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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuroprotection of catalpol and its mechanism was evaluated in cerebral ischemic model in gerbils. Three groups were designed as sham-operated, ischemia-treated, respectively, with catalpol and saline. Catalpol was injected intraperitoneally immediately after reperfusion and repeatedly at 12, 24, 48 and 72 h with the dose of 5.0 mg/kg. The neuroprotection was estimated by the indexes of behavior and histology. Behavioral testing was performed in Y-maze and the survival neurons in CA1 subfield were counted under a microscope after behavioral testing. In addition, apoptosis induced by ischemia was also examined by using the terminal deoxynucleotidyl transferase-mediated UTP nick end labeling method. It was shown that catalpol significantly attenuated apoptosis, rescued hippocampal CA1 neurons and reduced cognitive impairment. In order to make clear the mechanism of catalpol's neuroprotection, the activities of endogenous antioxidants and nitric oxide synthase together with the content of lipid peroxide in cortex and hippocampus were assayed. The results proved that catalpol significantly reduced the content of lipid peroxide, increased the activity of glutathione peroxidase and decreased the activity of nitric oxide synthase. All these suggested that catalpol was a potential neuroprotective agent and its neuroprotective effects were achieved at least partly by promoting endogenous antioxidant enzymatic activities and reducing the formation of nitric oxide.
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PMID:Neuroprotection of catalpol in transient global ischemia in gerbils. 1538 Mar 24

Cerebrovascular disease (CVD), as well as secondary ischemic brain injury from cardiovascular disease, are common causes of dementia and cognitive decline in the elderly. In addition, CVD frequently contributes to cognitive loss in patients with Alzheimer's disease (AD). Progress in understanding the pathogenetic mechanism involved in vascular cognitive impairment (VCI) and vascular dementia (VaD) has resulted in promising treatments of these conditions. Cholinergic deficits in VaD are due to ischemia of basal forebrain nuclei and of cholinergic pathways and can be treated with the use of the cholinesterase inhibitor agents used in AD. Controlled clinical trials with donepezil, galantamine and rivastigmine in VaD, as well as in patients with AD plus CVD, have demonstrated improvements in cognition, behavior and activities of daily living.
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PMID:Treatment of vascular dementia--evidence from clinical trials with cholinesterase inhibitors. 1553 22

The present study evaluated for the first time the dose-effectiveness, therapeutic time-window and long-term efficacy of the neuroprotection of catalpol by behavioral and histological measures in gerbils subjected to transient global cerebral ischemia. Catalpol (1 mg/kg ip) used immediately after reperfusion and repeatedly at 12, 24, 48 and 72 h significantly rescued neurons in the hippocampal CA1 subfield and reduced cognitive impairment. The neuroprotective efficacy of catalpol became more evident at the doses of 5 and 10 mg/kg. Of great importance were the findings that the neuroprotective efficacy of catalpol still could be seen even when the treatment was delayed 3 h and when the observational period was lasted out 35 days after ischemia. It was reasonable to draw the conclusion that catalpol was truly neuroprotective rather than simply delayed the onset of neuronal damage. These results suggested that catalpol might be of therapeutic value for global cerebral ischemia.
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PMID:Neuroprotective properties of catalpol in transient global cerebral ischemia in gerbils: dose-response, therapeutic time-window and long-term efficacy. 1554 72

Traumatic brain injury results from a sudden and external physical insult to the head, which is often accompanied by motor and cognitive impairment. Neurotrauma is characterized not only by focal abnormalities, but rather by multifocal, or even global structural and functional disturbances of the brain network. The impact initially causes necrotic cell death in the underlying tissue, followed by apoptotic cell death in the surrounding tissue due to multiple subsequent events, such as ischemia, excitotoxicity and altered gene expression. These pathological conditions are associated with high morbidity and mortality. Despite the high medical and economical relevance of neurotrauma there are currently no sufficient treatments. Supplementary therapeutic strategies have to be established. Many types of stem cells have the ability to engraft diffusely and become integral members of structures throughout the host CNS. Intrinsic factors appear to derive spontaneously from stem cells and seem to be capable of neuroprotective and/or neuroregenerative functions. Furthermore stem cells can be readily engineered to express specific genes. Such observations suggest that stem cells might participate in reconstructing the molecular and cellular milieu of traumatized brains. In this paper, the state of stem cell research is reviewed and its possible application in neurotrauma will be discussed.
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PMID:Potential stem cell therapy and application in neurotrauma. 1558 Dec 81

Studies reporting that ischemic vascular dementia (IVD), compared to Alzheimer's disease (AD), is associated with relatively greater impairment of executive function and relatively preserved episodic memory raise the question of whether there is a distinctive neuropsychological profile of impairment associated with IVD and whether this might be useful in clinical diagnosis. However, prior reports are almost all based on clinically diagnosed cases, raising obvious issues of possible circularity and leaving unanswered questions of validity. Here we report on clinical and neuropsychological findings in 18 prospectively studied cases that had substantial pathology-defined cerebrovascular disease (CVD) at autopsy. Nine cases had minimal AD pathology, while the remainder had moderate or severe degrees of AD pathology. Cognitive status at last evaluation ranged from mild cognitive impairment to moderate dementia. Clinical features were quite variable; only 40% of cases with high CVD levels had elevated Hachinski Ischemia Scale scores and neither abrupt onset nor stepwise progression was found in most high CVD cases, even when AD changes were essentially absent. The presence of dementia was predictably related to the level of neurofibrillary pathology, but was not related to the severity of CVD. Neuropsychologists expert in the evaluation of dementia used a priori criteria to diagnose neuropsychological protocols (blind to all other data) from cases with pathology-informed diagnoses of AD, IVD, and mixed dementia. Sensitivity and specificity were both high for AD, sensitivity for detecting pure IVD was poor, and values were intermediate for detecting IVD irrespective of AD levels. A illustrative case example is included. We conclude that the profile of cognitive impairment in IVD is highly variable, but that in clinical settings neuropsychological readings may contribute to the differential diagnosis of dementia.
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PMID:Clinical and neuropsychological features in autopsy-defined vascular dementia. 1559 59

Focal ischemia induces long-term pathophysiological consequences in widespread brain areas. Here we analyzed long-term effects of sequential cortical lesions on brain volume and cognitive function. Rats received either single photothrombotic lesions in the forelimb sensorimotor cortex (SL) or two lesions in sequence either immediately (DL0), 2 days (DL2), 7 days (DL7), or 10 days (DL10) after the first surgery in the homotopic contralateral area. Infarct and global brain volume were measured 7 days (SL and DL2 groups) and one month (all groups) after the last period of ischemia. In the weeks following a stroke, the single lesion shrank considerably. This shrinkage was accentuated by a further lesion received either earlier or later. Thirty-one days after obtaining the second lesion, the lesion scars on both sides had a mean volume of 5.8 +/- 2.3 mm3 in DL2 as compared to 8.5 +/- 3.5 mm3 in SL-animals. In addition, there was a super-additive loss of residual brain volume by 2.2-8.0% in each hemisphere in animals with sequential lesions. In the watermaze, this loss of brain volume corresponded to a slight but significant impairment in performance. The present study revealed a complex interaction of lesions in animals with sequential strokes associated with global reduction of brain volume and cognitive impairment indicating degenerative processes beyond the lesions itself.
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PMID:Long-term effects of sequential cortical infarcts on scar size, brain volume and cognitive function. 1568 Jan 95

With regards to the applications of three Chinese herbs poria, rhizoma atractylodis macrocephalae, and radix angelicae sinensis to vascular dementia (VD), the work was performed to assess the nootropic action and explore neuroprotective mechanisms of three herbs combinations (FBD) on mice injured by cerebral repetitive ischemia-reperfusion (IR). Aqueous extracts from FBD (115-460 mg/kg) administered p.o. significantly improved cognitive function through elongating latency and reducing number of errors in step-through test. Aqueous extracts from FBD inhibited lipid peroxidation (LPO), elevated activity in (Na+)-(K+)-ATPase and (Ca2+)-ATPase, reduced the production of nitric oxide (NO) in cortical tissue after IR, and artificial cerebrospinal fluid (ACSF) containing aqueous extracts from FBD (ACSF-FBD) (0.01-10 mg/L) protected also primary cortical cortex neurons (PCCN) from hypoxic and excitotoxic insult induced by sodium dithionite (1 mM) and monosodium glutamate (MSG) (0.5 mM) in vitro. Multiple anti-IR properties contributed probably FBD to ameliorate cognitive dysfunction shown in this murine model for VD.
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PMID:Protective effects of FBD--an experimental Chinese traditional medicinal formula on memory dysfunction in mice induced by cerebral ischemia-reperfusion. 1574 Aug 83

The authors investigated the effects of ischemia and reperfusion on the N-methyl-D-aspartate receptor (NMDAR) subunits 2A and 2B concentration in rat hippocampus. At the protein level, significant increase in the amounts of NMDAR 2A and NMIDAR 2B in the rat hippocampus was observed at 1 h after reperfusion compared with control group. These results suggested that the alteration in hippocampal NMDAR2 subunit concentrations after ischemia-reperfusion might be invovlved in cognitive dysfunction and excitotoxicity.
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PMID:Effects of ischemia-reperfusion on NMDA receptor subunits 2a and 2b level in rat hippocampus. 1580 17

Severe and prolonged stress but also long-term treatment with glucocorticoids (GCs) have been described to cause brain damage (especially hippocampal and striatal neurons) in humans as well as in animals. GCs potentiate stress or ischemia-induced accumulation of excitatory amino acids (EAA) in the extracellular space of the hippocampus. It was shown that EAA play a major role in various neurologic disorders with cognitive dysfunction. Many authors suggested the neuroprotective effect of N-methyl-D-aspartate (NMDA) glutamate receptor antagonists in some acute or chronic neurodegenerative diseases. On the other hand, many NMDAreceptor antagonists produce highly undesirable side-effects at the doses within their putative therapeutic range. The aim of the present study was to evaluate the behavioral effects (memory performance, motor coordination, lethality and body weight) of MK-801 or memantine (MEMAN, non-competitive NMDAreceptor antagonists) (at the doses of 25 and 50 microg/kg/day or 2.5 and 5.0 mg/kg/day, respectively) on neurotoxicity induced by dexamethasone (DEX) administered chronically at the doses of 40 or 80 mg/kg/day in mice. It was shown that prolonged treatment (for 10 days) with DEX at the dose of 80 mg/kg/day (but not at 40 mg/kg/day) significantly decreased the retention time in the memory task in mice and impaired the motor coordination in "chimney" test. Neither MK-801 nor MEMAN (at the both doses used) were able to counteract the behavioral impairment induced by DEX administration. Moreover, the potentiation of the body weight reduction and lethality induced by DEX were noted in mice co-treated with MK-801 or MEMAN. The above findings suggest that MK-801 or MEMAN at the doses used have no neuroprotective effect. On the contrary, both NMDA receptor antagonists potentiate the toxicity of DEX given chronically.
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PMID:Effect of NMDA receptor antagonists on behavioral impairment induced by chronic treatment with dexamethasone. 1584 76

Antiphospholipid syndrome can be associated with several neurological manifestations. The most common symptom is headache. It has also been associated with cognitive dysfunction, probably due to ischemia. A high prevalence of antiphospholipid antibodies has been found in patients with epilepsy and in transverse myelitis. The most common thrombotic manifestation is stroke. Venous thrombosis can also be found, yet it is less frequent. A stroke in a young person obliges to rule out the antiphospholipid syndrome. The neurological manifestations can mimic multiple sclerosis. Thus, determination of antiphospholipid antibodies is recommended in the study of patients with atypical manifestations of multiple sclerosis. Other manifestations associated with antiphospholipid antibodies include chorea, neurosensorial deafness, Guillain-Barre syndrome, and psychotic disorders.
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PMID:[Neurological manifestations of the antiphospholipid syndrome]. 1587 82


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