Relevant bibliographies by topics / Cerebral ischaemia

Academic literature on the topic 'Cerebral ischaemia'

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Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Cerebral ischaemia"

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Park, C. K., D. G. Nehls, D. I. Graham, G. M. Teasdale, and J. McCulloch. "Focal Cerebral Ischaemia in the Cat: Treatment with the Glutamate Antagonist MK-801 after Induction of Ischaemia." Journal of Cerebral Blood Flow & Metabolism 8, no. 5 (October 1988): 757–62. http://dx.doi.org/10.1038/jcbfm.1988.124.

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The effects of the glutamate N-methyl-D-aspartate receptor antagonist MK-801 in reducing ischaemic brain damage have been examined in anaesthetised cats, with drug treatment being initiated 2 h after the induction of cerebral ischaemia. Focal cerebral ischaemia was produced by permanent occlusion of one middle cerebral artery, and the animals were killed 6 h later. The amount of early irreversible ischaemic damage was assessed at 16 predetermined stereotactic planes. Treatment with MK-801 (5 mg/kg, i.v.) 2 h after middle cerebral artery occlusion reduced significantly the volume of ischaemic damage (from 1,625 ± 384 mm3 of the cerebral hemisphere in vehicle-treated cats to 792 ± 385 mm3 in MK-801-treated cats). The demonstration of reduced ischaemic brain damage with MK-801, when the agent is administered after the induction of ischaemia, extends the therapeutic potential of such agents in the treatment of focal cerebral ischaemia in humans.
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Schwarting, Sönke, and Harald Neumann. "Immunoregulatory Neuroprotection of Cerebral Ischaemia by Haematopoietic Stem and Precursor Cells." European Neurological Review 4, no. 2 (2009): 42. http://dx.doi.org/10.17925/enr.2009.04.02.42.

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Cerebral ischaemia leads to early immune system activation followed by delayed immunosuppression. Post-ischaemic inflammation contributes to neurodegeneration. Although experimental approaches using adult stem or precursor cells have repeatedly demonstrated neuroprotective effects in cerebral ischaemia, the underlying mechanism of cell-mediated neuroprotection is still debated. It was suggested that stem or precursor cells invade ischaemic brain regions and act locally. However, recent data demonstrate that systemically transplanted stem or precursor cells have strong immunoregulatory effects leading to reduced post-ischaemic brain tissue inflammation. This article argues that the systemic balance of the immune system might explain the reduced neurodegeneration observed after stem cell treatment in cerebral ischaemia. Consequently, systemic immunoregulatory neuroprotection using stem and precursor cells should be considered an important therapeutic option to prevent post-ischaemic neurodegeneration in cerebral ischaemia.
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Li, Zy, B. Liu, J. Yu, Fw Yang, Yn Luo, and Pf Ge. "Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization." Journal of International Medical Research 40, no. 3 (June 2012): 954–66. http://dx.doi.org/10.1177/147323001204000314.

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OBJECTIVE: To investigate the effects of ischaemic postconditioning on brain injury and protein oxidization in focal ischaemia/reperfusion. METHODS: Adult male Wistar rats ( n = 30) were randomly divided into sham-operated, ischaemia, and ischaemic postconditioning groups. Ischaemia was produced by middle cerebral artery occlusion and ischaemic postconditioning was performed using three cycles of 30-s/30-s reperfusion/reocclusion after 2 h of ischaemia. Brain infarction size, hydrogen peroxide concentration, superoxide dismutase (SOD), catalase (CAT) and proteasome activities, protein carbonyl derivatives and advanced oxidized protein products (AOPPs) were evaluated. RESULTS: The size of brain infarction after ischaemic postconditioning was significantly smaller compared with the ischaemia group, and was concomitant with significant reduction in protein carbonyl derivatives and AOPPs. The activities of SOD, CAT and proteasomes were elevated by ischaemic postconditioning compared with the ischaemia group. CONCLUSIONS: Ischaemic post-conditioning is an effective way of reducing the size and effects of brain infarction caused by focal ischaemia/reperfusion, possibly due to a decrease in oxidized protein levels. Decreasing protein oxidization may, therefore, be a useful target for preventing cerebral injury.
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O'Shaughnessy, C. T., N. J. Rothwell, and J. Shrewsbury-Gee. "Effects of an analogue of thyrotrophin-releasing hormone, RX77368, on infarct size and cerebral blood flow in focal cerebral ischaemia in the rat." Canadian Journal of Physiology and Pharmacology 67, no. 10 (October 1, 1989): 1345–50. http://dx.doi.org/10.1139/y89-214.

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Effects of a stable analogue of thyrotrophin-releasing hormone, RX77368, on cerebral blood flow and infarct size have been studied in an acute model of cerebral ischaemia in the rat. Two hours after electrocoagulation of the left middle cerebral artery (MCA), the mean area of ischaemia (± SEM), determined histochemically, was 11.5 ± 2.2% of a single hemisphere and blood flow, determined using radiolabeled microspheres, was reduced by 40% in the left forebrain (p < 0.001 compared with sham-operated animals). Administration of RX77368 (50 μg/kg, intracerebroventricularly) within 10 min of arterial occlusion caused a significant (p < 0.01) reduction in mean lesion size to 3.7 ± 1.8% and stimulation of blood flow to the left ischaemic forebrain (60% above saline treated). Peripheral administration of RX77368 (1 mg/kg intraperitoneally) also significantly stimulated blood flow to the ischaemic forebrain and caused an apparent decrease in frequency of large infarcted areas of brain tissue, although mean lesion size was not significantly affected. These findings indicate that RX77368 ameliorates tissue damage in acute focal cerebral ischaemia. Such effects may be related to stimulation of cerebral blood flow.Key words: middle cerebral artery, focal cerebral ischaemia, cerebral blood flow, thyrotrophin-releasing hormone analogue.
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Kendall, B. "Cerebral Ischaemia." Rivista di Neuroradiologia 3, no. 2_suppl (September 1990): 35–38. http://dx.doi.org/10.1177/19714009900030s208.

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Bittencourt, P. R. M., S. Padilha, and S. Mazer. "Simple and safe heparin regimen for acute ischaemia." Arquivos de Neuro-Psiquiatria 44, no. 1 (March 1986): 32–37. http://dx.doi.org/10.1590/s0004-282x1986000100003.

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The risk/benefit ratio of acute anticoagulation in ischaemic cerebro-vascular disease is not clearly established. A simple and safe intermittent intravenous heparin regimen (20000 IU daily) was used prospectively in 50 patients of 57 ± 14 (m ± sd) years of age whose blood pressures ranged from normal to severe hypertension. Twenty-two patients had cardiogenic embolism and the remaining had recurrent severe transient ischaemic attacks of recent onset or progressive cerebral infarcts. Time of exposure to heparin was 6.4 ± 4 (m±sd) days. Two patients had recurrences of cerebral thromboembolism and none had bleeding complications. This is a safe and efficient method of anticoagulation for patients with cerebral ischaemia when continuous infusion of heparin or close monitoring of clotting times are not used routinely.
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Zhang, Pei-Lei, Hai-Tao Lu, Jun-Gong Zhao, and Ming-Hua Li. "Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischaemia-reperfusion injury in rats." Acta Neuropsychiatrica 25, no. 1 (February 2013): 12–17. http://dx.doi.org/10.1111/j.1601-5215.2012.00649.x.

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ObjectiveTo investigate the effect of dl-3n-butylphthalide (NBP) on the protection of cerebral tissue and possible mechanism on ischaemia-reperfusion injury, and to find out whether NBP therapy can extend the reperfusion window in an experimental stroke model in rats.MethodsSeventy-two Sprague-Dawley rats were randomly divided into sham operation, ischaemia-reperfusion and ischaemia-reperfusion with NBP groups. Focal cerebral ischaemia was induced using the modified intraluminal thread method and maintained for 2, 3 or 4 h. The ischaemia-reperfusion group received reperfusion immediately after ischaemia-reperfusion. The NBP group received intraperitoneal injection of NBP immediately after ischaemia, followed by reperfusion. The sham operation group received only injection of physiological saline. The cerebral infarction volume and neurological deficit were analysed, and vascular endothelial growth factor (VEGF) expression in brain tissues was visualised by immunohistochemistry.ResultsNBP treatment caused a significant decrease in both infarction volume and neurological deficit compared with the ischaemia-reperfusion group at corresponding time points in each (p < 0.05). In the NBP group, the infarction volume and neurological deficit did not change with different ischaemia times. The expression of VEGF was significantly decreased in the ischaemia-reperfusion group compared with the sham group (p < 0.01), while this change was partly prevented in the NBP group (p < 0.01). The expression of VEGF in brain tissue in both the NBP and ischaemia-reperfusion groups gradually decreased when the ischaemic period was prolonged.ConclusionNBP treatment has a protective effect against cerebral ischaemia; this possible mechanism maybe related to the VEGF expression and may extend the reperfusion window for subsequent salvage of cerebral ischaemia by reperfusion.
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Tian, Lin, Yunqian Li, Wei Hua, Ying Jia, Min Zhou, Yunhe Gu, and Jiping Qi. "Expression of Urotensin II During Focal Cerebral Ischemic in Diabetic Rats." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 4 (July 2014): 498–503. http://dx.doi.org/10.1017/s0317167100018552.

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Background:The objective of this study was to explore the expression of urotensin II (UII), its receptor (GPR14), and vascular endothelial growth factor (VEGF), as well as their associations in the ischaemic brains of rats with focal cerebral ischaemia, under normal and diabetic conditions.Methods:Diabetes mellitus (DM) was induced by injection of streptozotocin (STZ) into Sprague—Dawley rats. Focal cerebral ischaemia was induced by middle cerebral artery occlusion (MCAO) four weeks after DM onset by STZ. Rats (n=80) were divided into four groups: normal control, DM, MCAO, and DM/MCAO. Immunohistochemistry and reverse-transcriptase-polymerase chain reaction (RT-PCR) were used to detect the expression of UII, GPR14 and VEGF in the diabetic and ischaemic brain.Results:Expression of UII and GPR14 was increased at mRNA and protein levels in the DM and MCAO group compared with controls. In the DM/MCAO group, expression of UII and GPR14 was increased significantly in the ischaemic brain, and was accompanied by a significantly increased VEGF expression.Conclusion:Diabetes mellitus was seen to aggravate brain lesions after ischaemia, and UII may have an important role.
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Tang, LL, K. Ye, XF Yang, and JS Zheng. "Apocynin Attenuates Cerebral Infarction after Transient Focal Ischaemia in Rats." Journal of International Medical Research 35, no. 4 (July 2007): 517–22. http://dx.doi.org/10.1177/147323000703500411.

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This study investigated whether inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase attenuates cerebral infarction after transient focal ischaemia in rats. Focal ischaemia (1.5 h) was produced in male Sprague-Dawley rats (250 − 280 g) by middle cerebral artery occlusion. Some rats also received treatment with 50 mg/kg apocynin, a NADPH oxidase inhibitor, by intraperitoneal injection 30 min prior to reperfusion. Two hours after reperfusion, brains were harvested to measure NADPH oxidase activity and superoxide levels. After 24 h, the remaining brains were harvested to investigate infarct size. NADPH oxidase activity and superoxide level were all augmented 2 h after reperfusion compared with controls. Apocynin treatment significantly reduced NADPH oxidase activity and superoxide levels. Cerebral infarct size was significantly smaller in the apocynin-treated group compared with those undergoing ischaemia/reperfusion alone. These results indicate that inhibition of NADPH oxidase attenuates cerebral infarction after transient focal ischaemia in rats, suggesting that inhibition of NADPH oxidase may provide a therapeutic strategy for ischaemic stroke.
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Nunn, J. A., J. A. Gray, and H. Hodges. "Neurotoxic Dorsal CA1 Lesions versus 4 VO Ischaemic Lesions: Behavioural Comparisons." Behavioural Neurology 11, no. 4 (1999): 217–26. http://dx.doi.org/10.1155/1999/603123.

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Anterograde amnesia, a common consequence of transient cerebral ischaemia, has been attributed to cell loss in the hippocampal CA1 subfield. However, variable, widespread damage outside hippocampal CA1 can also occur following ischaemia. We compared the functional consequences of ischaemia and ibotenate acid CA1 lesions on 2 spatial memory tasks (water maze ‘place’ and ‘matching-to-position’) to address the possibility that extra-CA1 loss contributes to ischaemia-induced memory deficits in the rat. During place task acquisition, ischaemic rats showed deficits on more measures than ibotenic rats, and during a 1 min probe trial, only ischaemic rats were impaired. On the matching-to-position task, ibotenic rats showed greater impairment than ischaemic rats in terms of one-trial learning, whereas ischaemic rats were more impaired after Trial 2. Ischaemia and ibotenic acid lesions resulted in equivalent CA1 loss, but silver impregnation revealed additional extra-CA1 cell loss in ischaemic rats. Together with the greater behavioural deficits of ischaemic rats, these data indicate a role for extra-CA1 cell loss in ischaemia-induced memory impairments in both animals and humans.
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Dissertations / Theses on the topic "Cerebral ischaemia"

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Rowe, Jeremy Geraint. "Cerebral ischaemia complicating subarachnoid haemorrage." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320671.

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Peters, Elaine Elizabeth. "Inflammatory responses and cerebral ischaemia." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252469.

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Kelly, Stephen. "Neuroprotection and functional alterations in mice over-expressing heat shock protein 70i." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327580.

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Fitridge, Robert Alwyn. "Reperfusion injury in focal cerebral ischaemia /." Title page, table of contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09MS/09msf546.pdf.

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Yam, Philippa S. "Axonal injury following focal cerebral ischaemia." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298683.

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McCarter, Jennifer F. "Inflammatory mechanisms in focal cerebral ischaemia." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/28562.

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In this thesis, focal cerebral ischaemia was induced in three animal models in an attempt to investigate the contribution of the inflammatory response. The rat monofilament model of middle cerebral artery (MCA) occlusion, considered by some to be a pro-inflammatory model, was set up for the first time in Edinburgh and validated as suitable model for further investigation. Permanent and transient models were established to allow the evaluation of possible reperfusion injury. Both monofilament models were compared with the endothelin-1 model already established and routinely in use in the laboratory. Analysis of the volume of damage and distribution of the lesion revealed no differences between the three models. However this observation did not in itself rule out the possibility of different pathophysiological mechanisms in the three models that ultimately resulted in apparently similar sized lesions. FK506, a potent neuroprotectant widely used experimentally, exhibited different neuroprotective efficacies. In all models, FK506 significantly reduced the overall volume of both damage and oedema. The majority of the neuroprotection was observed in the cortex although striatal protection was seen in the transient rat monofilament model. The neuroprotection observed in the transient monofilament model was approximately twice that seen in the permanent model and similar to that in the endothelin-1 model suggesting distinct pathways that lead to cell death. Data for FK506 administration in the mouse monofilament model demonstrated neuroprotection for the first time in this species was included as an interesting comparison with the rat data. In summary, the re-introduction of blood to ischaemic tissue appears to alter the response of the individual cells although this does not change their ultimate fate. In instances where reperfusion is established, the tissue appears to be more amenable to neuroprotection by RK506. It is suggested that this is associated with the blockade of inflammatory mechanisms.
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Dreier, Jens P. "Cortical spreading ischaemia and delayed ischaemic neurological deficits after subarachnoid haemorrhage." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970109342.

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McCaig, David. "Characterisation of Gadd34 response after cerebral ischaemia." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433083.

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Lee, Vee Meng. "Magnetic resonance imaging of cerebral ischaemia models." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242995.

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Mokhtarudin, Mohd Jamil Mohamed. "Mathematical modelling of cerebral ischaemia-reperfusion injury." Thesis, University of Oxford, 2016. http://ora.ox.ac.uk/objects/uuid:3f5dd7cf-e403-4cf0-b725-4ac235c1b37e.

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Restoring cerebral blood flow using reperfusion treatment is a common method in treating ischaemic stroke. Reperfusion treatment should be given within 4.5 hours from stroke onset. However, reperfusion beyond this time window poses the risk of reperfusion injuries such as intracranial haemorrhage and cerebral tissue swelling. The focus of this thesis is to study the effect of cerebral tissue swelling after reperfusion as it can occur in a few hours after the treatment. Cerebral tissue swelling may cause brain structure movement and cerebral microvessel compression; the latter may then lead to secondary ischaemia occurrence. In this thesis, two mathematical models are presented. The first model investigates the effect of ischaemia-reperfusion in the formation of cerebral tissue swelling. This model provides the understanding of suitable reperfusion conditions to reduce the effect of tissue swelling and also becomes the basis for the subsequent model. Meanwhile, the second model studies the role of a water-transporting protein, aquaporin-4 in ischaemia-reperfusion and its potential as part of treatments for cerebral tissue swelling. In addition, the ionic concentration may change during ischaemia which may be a factor contributing to cerebral tissue swelling. Thus, the effect of ionic concentration on the swelling formation is also investigated. Finally, validations of these models are achieved by developing patient-specific geometries from available ischaemic stroke patient MRI data and utilising finite element analysis. Comparison between the simulation results and the MRI data is done by quantifying the brain ventricles movement during cerebral tissue swelling.
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Books on the topic "Cerebral ischaemia"

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Bories, Jacques, ed. Cerebral Ischaemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2.

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Loddick, Sarah Ann. The role of interleukin-1 in cerebral ischaemia. Manchester: University of Manchester, 1996.

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Nelson, Rachael M. Cellular effects of cerebral ischaemia in vitro: Cerebroprotective actions of GABAmimetic agents. Leicester: De Montfort University, 2002.

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Smith, T. C. G. 1939-, ed. Ischaemia in head injury: 10th European Congress of Neurosurgery, Berlin 1995 ; proceedings of a special symposium. Berlin: Springer, 1996.

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Kramer, G., W. Hacke, H. J. Gelmers, and M. Hennerici. Cerebral Ischaemia. Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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Krieglstein, Josef. Pharmacology of Cerebral Ischaemia. Elsevier, 1986.

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Cerebral Ischaemia: A Neuroradiological Study. Springer, 2011.

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Jacques, Bories, and Aymard A, eds. Cerebral ischaemia: A neuroradiological study. Berlin: Springer-Verlag, 1985.

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Alarcón, Gonzalo, Marian Lazaro, and Antonio Valentín. Migraine, stroke, and cerebral ischaemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0033.

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This chapter reviews the electroencephalographic changes associated with migraine, stroke and cerebral ischaemia, and their interpretation to aid in their differential diagnosis. The incidence of stroke and cerebral ischaemia is increasing with population aging. They are some of the most common problems faced in emergency medicine, and their diagnosis can be puzzling. This chapter describes and illustrates the patterns seen in such conditions, such as slowing, frontal intermittent delta activity (FIRDA), periodic lateralized epileptiform discharge (PLED), generalized periodic lateralized epileptiform discharge (GPED), and bilateral periodic lateralized epileptiform discharge (BiPED). The chapter reviews their prognostic value in critical care medicine and their differential diagnosis with status epilepticus.
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R, Caplan Louis, ed. Cerebrovascular ischaemia investigation and management. London: Med-Orion, 1996.

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Book chapters on the topic "Cerebral ischaemia"

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Bories, J. "Cerebral ischaemia: A neuroradiological study." In Cerebral Ischaemia, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_1.

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Thiebot, J., and E. Clavier. "The place of digital intravenous angiography in cerebral infarcts." In Cerebral Ischaemia, 89–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_10.

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Boespflug, O. J. M. "Ultrasonography of supra-aortic trunks." In Cerebral Ischaemia, 94–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_11.

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Natali, J., and C. Ruotolo. "Post-operative angiographic control." In Cerebral Ischaemia, 98–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_12.

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Carpena, J. H., J. Bories, and J. Chiras. "Post-operative angiographic control." In Cerebral Ischaemia, 107–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_13.

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Raybaud, C. A., Marie-Odile Livet, M. Jiddane, and Nicole Pinsard. "Radiology of ischemic strokes in children." In Cerebral Ischaemia, 117–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_14.

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Grosgogeat, Y. "Cerebral ischemic accidents of cardiac origin." In Cerebral Ischaemia, 129–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_15.

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Bousser, M. G., J. C. Baron, and J. Chiras. "Ischemic strokes and migraine." In Cerebral Ischaemia, 133–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_16.

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Godon-Hardy, S., J. F. Meder, A. Dilouya, V. Monsaingeon, and D. Fredy. "Ischemic strokes and oral contraception." In Cerebral Ischaemia, 138–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_17.

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Chiras, J., M. Dubs, and J. Bories. "Venous infarctions." In Cerebral Ischaemia, 143–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_18.

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Conference papers on the topic "Cerebral ischaemia"

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Dormandy, J. "RHEOLOGY AND ISCHAEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643989.

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While the previous presentations have dealt with the experimental evidence linking flow patterns and shear stress to thrombosis and atherogenesis, this presentation will concentrate on the clinical evidence linking Theological abnormalities to macro and micro-circulatory ischaemia. Whole blood viscosity undoubtedly influences blood flow along larger vessels as suggested by Poiseuille. The two important determinants of whole blood viscosity are the red cell concentration and plasma fibrinogen.There is overwhelming epidemiological evidence that the red cell concentration is a primary risk factor for the development of essential hypertension, myocardial, cerebral and leg ischaemia. It is also a secondary risk factor in patients who already had a clinical episode of ischaemia in any of these territories. There is similar evidence in relation to a high plasma fibrinogen.Furthermore therapeutic haemodilution or defibrinogenation are increasingly used in the prevention and treatment of ischaemia.Haemorheological factors in the microcirculation are probably equally important but more difficult to assess clinically. The concept of a 'vicious viscous spiral' in ischaemic tissue is gaining increasing support. Whatever the initial cause of the ischaemia, important secondary haemorheological changes occur which can perpetuate or aggravate the ischaemia. Most of the changes known to occur locally in ischaemic tissues such as hypoxia, acidosis, release of serotonin and platelet activation have been shown to impair the deformability of blood cells. This will be particularly important if the perfusion pressure is also decreased and may result in capillary plugging and uneven distribution of flow in the microcirculation. Abnormal blood cell filtrability, just as whole blood viscosity, has been shown to be associated with acute as well as chronic ischaemia in most territories. Furthermore there is a correlation between the magnitude of the haemorheological changes measured and the subsequent clinical course of the patient following an ischaemic injury.The newest aspect of haemorheology to attract clinical attention is the role of the white cell in ischaemia. Epidemiological as well as recent experimental and clinical studies suggest that the Theologically activated white cell may be the most dangerous component of blood in terms of perpetuating and extending tissue ischaemia.The assessment of the Theological properties of blood should form an integral part of studies looking at the causes and possible therapy of all forms of acute and chronic ischaemia.
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SLOTWINSKI, K., P. CALABRESE, R. PODEMSKI, and W. GEHLEN. "HEMISPHERIC LATERALIZATION OF FOCAL CEREBRAL ISCHAEMIA AS REFERRED TO MEMORY PROCESSES." In Proceedings of the International School of Biocybernetics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776563_0036.

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Farrell-Dillon, Keith, Paul Fraser, Giovanni Mann, and Sarah Chapple. "9 P62 deficiency protects against cerebral ischaemia in insulin resistant mice." In Abstracts from the Fellowship of Postgraduate Medicine Centenary Conference 2018: Transforming Health and Health Care. The Fellowship of Postgraduate Medicine, 2018. http://dx.doi.org/10.1136/postgradmedj-2018-fpm.20.

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Farrell-Dillon, Keith, Paul A Fraser, and Giovanni E Mann. "7 Dietary sulforaphane reduces peri-infarct constriction frequency in mouse brain following focal cerebral ischaemia via a Nrf2-independent mechanism." In Abstracts from the Fellowship of Postgraduate Medicine Centenary Conference 2018: Transforming Health and Health Care. The Fellowship of Postgraduate Medicine, 2018. http://dx.doi.org/10.1136/postgradmedj-2018-fpm.18.

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Nechipurenko, N., L. Vasilevskaya, J. Musienko, and G. Maslova. "THE INFLUENCE OF INTRAVENOUS LASER IRRADIATION OF BLOOD ON SOME METABOLIC AND FUNCTIONAL PARAMATERS IN INTACT RABBITS AND EXPERIMENTAL CEREBRAL ISCHAEMIA." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/ecbo.2007.6632_55.

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Nechipurenko, N., L. Vasilevskaya, J. Musienko, and G. Maslova. "The influence of intravenous laser irradiation of blood on some metabolic and functional parameters in intact rabbits and experimental cerebral ischaemia." In European Conference on Biomedical Optics, edited by Alfred Vogel. SPIE, 2007. http://dx.doi.org/10.1117/12.728721.

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Alessandri, C., F. Violi, M. Rasura, C. Caliendo, and P. Pelaia. "BEHAVIOUR OF ADREN0CHR0ME PATHWAY IN PATIENTS WITH CEREBROVASCULAR DISEASES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643169.

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Abstract:
Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a neutrophil oxidase able to convert,in vitro, adrenaline to adrenochrome.Aim of present study was to evaluate if neutrophil activation can be observed in patients with brain hemor ragie (BH) also.Six patients (females 1,males 5;age 68-79 years) suffering from BH and 15 patients (females 5, Males 10;age 58-86 years) affected by brain infarction (BI) were studied within 20-48 hours from acute episode.Diagnosis of stroke was made by computerized tomography.Neutrophil activation was studied in plasma evaluating the oxidation of adrenaline to adrenochrome according to Matthews and Campbell method.20 matched for age and sex healthy subjects were studied as control.A significant rise of plasma adrenaline oxidase activity was observed in patients with BI.This preliminary investigation suggests that neutrophil activation could be restricted to patients with BI.In fact,patients with BH had plasma oxidase activity similar to controls.Clinical data should be necessary to evaluate if a relation between leucocyte activation and the natural course of cerebral ischemia does exist.
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Zhou, Mingchao, Shanshan Ling, Hongxia Chen, and Ruihuan Pan. "Inhibition of notch signaling pathways contribute to neuroprotection effect by the combination of astragalus membranaceus and ligustrazine in rat model after thrombolysis of cerebral ischaemia." In 2017 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2017. http://dx.doi.org/10.1109/bibm.2017.8218051.

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Prins, M. H., G. J. H. den Ottolander, R. Gelsema, T. C. M. van Woerkom, A. K. Sing, and I. Heller. "DEEP VENOUS THROMBOSIS PR0FYLAXIS WITH A LMW HEPARIN (KABI 2165) IN STROKE PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643217.

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In a group of 60 patients entering our hospital for completed stroke, within 72 hours after onset of symptoms, treatment with Kabi 2165 2x 2500 anti-Xa U s.c. was compared to placebo 2x s.c. in a double blind trial to test the assumption that Kabi 2165 could prevent DVT, without causing cerebral bleeding in the ischaemic area. The diagnosis of stroke was made on clinical grounds. A.CT-scan of the head was performed before entering the trial to exclude cerebral bleeding or tumor. Follow-up during a trial period of 14 days included a Fibrinogen scan - if positive followed by flebografy. After the trial period or when clinical deterioration occurred a CT-scan of the head was repeated. Before and during the trial period haematologic and coagulation data were obtained and will be reported. Obduction was obtained whenever possible.The patient groups were comparable, except for a slight preponderance of disturbed consciousness and atrial fibrillation in the Kabi 2165-treated group. This difference did not reach statistic significance. In the Kabi 2165 group there were 6 cases of DVT compared to 15 in the placebo group (p=0,05). In the Kabi 2165-treated group there were slightly more cases of cerebral bleeding and death during trial, respectively 4 versus 2 and 9 versus 4 (both NS). Cerebral bleeding occurred only in patients with a bloodpressure above 150/90 mmHg on entering.Although the patient group is still small, we like to conclude that in normotensive stroke patients Kabi 2165 2x 2500 anti-Xa U s.c. per 24 hours, is a safe method of DVT profylaxis.
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Montecchio, G. P., P. Custodi, S. Carbone, C. Bendotti, and F. Piovella. "TICLOPIDINE AND INDOBUFEN: EFFECTS ON HAEMOSTATIC FUNCTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643418.

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Many different mechanisms are involved in thrombus formation. We compared the effects on haemostatic function of two drugs having different mechanism of action, the one interfering with arachidonic acid metabolic cascade (Indobufen) and the other (Ticlopidine) independent from it. 18 adult patients of both sexes suffering from cerebral Transient Ischaemic Attack (T.I.A.) or Reversible Ischaemic Neurologic Disability (R.I.N.D.) have been treated with Indobufen (400 mg daily) or Ticlopidine (500 mg daily) for three weeks. The effects on various haemostatic parameters including bleeding time, platelet adhesion to glass beads, platelet aggregation induced by ADP, collagen, platelet activating factor (PAF )f have been evaluated at the beginning and at the end of treatment. Both drugs prolonged the bleeding time, Ticlopidine being more effective than Indobufen. ADP-induced platelet aggregation was more effectively inhibited by Ticlopidine, while Indobufen was more effective on collagen-induced aggregation. PAF-induced platelet aggregation was inhibited by Ticlopidine, while Indobufen was ineffective. Platelet adhesion to glass beads was not influenced by treatment with either drugs. In conclusion, both drugs confirmed to be effective in inhibiting haemostatic function although with different mechanisms. Ticlopidine seems to be involved in more mechanisms, interfering with platelet aggregation induced by ADP, collagen, PAF and prolonging the bleeding time. Indobufen interferes with platelet aggregation induced by ADP and collagen, is less effective in prolonging the bleeding time, and does not affect PAF-induced platelet aggregation.
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