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

Several kinds of middle cerebral artery occlusion model in rats have been developed. Variable ischemic inductions are attributed to the different contributing factors in ischemic damage formation. In the present study, we examined the differences in ischemic induction attributed to chronic stage. Male Sprague-Dawley rats were subjected to two kinds of middle cerebral artery occlusion model, a thermocoagulation and a photothrombosis model. We compared the changes in body weight, neurological outcome, size of ischemic damage, brain edema and atrophy formation, and histological data for 84 days between a thermocoagulation and a photothrombosis model in rats. Although the time courses of infarction formation were no different, there were differences in the time courses of brain edema, atrophy formation, and neuronal deficits between the models. Microinfarction formation was observed as a characteristic of the photothrombosis model. The present study demonstrated that differences in ischemic induction did not affect maturation of infarct size, brain atrophy, or neuronal deficits 84 days after ischemia. However, the progress of maturation was different between the models. The possibility that reperfusion contributed to the time course of brain edema and atrophy was considered, and it was suggested that brain edema formation influenced neurological outcome.
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PMID:Time courses of progress to the chronic stage of middle cerebral artery occlusion models in rats. 1219 83

Experimental studies demonstrate an alkaline shift in brain intracellular pH (pH(i)) after hypoxia-ischemia (HI). In infants with neonatal encephalopathy after HI, our aims were to assess (1) brain pH(i) during the first 2 weeks after birth in infants categorized according to magnetic resonance imaging (MRI) during the first 2 weeks after birth and at more than 3 months of age, and neurodevelopmental outcome at 1 year; (2) the relationship between brain pH(i) and lactate/creatine; and (3) duration of alkaline brain pH(i). Seventy-eight term infants with neonatal encephalopathy were studied using MR techniques. One hundred and fifty-one studies were performed throughout the first year including 56 studies of 50 infants during the first 2 weeks after birth. pH(i) was calculated using phosphorus-31 MR spectroscopy and lactate/creatine was measured using proton MRS. The mean (standard deviation [SD]) brain pH(i) during the first 2 weeks after birth in infants with severely abnormal versus normal MRI was 7.24 (SD, 0.17) versus 7.04 (SD, 0.05; p < 0.001); in infants who subsequently developed cerebral atrophy versus those who did not: 7.23 (SD, 0.17) versus 7.06 (SD, 0.06; p < 0.05); in infants who died or had a severe neurodevelopmental impairment versus normal outcome: 7.28 (SD, 0.15) versus 7.11 (SD, 0.09; p < 0.05). Brain alkalosis was associated with increased brain lactate/creatine (p < 0.001). pH(i) remained more alkaline in the severe outcome group up to 20 weeks after birth (p < 0.05).
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PMID:Brain alkaline intracellular pH after neonatal encephalopathy. 1244 26

Vascular damage and reactive gliosis are found colocalized with amyloid deposits in Alzheimer's disease brain, suggesting that the cerebrovasculature may be a clinically relevant site of Alzheimer's disease pathology and may contribute to the neurodegeneration process in Alzheimer's disease. In ischemic conditions, amyloid precursor protein and amyloid peptide are reported to be upregulated in neurons and in extracellular space. Expression and distribution of amyloid precursor protein and amyloid peptide in astroglial cells were examined immunohistochemically after 10-min cardiac arrest. After reperfusion for 2, 7, and 14 days and 1, 6, 9, and 12 months, brains were immunostained. The indirect reactive astrocytes with fragments of the full-length amyloid precursor protein were observed in brains until 7 days postischemia. Direct immunoreactivity only of amyloid peptide and the C-terminal of amyloid precursor protein was also localized in the reactive astrocytes in ischemic brains at 6 months after ischemia. Ischemia temporarily induced amyloid peptide overexpression in reactive astrocytes, but this expression peaked at 7 days and 6 months. A glial appearance of amyloid peptide and C-terminal of amyloid precursor protein staining occurred when extensive neuronal loss and the onset of brain atrophy were evident. The localization of the C-terminal of amyloid precursor protein within ischemic astroglial cells underscores the likely importance of the C-terminal of amyloid precursor protein in the pathogenesis of ischemia as in Alzheimer's disease.
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PMID:Astroglial expression of the beta-amyloid in ischemia-reperfusion brain injury. 1248 Jul 38

Elevated fasting plasma total homocysteine concentration (tHcy) and lower vitamin status are associated with atherosclerotic states. Silent brain ischemic lesions and brain atrophy, prevailing in the elderly, are affected by tHcy and vitamin status. The study was performed on 56 outpatients who had undergone brain computed tomography (CT) before the onset of the study. According to brain CT evaluation, three groups were set: minor brain ischemia, brain atrophy and control. Brain CT, tHcy, plasma pyridoxal phosphate (PLP), vitamin B(12), folic acid and cognitive and functional capacities were measured or evaluated in all of the subjects. Plasma vitamin score for three vitamins was calculated. In subjects with minor brain ischemic lesions (n = 21), tHcy was higher by 5.6 microM, whereas vitamin score and cognitive function were lower than in controls (n = 24). In subjects with brain atrophy (n = 11), plasma PLP and cognitive function were lower. Particular attention should be paid to tHcy monitoring, vitamin status assessment and brain impairment evaluation.
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PMID:Hyperhomocysteinemia and vitamin score: correlations with silent brain ischemic lesions and brain atrophy. 1271 99

Fifty-two patients with cerebrovascular risk factors without neurological abnormalities were examined by magnetic resonance imaging and were evaluated for their periventricular hyperintensity (PVH) on T2-weighted images. We assumed that PVH was not a mere focal finding of the brain but a kind of marker for condition related to arteriosclerosis and cerebral ischemia, and we tried to devise a model screening test, using common parameters available in most ordinary hospitals, to predict PVH. Multiple regression analysis was performed by setting up the PVH% (the volume percentage of PVH to cranial cavity) as a dependent variable and twenty-seven variables associated with general medical examination and brain atrophy as explanatory variables. We found that arteriosclerotic changes in the body as well as brain atrophy were significantly correlated with PVH, and that PVH could be predicted with a high contribution ratio of 0.70. It is clinically important to examine the elderly with our screening test to predict PVH in order to detect the early stages of ischemia.
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PMID:A study of periventricular hyperintensity. I. Normal brain aging. 1537 3

The role of complement in post-ischemic cerebral injury is incompletely understood. Therefore, experiments were designed to test the effect of complement depletion on cerebral infarct volume in adult rats and cerebral atrophy in neonatal rats. Cerebral infarcts were induced in adult rats by transient filamentous occlusion of the right middle cerebral artery (MCAO). Cerebral atrophy was induced by subjecting 7-day-old rats to ligation of the right common carotid artery followed by 2.5h of hypoxia (8% O2). Forty-eight hours after MCAO, coronal sections of adult brains were obtained and stained with 2,3,5-triphenyl tetrazolium chloride. The infant rat brains were removed for analysis 6 weeks after the hypoxic-ischemic insult. Volumes of infarcts and normal hemispheric parenchyma were quantified by computer-based planimetry. Twenty-four hours prior to MCAO (adults) or hypoxia-ischemia (neonates), each animal received an i.p. injection of either 1 mcg/g body weight cobra venom factor (CVF; adult n=11; neonatal n=20) or normal saline (adult n=12; neonatal n=24). In the neonates, a second dose of CVF or saline was administered 2 days after hypoxia-ischemia. The administration of CVF significantly reduced: (1) post-ischemic cerebral infarct volume in the adults and (2) post-hypoxic-ischemic cerebral atrophy in the neonates. Therefore, complement activation augmented post-ischemic cerebral injury in adult and neonatal rats. Complement depletion induced by CVF significantly reduced post-ischemic cerebral infarct volume and atrophy in adult and neonatal rats.
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PMID:The administration of cobra venom factor reduces post-ischemic cerebral injury in adult and neonatal rats. 1585 49

Understanding of the molecular basis of dementias such as Alzheimer's disease has not improved greatly in recent years. In this situation the study of neurobiology of Alzheimer's disease, now more than ever, needs an infusion of new concept. Recent evidence suggests that the neuropathological picture of Alzheimer's disease comprises more than amyloid accumulation, neurofibrillary tangles and finally brain atrophy. At least one third of Alzheimer type of dementia cases exhibit different cerebrovascular diseases. In addition, micro- and macro-infarctions and ischemic white matter changes are also evident in brains of Alzheimer's disease patients. The presence of vascular abnormalities seems usually ignored and regarded by researchers as insignificant or considered incidental in Alzheimer's disease etiology. The "ischemia-reperfusion hypothesis" was primarily aimed at stimulating research and redirecting the focus of studies towards ischemic cellular mechanisms of Alzheimer's disease. Considerable progress has been made in recent years in understanding the role of ischemia in the aging process and in contributing to the development of Alzheimer's disease. To accommodate the recent ischemic progress of study in Alzheimer's disease there is a need to synthesize all the divergent pieces of data into a coherent story. In this review, current knowledge on the relation between cerebrovascular disease factors and Alzheimer's type dementia will be reviewed. We will summarize the results with a special focus on Alzheimer lesions in experimental brain ischemia.
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PMID:From brain ischemia-reperfusion injury to possible sporadic Alzheimer's disease. 1618 Oct 92

Recent studies have indicated the beneficial effects of vascular endothelial growth factor (VEGF), and transplanted neural stem cells (NSCs) in cerebral ischemia. We investigated the effects of the combined administration of NSCs and VEGF on focal cerebral ischemia in adult rats. Four groups (n = 12, respectively)--group 1 (ischemia-only), group 2 (ischemia + VEGF), group 3 (ischemia + NSCs) and group 4 (ischemia + NSCs + VEGF)--were compared. Human NSCs (HB1.F3), labeled with Lac Z+ or PKH26, were given intravenously 24h after surgery (5 x 10(6) cells). At 48 h after surgery, recombinant human VEGF (50 microg/kg) was infused intravenously (1 microg/(kg min)). Behavioral tests using the modified limb placing and rotarod tests were performed every week following ischemia. Immunohistochemistry for endothelial barrier antigen (EBA), VEGF and Nissl staining were performed at day 35 after ischemia. Group 4 showed better behavioral recovery at 7, 14 and 28 days than group 3 (p = 0.020, 0.005 and 0.043, respectively). These functional recoveries were correlated with enhanced EBA immunoreactivities at day 35 after ischemia, especially in the ipsilesional striatum. Group 4 showed lesser degree of brain atrophy in cortex and striatum, when compared with other groups. The distribution of VEGF was not co-localized with NSCs. Our results suggest that VEGF may act synergistically on NSC-transplanted, ischemic brain via a pro-angiogenic effect.
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PMID:Combined treatment of vascular endothelial growth factor and human neural stem cells in experimental focal cerebral ischemia. 1619 14

In addition to the well-documented mood-stabilizing effects of lithium in manic-depressive illness patients, recent in vitro and in vivo studies in rodents and humans have increasingly implicated that lithium can be used in the treatment of acute brain injuries (e.g., ischemia) and chronic neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, tauopathies, and Huntington's disease). Consistent with this novel view, substantial evidences suggest that depressive illness is not a mere neurochemical disease, but is linked to gray matter atrophy due to the reduced number/size of neurons and glia in brain. Importantly, neurogenesis, that is, birth/maturation of functional new neurons, continues to occur throughout the lifetime in human adult brains (e.g., hippocampus); the neurogenesis is impaired by multiple not-fully defined factors (e.g., aging, chronic stress-induced increase of glucocorticoids, and excitotoxicity), accounting for brain atrophy in patients with depressive illness and neurodegenerative diseases. Chronic treatment of lithium, in agreement with the delayed-onset of mood-stabilizing effects of lithium, up-regulates cell survival molecules (e.g., Bcl-2, cyclic AMP-responsive element binding protein, brain-derived neurotrophic factor, Grp78, Hsp70, and beta-catenin), while down-regulating pro-apoptotic activities (e.g., excitotoxicity, p53, Bax, caspase, cytochrome c release, beta-amyloid peptide production, and tau hyperphosphorylation), thus preventing or even reversing neuronal cell death and neurogenesis retardation.
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PMID:Lithium: potential therapeutics against acute brain injuries and chronic neurodegenerative diseases. 1634 Jan 57

Cilostazol, a selective inhibitor of phosphodiesterase 3, exerts neuroprotective effects on acute brain injury after cerebral ischemia in rats. However, it is unknown whether cilostazol affects the subacute or chronic ischemic injury. In the present study, we evaluated the dose- and time-dependent effects of cilostazol on acute ischemic brain injury and the long-lasting effect on the late (subacute/chronic) injury in mice with focal cerebral ischemia induced by transient middle cerebral artery occlusion. We found that pre-treatment of cilostazol (injected i.p. at 30 min before ischemia) significantly ameliorated the acute injury 24 h after ischemia, and the effective doses were 3-10 mg/kg. The post-treatment of cilostazol (10 mg/kg) was effective on the acute injury when it was injected 1 and 2 h after ischemia. In addition, for the late injury, post-treatment of cilostazol (10 mg/kg, i.p., for 7 consecutive days after ischemia) attenuated neurological dysfunctions, brain atrophy and infarct volume. It also inhibited astrocyte proliferation/glial scar formation and accelerated the angiogenesis in the ischemic boundary zone 7 and 28 days after ischemia. Thus, we conclude that cilostazol protects against not only the acute injury, but also the late injury in mice with focal cerebral ischemia; especially it can modify brain remodeling, astrogliosis and angiogenesis.
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PMID:Cilostazol, a phosphodiesterase 3 inhibitor, protects mice against acute and late ischemic brain injuries. 1716 38


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