidence that the hippocampus is a focal site of pathological change in cerebral ischemia, and that damage limited to the hippocampus is sufficient to impair memory.
 ...
PMID:Enduring memory impairment in monkeys after ischemic damage to the hippocampus. 161 49

To examine the working memory performance, gerbils were tested in the delayed nonmatching to position task using a T-maze, and the effects of cerebral ischemia on the performance were examined. There were no significant differences between gerbils and rats in the alternation performance without delay and with the interrun intervals ranging from 10 to 810 sec. These data suggest that this task is useful for assessing working memory in gerbils as well as in rats. Scopolamine (0.1 and 0.2 mg/kg) impaired the working memory performance in both species. Bilateral occlusion of the common carotid arteries for 5 min severely impaired the choice accuracy in the gerbils 1 to 3 days after the operation. This memory impairment was observed even at the shortest interval. One month after the operation, partial behavioral recovery was observed in the ischemic gerbils, in spite of a marked loss of the pyramidal cells in the hippocampus CA1 sector. These data indicate that the working memory performance is highly vulnerable to the cerebral ischemia and that the ischemic operation transiently but severely impairs the acquisition process of the working memory in gerbils.
 ...
PMID:Effects of transient cerebral ischemia in gerbils on working memory performance in the delayed nonmatching to position task using a T-maze. 180 68

Ergot alkaloids are commonly used as cerebroprotective drugs. Their efficacy has been demonstrated experimentally in animals submitted to acute cerebral anoxia or ischaemia, at dose levels hugely superior to dose levels usually administered in humans. In the present experiments, dihydroergocryptine (DHEC), a constituent of dihydroergotoxine (DHET), was administered at doses closely related to human doses, preventively (in experiments where animals survived only for a short while after ischaemic insult) or curatively, and its efficacy tested through refined neurological and biochemical evaluation of experimental cerebral ischaemia sequelae. DHEC was administered orally (30 micrograms or 150 micrograms/kg body weight (bwt) twice daily) for 3 days, following transient cerebral ischaemia induced by a 60-min carotid occlusion plus sodium nitroprusside (1.1 mg/rat s.c.) injection, or, in a second experiment, prophylactically (60 micrograms or 300 micrograms/kg bwt/day) for 4 days prior to multiple cerebral infarct induced by sodium arachidonate injection into the left internal carotid artery. The neurological sequelae were evaluated by the Irwin visual placing response or by a battery of behavioural tests. Na-K-ATPase enzyme activity in cerebral homogenates was measured; decreases in this enzyme activity are considered to reflect the neuronal membrane consequences of the neurocell energetic metabolism alterations caused by cerebral ischaemia. Low dose oral DHEC treatment prevented the behavioural abnormalities and memory impairment arising after transient cerebral ischaemia and there was a marked trend in improving the behavioural abnormalities observed in animals submitted to massive cerebral infarction, in spite of the model severity. DHEC prevented reduction in cerebral Na-K-ATPase activity after cerebral multiinfarction. These effects of DHEC were observed with doses and administration route close to the usual therapeutic regimen.
 ...
PMID:The effects of dihydroergocryptine on the neurological and enzyme disorders induced by cerebral ischaemia in rats. 255 45

Two rat models of memory impairment in passive avoidance learning induced by cerebrovascular disturbance, were established to estimate the effects of a cerebral metabolic enhancer, idebenone. Transient and global cerebral ischemia in rats, produced by 4-vessel occlusion for 200 s immediately after the acquisition trial of passive avoidance learning, shortened the latencies in the retention test trial performed 24 h later. This retrograde amnesia was reversed significantly by idebenone administered orally or intraperitoneally at the doses of 10 and 30 mg/kg before the retention test trial. Idebenone at a dose of 10 mg/kg, given intraperitoneally before or immediately after the ischemia, also markedly inhibited the appearance of amnesia. In the second model, permanent and cerebral hemisphere embolization produced by injecting 2,000 microspheres into the internal carotid artery, significantly impaired passive avoidance learning performed 7 days later. The repeated administration of idebenone (30 mg/kg, i.p.). once a day after the embolization, significantly improved the impairment of passive avoidance learning in the embolized rats. Furthermore, physostigmine and arginine-vasopressin as reference compounds improved the impairment of passive avoidance learning in these models. These findings suggest that idebenone ameliorates memory impairment induced by cerebral vascular disturbance in rats.
 ...
PMID:Effects of idebenone on memory impairment induced in ischemic and embolization models of cerebrovascular disturbance in rats. 276 39

30 patients aged between 45 and 78 years and who had suffered from transient global amnesia (TGA), were seen at the Department of Neurology, Pordenone Public Hospital, in the period 1978 to 1982. 25 patients had one or more risk factors for cerebrovascular disease, such as hypertension, cardiac abnormalities, diabetes and hyperlipidemia. EEG examination revealed abnormal activity only in 7 patients. Brain Computed Tomography showed cerebral atrophy in 10 and hypodense lesions in 3 patients. 16 patients had been followed up for a mean interval of 20 months. During the follow-up period, 4 patients had recurrent TGA and one had a transient ischemic attack in the vertebrobasilar arterial system. In the follow-up group, 15 patients showed permanent memory impairment. The high incidence of risk factors for cerebrovascular disease seems to confirm that TGA is probably due to transient cerebral ischemia. The high rate of permanent memory impairment, almost always connected with the coexistence of cerebrovascular risk factors, is not in agreement with the postulated good prognosis of TGA.
 ...
PMID:Transient global amnesia. 651 86

28 patients with transient global amnesia (TGA) were followed for a mean period of 73 months. The patients fell into 3 diagnostic groups: a group where patients had associated symptoms and signs of transient focal cerebral ischemia (TIA), a migraine group and a miscellaneous group. 22 patients had evidence of cerebrovascular disease or risk factors for cerebrovascular disease, and a vascular basis for the amnesic attack was highly suggestive in 25 patients. During the follow-up period 2 patients died, 3 had recurrent TGA and 13 developed a completed stroke or suffered from further TIA's. Permanent memory impairment was encountered in 9 cases. An unfavourable course was related to the presence of other TIA manifestations and/or risk factors for cerebrovascular disease. The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.
 ...
PMID:Transient global amnesia -- its clinical and pathophysiological basis and prognosis. 721 Nov 87

Ten patients with transient global amnesia (TGA) associated with symptoms of transient focal cerebral ischemia were seen at the University Department of Neurology, Arhus Kommunehospital in the period 1966-1978. All had either prior to or following the amnesic attack transient ischemic attacks (TIA) in the territory of the posterior cerebral circulation. On admission minor neurological deficits were noted in three and normal findings in the remaining seven. There was no evidence of epilepsy in any case. We studied the course (average, 77 months) and found that three had recurrent amnesic episodes. Four patients had only further transient focal cerebral ischemic attacks, while six developed a completed stroke, in five located in the distribution of the basilar artery. Seven patients had persistent memory impairment. TGA is one manifestation of TIA in the vertebrobasilar arterial system. When TGA appears in connection with other transient cerebral ischemic attacks, the prognosis is apparently grave with a great risk of a subsequent completed stroke or a permanent memory impairment.
 ...
PMID:Transient global amnesia as a manifestation of transient cerebral ischemia. 739 56

Active oxygen species are suggested to be concerned with various senile disorders. Tea catechins, (+)catechin (CA), (-)epicatechin (EC) and (-)epigallocatechin gallate, are polyhydroxy-fravan derivatives from tea leaves and have been proposed to possess active oxygen scavenging effect. Tea catechins protected the cultured newborn-mouse cerebral nerve cells from death induced by glucose oxidase. The protective potency of (-)epigallocatechin gallate was weaker than those of EC and CA. Learning ability of mice was assessed by a step-down-type passive avoidance test, and memory impairment of mice was achieved by intracisternal injection of glucose oxidase or cerebral ischemia induced by 10 min occlusion of the common carotid arteries. Intracisternal injection of EC improved the memory impairment induced by intracisternal glucose oxidase, and i.v. injection of CA or EC improved that induced by the cerebral ischemia. CA and EC depressed carrageenin-induced edema in rat hind paw, but (-)epigallocatechin gallate did not. These results suggest that tea catechins ameliorate the injuries or impairments induced by active oxygens through scavenging intracellular active oxygens, and might become useful for protecting human from senile disorders such as dementia.
 ...
PMID:Ameliorative effects of tea catechins on active oxygen-related nerve cell injuries. 763 19

We investigated the effect of N-benzyloxycarbonyl-thioprolyl-thioprolinal-dimethylaceta l (ZTTA), a novel postproline cleaving enzyme (prolyl endopeptidase, PPCE) inhibitor, on the in vitro activity of rat brain PPCE and memory impairment induced by cerebral ischemia. ZTTA noncompetitively inhibited rat brain PPCE (ki = 2.9 microM). Cerebral ischemia for 5 min increased the number of errors in a working memory task with a three-panel runway paradigm. ZTTA at 6 mg/kg, administered immediately after blood flow reperfusion, significantly reduced the increase in working memory errors expected to occur 24 h after 5 min of ischemia. The antiamnesic action of ZTTA may be ascribable to a neuroprotective effect on the central nervous system due to some neuropeptides that are substrates of PPCE in the brain.
 ...
PMID:ZTTA, a postproline cleaving enzyme inhibitor, improves cerebral ischemia-induced deficits in a three-panel runway task in rats. 895 74


1 2 3 4 5 6 7 8 9 10 Next >>