Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in acute ischemic stroke patients as compared with the controls. The altered CSF NSE levels correlated well with the infarct size in CT scan. The CSF NSE levels were higher in 6-multiinfarct dementia (MID) patients who were diagnosed after 6-month follow-up than those in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE in the study of dementia related to ischemic stroke is worth further studies.
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PMID:Neuron-specific enolase in patients with acute ischemic stroke and related dementia. 779 31

17 parameters of vital activity (VA) were scanned in 35 female and 12 male dependent geriatric patients (mean age 81). These included mental testing, Barthel score, lung function, urinanalysis, creatinine clearance, Hb, albumin, globulin and electrolytes, skin-folds, locomotion, presence of IHD, hemodynamic state, continence, infections, WBC and lymphocyte count, pressure sores and dysphagia, 4 main templates of VA deterioration identified were: IHD, hemisyndrome (due to CVA), vegetative state (post-CVA) and senile dementia (SDAT). The IHD template was characterized by marked variations in VA, ending in death due to cardiac complications (pulmonary edema, ischemia, etc.). In the 3 other templates VA gradually deteriorated. Gradual declining VA allowed assessment of individual mortality prognosis. Assessment was by approximation of the computed exponent of the extrapolated VA curves; the longer the observation, the fewer the mistakes in assessment. Epidemiologic prognosis data of 48 dependent patients is described; mean age was about 81 years. Hospitalization mean was 853.5 +/- 601 days and for patients with dementia, 1158.6 +/- 622.7 days.
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PMID:[Assessment of vital activity in geriatric patients]. 781 43

A study was performed to compare the follow-up results of superficial temporal artery-middle cerebral artery anastomosis between a group of nine elderly patients (aged 70 years or over) and another group of 24 non-elderly patients (aged less than 70 years) with cerebral ischemia. The 33 patients, comprising 26 males and seven females, were evaluated pre- and postoperatively by four-vessel angiography, CT scan, MRI and cerebral blood flow (CBF) examination using either xenon inhalation or 123I-IMP SPECT. In some patients, additional evaluations were done. For those with dementia, the minimental scale (MMS), P300 event-related potential, the Hachinski ischemia score, and the vowel word counting test (Kaneko's KANAHIROI) were used, and for the hemiplegic, the Barthel index indicating ability of daily life (ADL) was employed. The results of follow-up for periods ranging from 12 to 55 months were "excellent" (returned to previous job) or "good" (able to perform self-care) in 27 of the 33 patients (81.8%) including six (66.6%) of the elderly group and 21 (87.5%) of the non-elderly group. There was no significant difference between the two groups by statistical evaluation. Among the nine patients with dementia (five under 70, four 70 years of age or over), eight (four under 70, four 70 or over) showed "rapid recovery" with improved postoperative MMS, P300, vowel word counting score and CBF. One patient under 70 (Case 5; a 47-year-old male) with a delayed 2-day recovery from general anesthesia, took as long as 6 months to obtain the self-care ability in daily life. Excluding this patient, all of the remaining eight patients responded quickly to surgery and were able to go home with their families after 2 to 4 weeks, there being no significant difference between the two age groups. In the 14 patients with hemiplegia/paresis (nine under 70, five 70 or over), a definitely better result was obtained for the non-elderly group. Eight of the nine non-elderly patients (89%) showed full ADL (Barthel index 100), whereas only one of three elderly patients (33.3%) showed almost full ADL (Barthel index 97). In five progressive stroke patients, (three under 70, two 70 or over) ultra-early bypass was performed within 8 hours postictus. Definitely better results were obtained in the patients aged less than 70, who showed rapid recovery and were able to return to their previous jobs 1 to 3 months after surgery. In contrast, the two patients aged 70 or over showed no improvement. In this report, we discuss the clinical and physiological variables that may be important for selection of elderly patients for cerebrovascular bypass surgery.
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PMID:[Results of superficial temporal artery-middle cerebral artery anastomosis for elderly and non-elderly patients with cerebral ischemia]. 782 13

Adenosine is now widely accepted as the major inhibitory neuromodulator in the central nervous system besides GABA. It has been suggested to be an endogenous neuroprotective metabolite. In situations of metabolic stress, e.g. ischemia adenosine decreases energy demand and increases energy supply. Of particular relevance in this context is its modulation of glutamate release. A shift of this adenosine-glutamate balance in favor of adenosine helps to restore function at the cellular, organ and organism level. Adenosine A1 receptor agonists and metabolic inhibitors, e.g. of transport, deaminase and xanthine oxidase have been demonstrated to be effective in different animal models of ischemia. Nimodipine, a L-type channel calcium antagonist currently in clinical trials for stroke and dementia syndromes, has now been shown to be a potent adenosine transport inhibitor in clinically relevant concentrations. Increase of adenosinergic neuromodulation may well be one of several future therapeutic strategies in neuroprotection.
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PMID:Adenosine--an endogenous neuroprotective metabolite and neuromodulator. 788 4

Selective death of CA1 pyramidal neurons after transient forebrain ischemia has attracted interest for its possible relation to the pathogenesis of memory deficits and dementia. Using whole cell patch-clamp recording from CA1 pyramidal neurons in hippocampal slices of gerbils after ischemia we studied the intracellular signaling mechanisms related to the phosphoinositide cycle. Intracellular application of an antibody against phosphatidylinositol 4,5-bisphosphate rescued ischemic neurons from stimulus-induced irreversible depolarization. Furthermore, application of inositol 1,3,4,5-tetrakisphosphate in normal cells caused an irreversible depolarization in response to synaptic input, which mimicked the deterioration of ischemic neurons. Depolarization of both ischemic and normal neurons in the presence of inositol 1,3,4,5-tetrakisphosphate was prevented by the addition of the Ca2+ chelator, 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetra-acetate. Application of antibody against inositol 1,4,5-triphosphate 3-kinase, which blocks formation of inositol 1,3,4,5-tetrakisphosphate, also protected against cell deterioration. Our results suggest that the vulnerability of hippocampal pyramidal neurons following ischemia is caused by a disturbed phosphoinositide cascade, with one metabolite, inositol 1,3,4,5-tetrakisphosphate, playing a key role in the induction of Ca2+ accumulation, which leads to neuronal death.
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PMID:Inositol 1,3,4,5-tetrakisphosphate as a mediator of neuronal death in ischemic hippocampus. 800 93

A clinicomorphological analysis of 60 postmortem cases with brain circulation disturbances against the background of arterial hypertension (AH) is performed. Lacunar infarcts, areas of incomplete necrosis and perivascular encephalolysis, small hemorrhages, criblures, persistent oedema and widespread spongiosis are found in the white matter (WM) of the brain in cases of AH of long duration with dementia. An important role in the WM lesions belongs to its ischemia due to hypertension angiopathy and disturbances of hemodynamics and liquor circulation. Complex of these lesions is called "hypertension leucoencephalopathy".
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PMID:[Hypertensive angio-encephalopathy and vascular dementia]. 803 92

Excessive stimulation of glutamate receptors and elevation of intracellular calcium levels initiate the neurodegenerative process resulting from cerebral ischemia. However, the subsequent cascade of molecular changes which are of pathogenic significance is less well understood. Breakdown of the cytoskeleton may be involved in the progression from compromise of neuronal viability to irreversible damage. Alteration of the microtubule-associated protein tau, as reflected by increased Alz-50 immunoreactivity, was induced by permanent focal cerebral ischemia in vivo but only in a proportion of neurones. Alz-50 immunoreactive neurones did not exhibit the characteristics of irreversible ischemic cell damage. Increased immunoreactivity to the stress response protein ubiquitin was also induced by ischemia in a proportion of neurones. Both proteins are components of neurofibrillary tangles in Alzheimer's disease. Alterations of the microtubule-associated protein tau may be a feature of the early stages of the ischemia-induced degeneration and the ubiquitin response may be an attempt by compromised neurones to deal with the presence of abnormal proteins.
Dementia
PMID:Cerebral ischemia induces alterations in tau and ubiquitin proteins. 808 73

Increasing evidence supports the hypothesis that escalating levels of excitatory amino acids (EAAs) are responsible for neuronal cell death in a variety of acute neurological conditions including hypoxia/ischemia, trauma, seizures, and hypoglycemia. EAAs may also contribute to several chronic neurodegenerative diseases including Huntington's disease, parkinsonism, and acquired immunodeficiency syndrome dementia. A predominant form of neurotoxicity appears to be mediated by excessive activation of the N-methyl-D-aspartate subtype of glutamate receptor. This laboratory recently reported that memantine, an antiparkinsonian drug, is a potent N-methyl-D-aspartate antagonist capable of preventing the death of central neurons both in vitro and in vivo when given coincident to an EAA insult. In the present study, we found that 12 microM memantine prevented the death of neonatal rat retinal ganglion cells in primary culture when administered up to 4 hours after the initiation of N-methyl-D-aspartate receptor-mediated neurotoxicity.
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PMID:Delayed administration of memantine prevents N-methyl-D-aspartate receptor-mediated neurotoxicity. 809 95

The effects of pre-treatment with ENA-713, an acetylcholinesterase (AChE) inhibitor, on changes in pre- and postsynaptic cholinergic indices in gerbil brain following transient ischemia were studied at 4 and 14 days after recirculation. In the ischemic group, hippocampal acetylcholine (ACh) level was significantly reduced (to 23% of sham-operated controls) at 4 days post-ischemia, but this reduction was completely prevented by ENA-713 treatment. Choline acetyltransferase (ChAT) and cholinesterase (ChE) activities were not significantly changed at 4 and 14 days post-ischemia. Although the maximum number (Bmax) of muscarinic ACh receptor (mACh-R) binding in the hippocampus was decreased (to 44%) without any change in affinity at 14 days post-ischemia, this decrease was also inhibited by ENA-713 treatment. In addition, histological experiment indicated that ENA-713 inhibited ischemia-induced pyramidal cell loss in the hippocampal CA1 regions. Thus, these findings suggest that ENA-713 has protective, neurotrophic and therapeutic effects on cerebrovascular type dementia due to cerebral ischemia.
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PMID:Acetylcholinesterase inhibitor ENA-713 protects against ischemia-induced decrease in pre- and postsynaptic cholinergic indices in the gerbil brain following transient ischemia. 818 20

Middle aged rats (13 months) were subjected to chronic cerebrovascular insufficiency (CVI) for 9 weeks using a 3-vessel occlusion technique. This CVI injury targets CA1 neuron damage selectively. Three groups of rats had their cerebral blood flow restored after 1, 2 or 3 weeks following CVI by removal of their carotid artery occluders. Another rat group did not undergo deocclusion for the 9 week observation period. Rats were tested for memory acquisition and retention 6 and 9 weeks after CVI using a modified water maze test. At the end of the 9 weeks, cerebral blood flow was measured in the fronto-parietal cortex and rats were killed by fixation-perfusion. Hippocampal morphometry was done to assess the % of damaged CA1 neurons and the density of GFAP-positive hyperplasia and hypertrophy. Results show that restoration of cerebral blood flow 1 and 2 weeks after CVI but not after 3 weeks of CVI, reversed a significant increase in reactive astrocytosis and prevented memory impairment in these deoccluded rats when compared to the non-deoccluded group. It appears from these results that 'neuronal rescue' of CA1 neurons is possible when cerebral blood flow is restored in rats subjected to chronic CVI during a 2 week (but not 3 week) 'window of opportunity'. This chronic brain ischemia model may be useful in screening potential therapy in patients with dementia where spatial memory impairment and hippocampal damage may be manifested.
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PMID:Brain blood flow restoration 'rescues' chronically damaged rat CA1 neurons. 822 Oct 94


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