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Dissertations / Theses on the topic 'Cerebral ischaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Murray, Katie. "Actions of interleukin-1 in cerebral ischaemia." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-in-cerebral-ischaemia(76a8206b-4153-437d-9616-7d668a35db51).html.

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Cerebral ischaemia is characterised by an interruption in cerebral blood flow (CBF) leading to neuronal dysfunction and death. Pre-existing systemic inflammation is strongly associated with exaggerated brain injury following cerebral ischaemia with experimental studies showing that increased damage is mediated by interleukin (IL)-1 dependent pathways. The mechanisms through which systemic inflammation worsens stroke have yet to be elucidated, therefore in this thesis we sought to further determine how systemic inflammation affects outcome after acute cerebral ischaemia. The effects of acute pre-existing inflammation on cerebral perfusion and infarct volume after transient middle cerebral artery occlusion (MCAo) in rats were measured using magnetic resonance imaging (MRI). Systemic IL-1 caused a severe reduction in CBF and increase in infarct volume compared to vehicle. CBF changes were accompanied by upregulation of the vasoconstricting peptide endothelin (ET)-1. Blockade of ET-1 receptors reversed hypoperfusion, reduced ischaemic damage and improved functional outcome when assessed at 48h. Streptoccocus pneumoniae is the most common infection in patients at risk of stroke and is associated with an elevated inflammatory profile. The effect of an acute S. pneumoniae challenge on stroke outcome was assessed in mice and rats following transient MCAo. S. pneumoniae induced a systemic IL-1 response, exacerbated brain injury and increased platelet adhesion to the endothelium. Blockade of IL-1 with IL-1 receptor antagonist (IL-1Ra) and administration of glycoprotein (Gp) Ibα (to reduce platelet-endothelial interactions) reversed infection-mediated exacerbation of ischaemic injury and improved functional impairments after MCAo. Presence of chronic inflammation in the form of advanced age and obesity are associated with poorer outcomes following ischaemic stroke. The neuroprotective effects of delayed IL-1Ra on stroke outcome were assessed in aged lean and corpulent rats versus young rats at 7 days post-stroke. IL-1Ra reduced ischaemic damage, blood brain barrier (BBB) breakdown, improved functional outcomes and preserved neurogenesis in young and aged co-morbid rats at 24 hours and 7 days. Overall, these findings suggest systemic IL-1 is a common point of convergence in both acute and chronic pre-existing inflammatory disorders that are risk factors for stroke. Systemic IL-1 leads to excessive ischaemic damage through effects on the endothelium and the coagulation cascade. These results lend further support to the hypothesis that IL-1 is a potential therapeutic target in ischaemic stroke.

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12

Bowler, John Vaughan. "Cerebral infarction and '9'9Tc'm HMPAO SPECT." Thesis, King's College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260983.

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13

Pathmanathan, Saidharshini. "Development of in vitro models of cerebral ischaemia." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249162.

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14

Whitfield, Peter Cyril. "Gene expression after global and focal cerebral ischaemia." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242632.

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15

McMahon, Catherine Jane. "Inflammation and delayed cerebral ischaemia induced byaneurysmal subarachnoid haemorrhage." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491335.

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Stroke is a sudden, unpredictable, often devastating neurological event. The commonest cause of morbidity and mortality associated with subarachnoid haemorrhage (SAH) is delayed cerebral ischaemia (DCI). Ischaemic and haemorrhagic strokes are recognised to induce a significant peripheral and central inflammatory response. These responses may be important in the exacerbation of ischaemic damage and in the development and exacerbation of DCI after SAH. A number of studies have examined the potential contribution of pro-inflammatory cytokines, such as interleukin-l (IL-l) and interleukin-6 (IL-6), to damage caused by experimental ischaemia. Intracerebroventricular (ICV) injection of interleukin-lP(IL-l P) causes a marked exacerbation of ischaemic damage in experimental paradigms of cerebral ischaemia. Conversely, administration of the cytokine anatgonist, interleukin-l receptor antagonist (ILlRA), or other inhibitors of IL-l release and action confer neuroprotection; The aim of this work was to test two primary hypotheses, namely (1) circulating markers of inflammation, (specifically, C-reactive protein (CRP), IL-6 and IL-lRA) predict the development of DCI after SAH, and (2) that there is a direct relationship between peripheral and central inflammation. Clinicai predictors of any cerebrovascular event, and outcome after SAH, were also determined. In a prospective study of 179 aneurysmal SAH patients between January 2004 and August 2007, plasma samples (and in 25 patients CSF samples) were obtained over a period of 15 days after SAH. Levels of inflammatory markers and presenceÃ‚Â· or absence of DCI was determined. In case-control analysis of 159 patients, only rate of change of IL-6 (OR 2.3, CI 1.1 to 5, pO.03) was predictive of DCI. In a secondary analysis of Erythrocyte sedimentation rate (ESR) and WCC, initial ESR (OR 2.4, CI 1.3 to 4.6, pO.006) average ESR (OR 2.3, CI 1.3 to 4.2, pO.006), peak ESR (OR 2.1, CI 1.1 to 3.9, pO.02) and final ESR (OR 2.0, CI 1.2 to 3.3, pO.009) in addition to final WCC (OR 1.2, CI 1 to 1.3, pO.Ol) and rate of change of WCC (OR 1.3, CI 1 to 1.6, pO.OS) were significantly associated with the development of DCI. A direct relationship was not demonstrated between peripheral and central inflammation. In unifactorial analysis of the 179 patient cohort, female sex (HR 1.8, CI 1 to 3.1, pO.04) hypertension (HI3-Z-,_CL1)_J.Q__~:;?,. pO.OOS), statin use (HR 2, CI 1 to 3.8, pO.04), infection peri-study (HR 1.9, CI 1.2 to 3.0, pO.007), increasing WFNS grade (II & III, HR 2.5, CI 1.5 to 4.2, pO.OOO; IV & V, HR 3.8, CI 2to 7.3, p

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16

Stock, Christopher John. "Inflammatory cytokines in repair and recovery after cerebral ischaemia." Thesis, University of Manchester, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633022.

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The cytokines, a family of poly-peptides that are central to the coordination of the inflammatory response, exert significant influence on the progression of acute cerebral ischaemic injury, or 'stroke'. Evidence has accumulated for a similarly significant role for cytokines in physical repair and neurological recovery after stroke, via actions within the injured central nervous system and through mediation of peripheral inflammation. This thesis addresses the spatio-temporal expression profile of cytokines in response to cerebral ischaemia in the rat, and the influence of elevated peripheral cytokine concentration on physical repair of the CNS.

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17

Calamante, Fernando. "Diffusion and perfusion MRI and applications in cerebral ischaemia." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314345.

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18

Taylor, Deanna Lesley. "Alterations in interstitial acid-base homeostasis during cerebral ischaemia." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267025.

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19

Sibson, Nicola Ruth. "A magnetic resonance imaging study of experimental cerebral ischaemia." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360825.

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20

Greenhalgh, Andrew. "Actions of interleukin-1 receptor antagonist in cerebral ischaemia." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-receptor-antagonist-in-cerebral-ischaemia(50aacd97-68c1-4f91-90b5-8f8deff5d21d).html.

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Cerebral ischaemia, or stroke, is a leading cause of death and disability worldwide. Ischaemic stroke, as a result of arterial occlusion, and subarachnoid haemorrhage (SAH), as a consequence of arterial rupture in the subarachnoid space, are major subtypes of stroke. Treatment options for both are limited, and many therapeutic strategies have failed. In ischaemic stroke, lack of evidence of brain penetration of treatments has been cited as a major weakness and contributing factor to failed clinical trials. In SAH, animal models do not always mimic key pathophysiological hallmarks of the disease, hindering development of new therapeutics. Inflammation is strongly associated with brain injury after cerebral ischaemia and inhibition of the pro-inflammatory cytokine interleukin-1 (IL-1) represents apossible therapeutic target. Therefore, the key objectives of this thesis were; (1) to improve preclinical data on a promising stroke treatment, interleukin-1 receptor antagonist (IL-1Ra), by investigating its pharmacokinetic profile and brain penetration in a rat model of ischaemic stroke, (2) to investigate the endovascular perforation model of SAH in rat, as a tool for the investigation of neuroprotectants, and (3) to examine the role of the inflammatory response in the SAH model and the effects of IL-1Ra. The neuroprotective effect, pharmacokinetic profile and brain penetration of IL-1Ra were assessed after a single subcutaneous (s.c.) dose (100mg/kg) in rats, after transient (90 min) middle cerebral artery occlusion (MCAo). A single s.c. dose of IL-1Ra reduced neuronal damage, resulted in sustained, high concentrations of IL-1Ra in plasma and cerebrospinal fluid and also penetrated brain tissue exclusively in areas of blood brain-barrier (BBB) breakdown. An endovascular perforation model of SAH in rat was investigated and produced widespread multifocal infarcts. In this model, administration of IL-1Ra (s.c.) reduced BBB breakdown, which correlated with injury at 48 h. IL-1_ was expressed in the brain early after SAH in areas associated with haem oxygenase-1 (HO-1) expression, indicating the presence of free haem. Stimulation of primary mouse mixed glial cells in vitro with haem induced expression and release of IL-1 alpha but not IL-1 beta. These data, after MCAo in rat, are the first to show that a single s.c. dose of IL-1Ra rapidly reaches salvageable brain tissue and is neuroprotective. This allows confidence that IL-1Ra is able to confer its protective actions both peripherally and centrally. After experimental SAH, we suggest that haem, a breakdown product of haemoglobin, released from lysed red blood cells in the subarachnoid space, acts as a danger associated molecular pattern (DAMP) driving IL-1- dependent inflammation. These data provide new insights into inflammation after SAH-induced brain injury and suggest IL-1Ra as a candidate treatment for the disease. Overall, these findings strengthen preclinical data supporting IL-1Ra as a neuroprotective therapy for ischaemic stroke, and identify SAH as a new indication for treatment with IL-1Ra.

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21

Critchley, Giles Roderic. "Cerebral ischaemia following subarachnoid haemorrhage : a laboratory and clinical investigation of the cerebral microcirculation." Thesis, St George's, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268382.

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22

Pell, Gabriel Simon. "Perfusion and diffusion magnetic resonance imaging studies of cerebral ischaemia." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313382.

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23

Neuhaus, Ain. "The effects of cerebral ischaemia on pericytes and neurovascular function." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:836ac5ca-3f05-4a40-a19c-aec4f9c257af.

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Acute ischaemic stroke is a major cause of morbidity and mortality in the developed world, yet the treatment options available are limited to therapies that restore vessel patency. Recanalisation of the occluded artery does not necessarily result in reperfusion of the downstream microvasculature, however, and the pathomechanisms involved in this are incompletely understood. One putative mediator of this is the capillary pericyte, a vascular mural cell type that may constrict under ischaemic conditions. The overarching aim of this thesis was to characterise vascular function following cerebral ischaemia, using in vivo, ex vivo and in vitro approaches. First, I demonstrated that ischaemia reduced both ipsilateral and contralateral cerebral blood flow responses to hypercapnia, and diminished reactivity of isolated pressurised arteries. I then developed a novel assay to characterise human pericyte contractility in vitro, and demonstrated that they are responsive to vasoactive substances even in the absence of αSMA expression. In this assay, chemical ischaemia caused pericyte contraction and subsequent death, consistent with in vivo reports describing their role in the no-reflow phenomenon. Finally, I explored whether the voltage-gated Ca²⁺ channel antagonist nimodipine could improve reperfusion in cerebral ischaemia, and found that rats treated with nimodipine exhibited improved post-ischaemic cerebral blood flow and ameliorated neurological impairment. However, I did not find a direct effect of nimodipine on pericyte contractility during chemical ischaemia in vitro, indicating that nimodipine may be targeting other cell types in the vasculature. Together, these data highlight the importance of vascular function following stroke and shed light on putative vasculoprotective approaches, which have translational potential to improve reperfusion in patients receiving recanalisation therapy.

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24

Aspey, Benjamin Stephen. "Cerebral artheroembolism : an experimental study to determine the mechanism of cerebral vascular occlusion and ischaemia." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46653.

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25

Jones, Paul A. "Modulation of kainate-induced excitotoxicity in rats." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244361.

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26

Murdoch, Iain. "Presynaptic pathology after acute brain injury." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340811.

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27

Shrewsbury-Gee, Joanne. "An investigation of compounds of potential value in experimental cerebral ischaemia." Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329110.

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28

Lythgoe, Mark Francis. "Studies of experimental cerebral ischaemia using magnetic resonance imaging and autoradiography." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300464.

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29

Gill, Ramanjit. "Neuroprotective studies of excitatory amino acid antagonists in focal cerebral ischaemia." Thesis, Royal Veterinary College (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522532.

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30

McCracken, Eileen. "White matter damage after acute brain injury." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340812.

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31

Ben-Yoseph, O. "Multinuclear magnetic resonance spectroscopy studies of perturbed cerebral metabolism in vitro." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240078.

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32

Chrysanthou, Elvina. "The lectin pathway of complement activation in cerebral ischaemia and reperfusion injury." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28171.

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The complement system constitutes a critical component of the innate immune response. The lectin pathway is one of the three activation pathways of the complement activation cascade that can recognise and respond to structures on oxygen deprived cells and contribute to ischaemia and reperfusion injury (IRI). Cerebral IRI mediated inflammation is known to be responsible for secondary damage in the penumbra region surrounding the initial area of infarct and the prevention of IRI-mediated secondary damage provides an attractive target for therapeutic intervention. Mannose binding lectin associated serine protease 2 (MASP-2) is the key effector enzyme of the lectin pathway, since depletion of this enzyme completely ablates lectin pathway function or activity. This study assessed the impact of MASP-2 deficiency on cerebral IRI and to what extent MASP-2 targeting can reduce the secondary inflammatory damage following an ischaemic insult. The 3 vessel occlusion (3-VO) model of stroke was found to be the most appropriate model to use in this study, as it was shown to have a lower degree of variability than the middle cerebral artery occlusion (MCAO) stroke model. TTC staining revealed that MASP-2 -/- mice were significantly protected from cerebral damage, showing statistically significant smaller infarct sizes when compared to age and sex matched wild type controls. MASP-2 deficient mice showed reduced C3 deposition and a lower degree of astrocytic activation in brain sections from mice undergoing 3-VO and showed higher mRNA abundance of anti-inflammatory mediators (such as IL-10) and lower abundance of pro-inflammatory mediators (such as MIP-2) when compared to wild type control mice. Subsequently, a recombinant inhibitory anti-MASP-2 antibody, AbD04211, a murine specific MASP-2 inhibitor, was assessed for the therapeutic utility of MASP-2 inhibition in the 3-VO cerebral IRI model of stroke. The results revealed that the use of MASP-2 inhibitors at a dose of 5mg/kg of body weight achieved a statistically significant protective effect, with infarct sizes reduced by up to 30% in the anti-MASP-2 treated animals.

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33

McColl, Barry. "Pathophysiology of cerebral ischaemia : effects of APOE genotype on outcome and endocytosis." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4324/.

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Apolipoprotein E (apoE denotes protein: APOE denotes gene) is a lipid-transport protein abundantly expressed in the brain and strongly upregulated after acute brain injury. The APOE e4 allele is the major genetic risk factor for Alzheimer’s disease (AD) and has been associated with poorer outcome after various types of acute brain injury, including traumatic brain injury and subarachnoid haemorrhage. However, the role of APOE genotype in focal ischaemic stroke is less clear. The mechanism(s) by which APOE genotype may modulate outcome after acute brain injury are also unclear at present. Accordingly, the studies described in this thesis were undertaken to further address these issues. 1. Endocytic pathway alterations in human temporal lobe after global cerebral ischaemia and association with APOE genotype. 2. Characterisation and validation of the intraluminal filament model of focal cerebral ischaemia in C57BI/6J mice. 3. Association between APOE genotype and differences in outcome and endocytic pathway alterations after focal cerebral ischaemia in mice. 4. Adenovirus-mediated gene transfer of APOE e3 markedly reduces ischaemic brain damage after focal cerebral ischaemia in mice. The data presented in this thesis indicate an important role for APOE genotype in modulating outcome after ischaemic brain injury, further highlighting the favourable effects associated with the APOE e3 allele. APOE genotype-dependent alterations in the endocytic pathway are mechanisms which could contribute to differences in outcome. These data also highlight the neuroprotective effects achieved by manipulating apoE levels to promote the beneficial effects of apoE3. An apoE-based therapeutic strategy may be a potential approach for treatment of ischaemic brain injury in humans.

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Smith, Sharon Lesley. "Production of markers of neurological damage induced by cerebral ischaemia or neurotoxins." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359770.

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35

Gregory, Lloyd James. "Monitoring the neuropathogenic processes following global cerebral ischaemia using magnetic resonance imaging." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325067.

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36

Nelson, Rachael Mary. "Cellular effects of cerebral ischaemia in vitro : cerebroprotective actions of GABAmimetic agents." Thesis, De Montfort University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393498.

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37

Mullins, Paul Gerald Mark. "Magnetic resonance imaging in the study of animal models of cerebral ischaemia /." [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16186.pdf.

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38

Marquardt, Lars. "Large artery disease in patients with cerebral ischaemia : frequency, investigation and management." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:70b598c5-97ca-4567-ac32-ed5092972a16.

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Stroke is the third leading cause of death in the developed world and is the leading neurological cause of disability with a massive impact on personal life and society. Large artery atherosclerosis is one of the main causes of ischaemic stroke. However, in several aspects of this condition there is still a significant amount of uncertainty about its prevalence, appropriate investigation and possible treatment. Reliable data on epidemiology are therefore necessary to provide clinicians and researchers with crucial information to guide diagnostic and therapeutic management as well as further research. With this thesis I aimed to provide useful information about the prevalence of large artery disease in certain groups of patients, and to contribute to investigation- and managementstrategies using data from a large population based study, the Oxford Vascular Study (OXVASC). OXVASC is a prospective, population-based incidence study of vascular disease in Oxfordshire, UK, which started in 2002 and is ongoing. The study population comprises all 91,106 individuals registered with nine general practices and uses multiple methods of case ascertainment to identify all patients with vascular events. Firstly, I have shown that the prevalence of ≥50% vertebral or basilar artery stenosis in posterior circulation TIA or minor stroke is more than twice as high as the prevalence of ≥50% carotid stenosis in patients with carotid territory events, and is associated with a very high early risk of stroke of 22% and TIA of 46%. Furthermore, severe vertebral and/or basilar artery stenosis is associated with multiple TIAs at first presentation. Secondly, I have shown that early risk of stroke was higher after posterior circulation TIA, with a 1-year risk of 16%, than after carotid territory TIA, with a 1-year risk of 9%. In addition, I was able to show for the first time, that the ABCD2 score was predictive of early stroke not only in patients with carotid circulation TIA but also in patients with vertebrobasilar TIA. Thirdly, in a pilot feasibility study about arterial spin labelling magnetic resonance imaging in patients with large artery disease in the vertebrobasilar circulation I have shown that patients with severe large artery disease have significantly impaired occipital brain perfusion. My results suggest that this new technique might be a useful tool to identify suitable patients for interventional treatment of vertebrobasilar large artery disease. Fourthly, I was able to show that the risk of ipsilateral stroke and TIA in patients with an asymptomatic carotid stenosis is very low with contemporary best medical treatment alone, suggesting that routine carotid endarterectomy for asymptomatic carotid stenosis might not longer be feasible. Finally, I have clarified that lower rates of intervention for moderate to severe symptomatic carotid stenosis in women than in men can be explained by sex-differences in the populationbased incidence of carotid large artery disease and not due to under-investigation or reluctance amongst women to undergo investigation or treatment.

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39

Price, Christopher John Simon. "Patterns of inflammation and their role in the pathophysiology of cerebral ischaemia." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612974.

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40

Smart, Sean Christopher. "NMR examinations of control and ischemic rodent brain tissue." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309450.

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41

McKittrick, Craig Martin. "The role of mast cells in a mouse model of focal cerebral ischaemia." Thesis, University of Strathclyde, 2013. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=22406.

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Treatments for ischaemic stroke are limited and have low efficacy despite many years of promising research uncovering many potential therapeutic targets. As a result, stroke ranks as the third leading cause of death and the leading cause of disability worldwide. Mast cells have been identified as contributors to ischaemic stroke pathology, and are therefore a novel candidate for targeted stroke therapy. Indeed, genetic mast cell deficiency prior to onset of transient middle cerebral artery occlusion (tMCAo) in rats resulted in a significant reduction in blood brain barrier (BBB) permeability, oedema and neutrophil recruitment. Therefore the hypothesis of this thesis was that mast cells are active in the acute phase of experimental focal cerebral ischaemia, and interact with the brain to potentiate ischaemic pathology by release of a plethora of pro-inflammatory, vasoactive and proteolytic mediators. These mediators could degrade the BBB leading to vasogenic oedema, and may also prom ote an inflammatory milieu within the brain. Using wild type C57BL6/J (WT) and, mast cell deficient, C57BL6/J Kit w-sh/w-sh (Kit) mice in the tMCAo model of focal cerebral ischaemia, we found a significant reduction of BBB permeability, oedema and neutrophil recruitment. Additionally, sodium cromoglycate (SCG) treatment prior to tMCAo had the added effect of reducing lesion volume in WT mice. Seventy two hours post-tMCAo, genetic mast cell deficiency did not result in reduction of any of the parameters analysed. Investigation of protein expression in brain homogenates, twenty minutes and forty-five minutes post-tMCAo, indicated that tumour necrosis factor-alpha (TNF-α) was not responsible for the pathology seen in the WT mice, as it was found at similar concentrations in both mouse strains. However, endothelin-1, endoglin and matrixmetaloproteinase-9 were highly expressed in the WT mice, but not in the Kit mice forty five minutes post tMCAo. Further studies are required to elucidate whether the absence of these mediators is responsible for the reduced pathology in the Kit mice. In conclusion, the present study has provided an insight into mast cell responses following tMCAo, and has highlighted potential mechanisms by which mast cells mediate their response.

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42

Thomas, David Lee. "Magnetic resonance imaging of diffusion and perfusion : techniques and applications to cerebral ischaemia." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391829.

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43

Henshall, David C. "The development of a novel model of focal cerebral ischaemia using endothelin isopeptides." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21300.

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Several animal models of focal cerebral ischaemia have been developed to gain insight into the pathophysiology and possible therapeutic treatment of stroke. This thesis aimed to optimise & characterise a model of focal cerebral ischaemia that utilises perivascular microinjection of endothelin-1 (ET-1) to occlude the middle cerebral artery (MCA) of the rat, and to develop a novel model of endothelin-induced MCA occlusion with controlled reperfusion. The MCA of the anaesthetised rat was occluded by the intracerebral microinjection of ET-1 into the outer layers of cortex adjacent to the MCA. Elistopathological analysis of ischaemic brain damage three days following injection, determined that ET-1 produced a large volume of ischaemic brain damage confined to the vascular territory of the MCA within the dose range 33-300 pmols, whilst a 10 pmol injection was ineffective. The optimal injection volume was found to be in the range 1-3pi. The isopeptide ET-3 was found to be equipotent with ET-1 in the ischaemic insult it produced, having the same minimal effective dose, and being effective over the same dose range. This is the first demonstration that ET-3 is capable of producing ischaemic damage by constricting a major cerebral artery. The equipotency of ET-1 and ET-3 in terms of histopathological outcome in this experimental model of stroke, was supported by laser Doppler flowmetry (LDF) recordings of perfusion velocity from the parietal cortex, in which the severity and duration of ischaemia was found to be the same between isopeptides. These isopeptides are only equipotent at the ET0 receptor, however, ETB receptor involvement was excluded by the ineffectiveness of the selective ETB receptor agonists BQ3020 and IRL1620 in producing MCA occlusion. Furthermore, whilst intracerebral injection of the specific ETA receptor antagonist FR139317 (3 nmols in 3 pi) 10 minutes before ET-3, blocked MCA occlusion, this dose of FR13 9317 was ineffective against ET-1 -induced MCA occlusion. This suggests the involvement of an atypical receptor in the contractile response of the rat MCA to endothelin isopeptdies. Intracerebral probes determined that striatal temperature remained unchanged following ET-1-induced MCA occlusion. By contrast, striatal oxygen tension, measured by intracerebral oxygen electrodes, and cortical tissue perfusion velocity, measured by laser Doppler flowmetry (LDF) fell rapidly following ET-1 injection. Oxygen tension did not recover for 3 hours following ET-1 injection, whilst the LDF signal showed some recovery but still remained below 50% of baseline levels after 2 hours. [l4C]iodoantipyrine autoradiography determined that local cerebral blood flow (CBF) was profoundly reduced throughout much of the vascular territory of the MCA three hours after injection of ET-1. This pathophysiological profile suggests that ET-1-induced MCA occlusion represents a model of permanent focal cerebral ischaemia in which reperfusion is limited. A 17mer sequence of the secreted form of (β-amyloid precusor protein (βAPP), which has previously been shown to possess trophic and neuroprotective properties, was evaluated using this experimental model of stroke. The 17mer peptide was found to confer neuroprotection to both cortex and striatum, when delivered intracerebroventricularly for three days before inducing ET-1-induced MCA occlusion. However, the 17mer peptide did not improve functional recovery following ET-1-induced MCA occlusion as assessed by a model of skilled motor control.

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Tseng, Ming-Yuan. "Maintenance of cerebral autoregulation and enhancement of blood flow as a therapeutic strategy against cerebral ischaemia following aneurysmal subarachnoid haemorrhage." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612923.

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45

Johnston, Andrew. "An investigation of free radical involvement in cell death in a cell culture model of ischaemia." Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343128.

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46

Sutherland, Brad Alexander, and n/a. "Heme oxygenase and the use of tin protoporphyrin in hypoxia-ischaemia-induced brain damage : mechanisms of action." University of Otago. Department of Pharmacology & Toxicology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090119.150318.

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Stroke is the third largest cause of death, and the leading cause of disability worldwide. Treatments are sought to reduce mortality, and increase survival time following an ischaemic stroke. Hypoxia-ischaemia (HI) is the combination of cerebral ischaemia and global hypoxia that can lead to neuronal damage, particularly perinatally. The complex neurodegenerative cascade following ischaemic stroke and HI activates many stress pathways, including heme oxygenase (HO). HO metabolises free heme to release iron, carbon monoxide, and biliverdin, which is subsequently metabolised to bilirubin. This thesis aims to elucidate the role HO plays following HI, and assess any neuroprotective mechanisms using HO modulators. The 26 day old rat model of HI was used to induce the neurodegenerative cascade. All animals were sacrificed 3 days post-insult. Immunohistochemistry and Western blotting demonstrated that HO-1 was increased in the ipsilateral hemisphere of both HI (by 1.7 � 0.1 fold: p = 0.016, n = 4) and middle cerebral artery occlusion (MCAO) brains (by 1.6 � 0.1 fold: p = 0.037, n = 4), compared to controls. HO-2 was constitutively expressed throughout the control brain, but HI upregulated HO-2 expression (by 1.7 � 0.2 fold: p = 0.027, n = 4) ipsilaterally, whereas MCAO did not alter HO-2 expression. Administration of the HO inhibitor tin protoporphyrin (SnPP; 30[mu]mol/kg intraperitoneally) daily, beginning 1 day prior to HI until sacrifice, reduced infarct volume to 50% � 10 of saline-treated animals (p = 0.039, n = 6-8). The HO inducer ferriprotoporphyrin (FePP; 30[mu]mol/kg) had no effect on infarct volume. HO activity and protein expression were not significantly altered following treatment with SnPP. Therefore, the neuroprotective actions of SnPP may be through alternative mechanisms. SnPP treatment increased HI + saline-induced total nitric oxide synthase (NOS) activity by 1.5 � 0.06 fold (p < 0.001, n = 6-8). Conversely, SnPP inhibited both inducible NOS (50% � 7 of HI + saline; p = 0.045, n = 7-8) and cyclooxygenase (COX) activity (32% � 6 of HI + saline; p = 0.049, n = 4-8). SnPP treatment also increased mitochondrial complex I activity by 1.6 � 0.25 fold (p = 0.04, n = 4-8) and complex V activity by 1.7 � 0.26 fold (p = 0.046, n = 4-8) in the ipsilateral hemisphere. It appears that SnPP is acting on inflammatory and mitochondrial enzymes to produce neuroprotection. In vitro analysis of cultured RAW264.7 macrophages exposed to lipopolysaccharide (LPS; 10[mu]g/mL) treated with SnPP (dose range: 10⁻�⁰M - 10⁻⁵M) did not alter nitrite levels or cell viability. However, high dose SnPP (10⁻⁵M) in the absence of LPS increased nitrite levels from control cells by 2.7 � 0.7 fold (p = 0.043, n = 6), complementing the in vivo total NOS data. Other mechanisms such as NMDA receptor activation were not affected by 100[mu]M SnPP or 100[mu]M SnCl₂ in patch clamped cortical pyramidal neurons. Overall, the role that HO plays following HI remains unclear, but this thesis provides definitive evidence that SnPP (an established HO inhibitor) provides neuroprotection. This neuroprotection may be due to its effects on inducible pathways such as NOS and COX. Therefore, further experimentation is required to fully elucidate the role that HO plays following cerebral ischaemia, and additional in vivo evidence will be necessary to establish HO inhibitors as a putative candidate for cerebral ischaemia neuroprotection.

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47

Kenny, Barry. "Differentiation between calcium antagonists in vitro and their effects in models of cerebral ischaemia." Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33589.

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Different classes of calcium antagonist were defined in vitro using radioligand binding studies and the efficacy of the classes as neuroprotective agents was assessed in vivo using a novel model of cerebral ischaemia. Radioligand binding studies indicated that the interactions of both class I (dihydropyridines) and class II (verapamil and diltiazem) calcium antagonists was temperature-, ligand- and tissue-dependent. Specific binding sites for class III antagonists (flunarizine, fluspirilene, etc.), labelled by [3H] fluspirilene in skeletal muscle, were not identified in brain membranes, although these compounds allosterically regulated [3H] dihydropyridine binding in brain. All class III compounds displayed high affinity for the [3H] fluspirilene site in skeletal muscle membranes and thus fluspirilene appeared to be prototypical of this class of compound. The calcium antagonist SR 33557 identified a novel high affinity binding site in brain membranes. This putatative fourth site for a calcium antagonist appeared to be tightly coupled to the dihydropyridine site. Class III calcium antagonists displayed a range of affinities for other receptor and ion channel sites but all class III calcium antagonists showed high affinity for rat brain sodium channels labelled by [3H] batrachotoxinin-A-20-a-benzoate. In the Mongolian gerbil, forebrain ischaemia (10 min but not 5 min) with 7 days recovery produced a significant reduction in the number of [3H] PN 200-110 binding sites in hippocampal membranes. However, an w3 ligand, [3H] PK 11195 was shown to be a better marker of ischaemic damage. Binding experiments and autoradiographic analysis demonstrated a significant ischaemia-induced increase in the density of w3 sites after 5 min forebrain ischaemia and 7 days recovery in the gerbil. The distribution and pharmacology of w3 sites was very species dependent. [3H] PK 11195 was successfully used to establish a model of focal ischaemia in the mouse, in which a variety of class III calcium antagonists were found to be neuroprotective. The anticonvulsant phenytoin was active in the mouse focal ischaemia model and in an in vitro model of ischaemia (using the rat hippocampal slice). The interaction of calcium antagonists with both Na+ and Ca2+ channels is proposed to be important as a mechanism whereby these agents confer neuroprotection.

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48

Clarkson, Andrew N., and n/a. "Lasting neuroprotection with clomethiazole following hypoxia-ischaemia-induced neurodegeneration : a mechanistic study." University of Otago. Department of Pharmacology & Toxicology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070424.120005.

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Subsequent to an hypoxic-ischaemic (HI)-insult a multi-faceted complex cascade of events occurs that ultimately results in cellular and neurological impairments within cortical and sub-cortical central nervous system (CNS) regions. In the present studies a modified �Levine� rat-pup model of HI (left carotid artery ligation + 1 hour global hypoxia on post-natal day (PND) 26) was employed to assess the neuroprotective properties of clomethiazole (CMZ; a γ-aminobutyric acid (GABA)A receptor agonist). In this study, histological and electrophysiological paradigms were used to assess the long-term neuroprotective properties of CMZ (414mg/kg/day via mini-pumps). Key enzymes involved in inflammation, namely nitric oxide synthase (NOS) and arginase, were also examined to assess other potential CMZ mechanisms. Assessments were carried out 3- and 90-days post-HI, with extensive ipsilateral CNS lesions evident at a gross histological level, at both the early and long-term stages, with CMZ significantly decreasing the lesion size at 3- and 90-days (P<0.01; P<0.05). Evoked field potential analyses were used to assess hippocampal CA1 neuronal activity ex vivo. Electrophysiological measurements contralateral to the occlusion revealed impaired neuronal function following HI relative to short- and long-term controls (P<0.001, 3- and 14-days; P<0.01, 90-days), with CMZ providing near complete protection (P<0.001 at 3- and 14-days; P<0.01 at 90-days). Both inducible NOS (iNOS) and arginase activities were significantly increased at 3-days (P<0.01), with arginase activity remaining elevated at 90-days post-HI (P<0.05) ipsilaterally. CMZ suppressed the HI-induced increase in iNOS and arginase activities (P<0.001; P<0.05). These data provide evidence of long-term functional neuroprotection afforded by CMZ in a model of HI-induced neurodegeneration. In addition, under conditions of HI, functional deficits were not restricted to the ipsilateral hemisphere and were due, at least in part, to changes in the activity of NOS and arginase. Underlying mitochondrial dysfunction is eminently present in many neuropathological conditions. The full extent of mitochondrial dysfunction in cortical, hippocampal and cerebellar tissues was assessed following HI. Assessment of mitochondrial FAD-linked respiration at both 1- and 3-days post-HI revealed a significant decrease in activity from ipsilateral cortical and hippocampal regions (P<0.001). In addition, significant changes in respiratory function were also evident in contralateral regions and cerebellum, 3-days post-HI (P<0.05). Assessment of the mitochondrial electron transport chain (complexes I-V) and mitochondrial markers of integrity (citrate synthase) and oxidative stress (aconitase) confirmed ipsilateral mitochondrial impairment following HI. Complexes I, II-III, V and citrate synthase were also impaired, in contralateral regions and cerebellum, 3-days post-HI. CMZ treatment provided significant protection to all mitochondrial aspects of neuronal tissue assessed. This study provides evidence of the full extent of mitochondrial damage following an HI-insult and may contribute, in part, to the impairment seen contralaterally. In addition, protection afforded by CMZ extends to preservation of mitochondrial function and integrity. Cerebral ischaemia-induced angiogenesis has been shown within and around infarcted regions and may contribute to a more favourable neurological outcome. The level of angiogenesis was examined using platelet endothelial cell adhesion molecule-1 (PECAM-1 / CD31). CD31 immunolabelling 7-days post-HI revealed a significant increase in angiogenesis compared with non-intervention controls (P<0.001). Treatment with CMZ decreased the level of angiogenesis compared to HI + saline (P<0.001) back to non-intervention control levels. Conversely, N[omega]-nitro-L-arginine methyl ester (L-NAME) treatment (5mg/kg/day) exacerbated the ischaemic lesion (P<0.001) and resulted in a marked decrease in angiogenesis compared to non-intervention controls (P<0.001). The extent of cerebral infarction in these studies is dependent on the level of NOS activity with CMZ increasing total NOS levels compared to HI + saline, while L-NAME halted the HI-induce increase in total NOS activity (P<0.001). These results show for the first time, that angiogenesis may be used as an assessment of neurodegeneration / neuroprotection in pathologies of cerebral ischaemia and are directly correlated with changes in NOS activity. These studies have therefore shown that following HI, damage also occurs contralateral to the occlusion, and is not restricted to the ipsilateral hemisphere. In addition, the neuroprotective effects of CMZ have been shown to extend out to 90-days post-HI, whereby significant protection to CA1 neuronal activity was seen. These studies also provide in vivo evidence that CMZ may also afford neuroprotection via anti-inflammatory pathways, as evidenced by a decrease in iNOS and arginase activities. Furthermore, these studies have also show evidence that angiogenesis (CD31) can be used as a diagnostic tool to assess neuroprotection / neurodegeneration.

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Gordon, Kirsty. "Investigation of the effects of oestrogen in rodent models of cerebral ischaemia and brain injury." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433066.

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50

Ekelund, Anders. "Detection and haemodilutive treatment of cerebral arterial vasospasm and delayed ischaemia after aneurysmal subarachnoid haemorrhage." Lund : Lund University, 1999. http://catalog.hathitrust.org/api/volumes/oclc/68945106.html.

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