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Journal articles on the topic 'Cerebral ischaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

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 d

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2

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

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3

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

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4

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 art

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5

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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6

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 an

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7

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

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8

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. Immunoh

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9

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

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10

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 rat

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11

Sutherland, Brad A., Jonas C. Fordsmann, Chris Martin, Ain A. Neuhaus, Brent M. Witgen, Henning Piilgaard, Micael Lønstrup, et al. "Multi-modal assessment of neurovascular coupling during cerebral ischaemia and reperfusion using remote middle cerebral artery occlusion." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (October 1, 2016): 2494–508. http://dx.doi.org/10.1177/0271678x16669512.

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Hyperacute changes in cerebral blood flow during cerebral ischaemia and reperfusion are important determinants of injury. Cerebral blood flow is regulated by neurovascular coupling, and disruption of neurovascular coupling contributes to brain plasticity and repair problems. However, it is unknown how neurovascular coupling is affected hyperacutely during cerebral ischaemia and reperfusion. We have developed a remote middle cerebral artery occlusion model in the rat, which enables multi-modal assessment of neurovascular coupling immediately prior to, during and immediately following reperfusio

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12

Todd, Nicholas V., Piero Picozzi, and H. Alan Crockard. "Quantitative Measurement of Cerebral Blood Flow and Cerebral Blood Volume after Cerebral Ischaemia." Journal of Cerebral Blood Flow & Metabolism 6, no. 3 (June 1986): 338–41. http://dx.doi.org/10.1038/jcbfm.1986.57.

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CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 ± 6 ml 100 g−1 min−1, which fell to 5.5 ± 0.5 ml 100 g−1 min−1 during ischaemia. There was a marked early postischaemic hyperaemia (262 ± 18 ml 100g−1 min−1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 ± 3 ml 100 g−1 min−1). Mean cortical dextran space

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13

Schwaninger, M., I. Inta та O. Herrmann. "NF-κB signalling in cerebral ischaemia". Biochemical Society Transactions 34, № 6 (25 жовтня 2006): 1291–94. http://dx.doi.org/10.1042/bst0341291.

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In acute stroke, neuronal apoptosis and inflammation are considered to be important mechanisms on the road to tissue loss and neurological deficit. Both apoptosis and inflammation depend on gene transcription. We have identified a signalling pathway that regulates transcription of genes involved in apoptosis and inflammation. In a mouse model of focal cerebral ischaemia, there is an induction of the cytokine TWEAK (tumour necrosis factor-like weak inducer of apoptosis) and its membrane receptor Fn14. TWEAK promotes neuronal cell death and activates the transcription factor NF-κB (nuclear facto

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14

Villacorta, J., F. Kerbaul, F. Collart, C. Guidon, M. Bonnet, J. C. Guillen, and F. Gouin. "Perioperative Cerebral Ischaemia in Cardiac Surgery and BIS." Anaesthesia and Intensive Care 33, no. 4 (August 2005): 514–17. http://dx.doi.org/10.1177/0310057x0503300415.

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A 46-year-old woman was monitored by bispectral index monitoring (BIS) during redo aortic and mitral valve replacement. On release of the aortic cross clamp there was a sudden, severe, unexplained, and sustained fall in the BIS value. Postoperatively, a CT scan was consistent with multiple ischaemic lesions. The lesions were presumed to be due to air embolism. This case suggests that a sudden unexplained and persistent fall in BIS may indicate cerebral ischaemia.

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15

&NA;. "Anticoagulants in cerebral ischaemia." Inpharma Weekly &NA;, no. 1122 (January 1998): 15. http://dx.doi.org/10.2165/00128413-199811220-00028.

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16

Elwood, P. C. "SMOKING AND CEREBRAL ISCHAEMIA." Lancet 334, no. 8668 (October 1989): 923. http://dx.doi.org/10.1016/s0140-6736(89)91589-4.

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17

Siesjö, Bo K. "Pathophysiology of cerebral ischaemia." European Journal of Anaesthesiology 17, Supplement 18 (2000): 6–7. http://dx.doi.org/10.1097/00003643-200000001-00005.

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18

Walker, Richard, and Mark Sair. "Coma and cerebral ischaemia." Anaesthesia & Intensive Care Medicine 8, no. 10 (October 2007): 403–4. http://dx.doi.org/10.1016/j.mpaic.2007.08.003.

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19

Khan, Sibghat Ullah, Naveed Aslam Lashari, Nadia Irum Lakho, Ambreen Faisal, and Aamir Hussain. "CEREBRAL ISCHAEMIA AND STROKE;." Professional Medical Journal 24, no. 12 (November 29, 2017): 1823–27. http://dx.doi.org/10.29309/tpmj/2017.24.12.564.

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Introduction: Colour Doppler sonography is a well-established widely available,noninvasive, cost effective and a reliable method for assessing cerebrovascular circulation.It has become a valuable completion of the sonographic workup in patients with cerebralischaemia and infarction. Its accuracy is close to angiography. Objectives: To determine thefrequency of significant carotid artery stenosis in patients of cerebral ischaemia/stroke and itscharacterized sonographic appearance of plaque. Study Design: Cross sectional study, basedon nonprobability convenience sample technique. Setting: Depart

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20

Loddick, Sarah A., and Nancy J. Rothwell. "Neuroprotective Effects of Human Recombinant Interleukin-1 Receptor Antagonist in Focal Cerebral Ischaemia in the Rat." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 932–40. http://dx.doi.org/10.1097/00004647-199609000-00017.

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Recombinant human interleukin-1 receptor antagonist (rhIL-1ra) markedly protects against focal cerebral ischaemia in the rat, implicating endogenous IL-1 in the events leading to cerebral infarction. The present experiments investigated the effect of intracerebroventricular (i.c.v.) administration of IL-1β or rhIL-1ra on ischaemia damage and physiological parameters after permanent middle cerebral artery occlusion in the rat. IL-1β (5 ng, i.c.v.) markedly (92%) enhanced infarct volume and caused a significant rise in body temperature, but rhIL-1ra (10 μg, i.c.v.) significantly reduced infarct

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21

Moxon, Joseph V., Alexandra F. Trollope, Brittany Dewdney, Catherine de Hollander, Domenico R. Nastasi, Jane M. Maguire, and Jonathan Golledge. "The effect of angiopoietin-1 upregulation on the outcome of acute ischaemic stroke in rodent models: A meta-analysis." Journal of Cerebral Blood Flow & Metabolism 39, no. 12 (October 4, 2019): 2343–54. http://dx.doi.org/10.1177/0271678x19876876.

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Clinical studies report that low circulating angiopoietin-1 concentration at presentation predicts worse outcomes after ischaemic stroke. Upregulating angiopoietin-1 may therefore have therapeutic benefit for ischaemic stroke. This systematic review assessed whether upregulating angiopoietin-1 improved outcomes in rodent models of ischaemic stroke. Random-effects models quantified the effect of angiopoietin-1 upregulation on stroke severity in terms of the size of cerebral infarction and the extent of blood–brain barrier permeability. Eleven studies utilising rat and mouse models of ischaemic

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22

Gong, Zhe, Jingrui Pan, Xiangpen Li, Hongxuan Wang, Lei He, and Ying Peng. "Hydroxysafflor Yellow A Reprograms TLR9 Signalling Pathway in Ischaemic Cortex after Cerebral Ischaemia and Reperfusion." CNS & Neurological Disorders - Drug Targets 17, no. 5 (August 7, 2018): 370–82. http://dx.doi.org/10.2174/1871527317666180502110205.

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Background and Objective: Hydroxysafflor yellow A (HSYA) was reported to suppress inflammation in ischaemic microglia. However, the mechanism through which HSYA inhibits inflammation caused by cerebral ischaemia and reperfusion injury remains unknown. Here, we have mimicked acute cerebral ischaemia and reperfusion injury by subjecting male Sprague-Dawley rats to transient middle cerebral artery occlusion for 90 minutes and have demonstrated that toll-like receptor 9 (TLR9) was upregulated from day 3 after reperfusion, accompanied by the persistent activation of the pro-inflammatory nuclear fac

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23

Picozzi, Piero, Nicholas V. Todd, and H. Alan Crockard. "Regional Blood-Brain Barrier Permeability Changes after Restoration of Blood Flow in Postischemic Gerbil Brains: A Quantitative Study." Journal of Cerebral Blood Flow & Metabolism 5, no. 1 (March 1985): 10–16. http://dx.doi.org/10.1038/jcbfm.1985.2.

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A quantitative technique utilising [14C]α-aminoisobutyric acid as a tracer was used to study cerebrovascular permeability in 22 Mongolian gerbils. Seven other animals were used to measure cerebral blood volumes. Global cerebral ischaemia was produced by temporary bilateral carotid artery occlusion (60 min) in 16 gerbils that were sacrificed at 1, 2, and 3 h following reperfusion. The blood-to-brain transfer constant was significantly increased after 2 h of reperfusion in the ischaemic zones and also in structures, like the cerebellum, not supplied by the carotid artery and not ischaemic during

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24

Baker, A. B., and A. J. Roxburgh. "Computerised EEG Monitoring for Carotid Endarterectomy." Anaesthesia and Intensive Care 14, no. 1 (February 1986): 32–36. http://dx.doi.org/10.1177/0310057x8601400108.

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A prospective study was undertaken in twenty patients undergoing carotid endarterectomy using computerised EEG monitoring in the form of a density-modulated spectral array, spectral edge frequency and integrated EEG power for monitoring cerebral ischaemia. This form of monitoring proved to be easy to use and understand. Because ischaemic EEG events longer than one minute were not necessarily followed by postoperative deficits, the definition of significant events that would cause ischaemia may need to be modified.

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25

Ilic, Miodrag, Slobodan Tanaskovic, Nenad Ilijevski, and Djordje Radak. "Acute reversible ischaemic neurological deficit induced by internal carotid artery kinking: Case report." Srpski arhiv za celokupno lekarstvo 139, no. 1-2 (2011): 92–94. http://dx.doi.org/10.2298/sarh1102092i.

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Introduction. Internal carotid artery (ICA) kinking is a pathological malformation with angulation of the vessel?s axis of 90? or less. It is known that kinking causes the reduction of flow within the vessel that may be exacerbated by progressive head rotation up to the point that causes complete cessation of flow. In this article, we report on the case of acute reversible ischaemic deficit induced by internal carotid artery kinking and immediate neurological recovery following surgical reconstruction. Case Outline. A 64-year-old woman was admitted to Vascular Surgery Clinic due to severe dizz

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26

Liao, Boya, Leiluo Geng, Fang Zhang, Lingling Shu, Ling Wei, Patrick K. K. Yeung, Karen S. L. Lam, et al. "Adipocyte fatty acid-binding protein exacerbates cerebral ischaemia injury by disrupting the blood–brain barrier." European Heart Journal 41, no. 33 (April 29, 2020): 3169–80. http://dx.doi.org/10.1093/eurheartj/ehaa207.

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Abstract Aims Adipocyte fatty acid-binding protein (A-FABP) is an adipokine implicating in various metabolic diseases. Elevated circulating levels of A-FABP correlate positively with poor prognosis in ischaemic stroke (IS) patients. No information is available concerning the role of A-FABP in the pathogenesis of IS. Experiments were designed to determine whether or not A-FABP mediates blood–brain barrier (BBB) disruption, and if so, to explore the molecular mechanisms underlying this deleterious effects. Methods and results Circulating A-FABP and its cerebral expression were increased in mice

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27

Flynn, Liam, and Peter Andrews. "Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage." F1000Research 4 (November 2, 2015): 1200. http://dx.doi.org/10.12688/f1000research.6635.1.

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Delayed cerebral ischaemia has been described as the single most important cause of morbidity and mortality in patients who survive the initial aneurysmal subarachnoid haemorrhage. Our understanding of the pathophysiology of delayed cerebral ischaemia is meagre at best and the calcium channel blocker nimodipine remains the only intervention to consistently improve functional outcome after aneurysmal subarachnoid haemorrhage. There is substantial evidence to support cerebral vessel narrowing as a causative factor in delayed cerebral ischaemia, but contemporary research demonstrating improvement

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28

Chen, Lucia Y., Charlotte Ainscough, Mohamed Sayed, and Maneesh Bhargava. "Simultaneous treatment of ischaemic bowel and ischaemic stroke with intravenous thrombolysis therapy." BMJ Case Reports 11, no. 1 (November 2018): e227126. http://dx.doi.org/10.1136/bcr-2018-227126.

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Novel treatment of simultaneous mesenteric and cerebral ischaemia with systemic thrombolysis. A 75-year-old man presented to the acute stroke team with aphasia, right-sided weakness and distressed with a pain he was unable to localise. He was treated with intravenous thrombolysis with tissue plasminogen activator for a left middle cerebral artery stroke. Decompensation on the ward during thrombolysis with worsening abdominal distension and pain, hypotension and tachycardia prompted a CT angiogram scan, which displayed proximal inferior mesenteric artery occlusion. Thrombolysis treatment result

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29

Liu, Shuiqiao, Song Han, Qingqing Dai, Shujuan Li, and Junfa Li. "BICAO-induced ischaemia caused depressive-like behaviours and caspase-8/-9-dependent brain regional neural cell apoptosis in mice." Stroke and Vascular Neurology 3, no. 1 (December 17, 2017): 1–8. http://dx.doi.org/10.1136/svn-2017-000109.

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IntroductionCerebral ischaemia-induced depression is among the most frequent neuropsychiatric consequences and adversely impact the prognosis and recovery of patients. Although several brain regions have been implied in the development of ischaemia-induced depression, the brain region-specific neural cell apoptosis pathways have not been clarified yet.MethodsIn this study, bilateral internal carotid artery occlusion (BICAO) mouse model was established to induce cerebral ischaemia. Sucrose preference, tail suspension and forced swim tests were conducted on mice at 7, 21 and 30 days after BICAO

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30

Todd, N. V. "Reflow following experimental cerebral ischaemia." British Journal of Plastic Surgery 38, no. 3 (July 1985): 441. http://dx.doi.org/10.1016/0007-1226(85)90273-5.

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31

Moulin, Solène, and Didier Leys. "Management of acute cerebral ischaemia." La Presse Médicale 45, no. 12 (December 2016): e451-e455. http://dx.doi.org/10.1016/j.lpm.2016.10.008.

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32

Choi, Dennis. "Neuroprotective Agents and Cerebral Ischaemia." Trends in Neurosciences 21, no. 8 (August 1998): 363. http://dx.doi.org/10.1016/s0166-2236(98)01257-0.

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Minhas, P. S., D. K. Menon, N. J. Herrod, S. PMJ Downey, J. C. Clark, P. M. Kemp, I. V. Kendall, A. Datta, T. A. Carpenter, and J. D. Pickard. "CEREBRAL ISCHAEMIA ASSOCIATED WITH HYPERVENTILATION." Journal of Neurosurgical Anesthesiology 9, no. 4 (October 1997): 380. http://dx.doi.org/10.1097/00008506-199710000-00022.

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34

Smith, Maj-Lis. "Cerebral ischaemia and brain protection." Current Opinion in Anaesthesiology 5, no. 5 (October 1992): 626–31. http://dx.doi.org/10.1097/00001503-199210000-00003.

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35

Flynn, R. W. V., R. S. M. MacWalter, and A. S. F. Doney. "The cost of cerebral ischaemia." Neuropharmacology 55, no. 3 (September 2008): 250–56. http://dx.doi.org/10.1016/j.neuropharm.2008.05.031.

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36

Petty, M. A., and J. G. Wettstein. "Elements of cerebral microvascular ischaemia." Brain Research Reviews 36, no. 1 (August 2001): 23–34. http://dx.doi.org/10.1016/s0165-0173(01)00062-5.

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37

Andreasson, Katrin. "Prostaglandin signalling in cerebral ischaemia." British Journal of Pharmacology 160, no. 4 (March 2, 2010): 844–46. http://dx.doi.org/10.1111/j.1476-5381.2010.00715.x.

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38

Reid, John L., Deborah Dawson, and I. Mhairi Macrae. "Endothelin, Cerebral Ischaemia and Infarction." Clinical and Experimental Hypertension 17, no. 1-2 (January 1995): 399–407. http://dx.doi.org/10.3109/10641969509087080.

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39

Hommel, Marc, and Julien Bogousslavsky. "Thrombolytics in acute cerebral ischaemia." Expert Opinion on Investigational Drugs 3, no. 10 (October 1994): 1011–20. http://dx.doi.org/10.1517/13543784.3.10.1011.

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40

Marangos, Paul J., Catherine C. Turkel, Zofia E. Dziewanowska, and Anthony W. Fox. "Dichloroacetate and cerebral ischaemia therapeutics." Expert Opinion on Investigational Drugs 8, no. 4 (April 1999): 373–82. http://dx.doi.org/10.1517/13543784.8.4.373.

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41

Ahmed, Shahzada K., and Patrick L. Semple. "Cerebral ischaemia in pituitary apoplexy." Acta Neurochirurgica 150, no. 11 (October 29, 2008): 1193–96. http://dx.doi.org/10.1007/s00701-008-0130-3.

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42

Limburg, M. "Cerebral ischaemia — A neuroradiological study." Journal of the Neurological Sciences 78, no. 3 (May 1987): 361. http://dx.doi.org/10.1016/0022-510x(87)90051-7.

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43

Laufs, Ulrich, Uta C. Hoppe, Stephan Rosenkranz, Paulus Kirchhof, Michael Böhm, Hans-Christoph Diener, Matthias Endres, et al. "Cardiological evaluation after cerebral ischaemia." Clinical Research in Cardiology 99, no. 10 (August 3, 2010): 609–25. http://dx.doi.org/10.1007/s00392-010-0200-4.

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44

Pfurtscheller, G., L. Auer, and V. Köpruner. "Quantitative EEG in cerebral ischaemia." Electroencephalography and Clinical Neurophysiology 61, no. 3 (September 1985): S81. http://dx.doi.org/10.1016/0013-4694(85)90331-1.

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45

Patel, Toshal R., Samuel Galbraith, David I. Graham, Hussein Hallak, Annette M. Doherty, and James McCulloch. "Endothelin Receptor Antagonist Increases Cerebral Perfusion and Reduces Ischaemic Damage in Feline Focal Cerebral Ischaemia." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 950–58. http://dx.doi.org/10.1097/00004647-199609000-00019.

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These investigations characterised the cerebrovascular effects of an endothelin ETA-receptor antagonist PD156707 in normal and ischaemic cat brain. A dose of PD156707 that inhibited the effects of exogenous endothelin-1 was established in nonischaemic cerebral resistance arterioles. Perivascular microapplication of the endothelin–receptor antagonist PD156707 (0.03–3 μ M) had a minimal effect on nonischaemic pial resistance arterioles. The perivascular coapplication of PD156707 and ET-1 (10 n M) effected a dose-dependent attenuation of the ET-1 vasoconstrictive response (IC50 = 0.1 μ M). Intrav

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Segan, Louise, Fiona Permezel, Wei Ch’ng, Ian Millar, Mark Brooks, Matt Lee-Archer, and Geoffrey Cloud. "Cerebral arterial gas embolism from attempted mechanical thrombectomy: recovery following hyperbaric oxygen therapy." Practical Neurology 18, no. 2 (December 28, 2017): 134–36. http://dx.doi.org/10.1136/practneurol-2017-001828.

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Cerebral arterial gas embolism is a recognised complication of endovascular intervention with an estimated incidence of 0.08%. Its diagnosis is predominantly clinical, supported by neuroimaging. The treatment relies on alleviating mechanical obstruction and reversing the proinflammatory processes that contribute to tissue ischaemia. Hyperbaric oxygen therapy is an effective treatment and has multiple mechanisms to reverse the pathological processes involved in cerebral arterial gas embolism. Symptomatic cerebral arterial gas embolism is a rare complication of endovascular intervention for acut

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Erecińska, Maria, and Ian A. Silver. "Relationships between ions and energy metabolism: cerebral calcium movements during ischaemia and subsequent recovery." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S190—S193. http://dx.doi.org/10.1139/y92-262.

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Intra- and extra-cellular concentrations of calcium were measured in hippocampal neurones of areas CA1 and CA3 during 8 min ischaemia and short-term (up to 60 min) recovery. During an ischaemic insult, [Ca2+]i increased progressively and [Ca2+]e decreased. There were large interneuronal differences, although, in general, rises in [Ca2+]i were much larger in area CA1 than in CA3. Restitution of blood flow was followed by movements of calcium in the directions opposite to those seen during ischaemia: [Ca2+] in the extracellular space gradually rose whereas that inside neurones fell. Within 30 –

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Malfertheiner, Maximilian Valentin, Andrea Koch, Christoph Fisser, Jonathan Edward Millar, Lars Sigfried Maier, Florian Zeman, Florian Poschenrieder, Matthias Lubnow, Alois Philipp, and Thomas Müller. "Incidence of early intra-cranial bleeding and ischaemia in adult veno-arterial extracorporeal membrane oxygenation and extracorporeal cardiopulmonary resuscitation patients: a retrospective analysis of risk factors." Perfusion 35, no. 1_suppl (May 2020): 8–17. http://dx.doi.org/10.1177/0267659120907438.

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Background: Cerebral complications in veno-arterial extracorporeal membrane oxygenation are known to have a strong impact on mortality and morbidity. Aim of this study is to investigate the early incidence, risk factors and in-hospital mortality of intra-cranial ischaemia and haemorrhage in adults undergoing veno-arterial extracorporeal membrane oxygenation treatment. Methods: This study is a single-centre retrospective analysis on adult patients undergoing veno-arterial extracorporeal membrane oxygenation for different indications. The inclusion criterion included patients with early routine

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Ploen, Robert, Markus Zorn, Li Sun, Wei Zhou, and Roland Veltkamp. "Anticoagulation with dabigatran does not increase secondary intracerebral haemorrhage after thrombolysis in experimental cerebral ischaemia." Thrombosis and Haemostasis 110, no. 07 (2013): 153–61. http://dx.doi.org/10.1160/th12-12-0942.

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SummaryDabigatran etexilate (DE) has recently been introduced for stroke prevention in atrial fibrillation, but management of acute ischaemic stroke during therapy with DE is a challenge. Thrombolysis is contrain-dicated because of a presumed increased risk of intracerebral haemorrhagic complications. We studied in different ischaemia models whether DE increases secondary haemorrhage after thrombolysis. C57BL/6 mice were anticoagulated with high-dose DE or warfarin. After 2 hour (h) or 3 h transient filament MCAO, rt-PA was injected. At 24 h after MCAO, secondary haemorrhage was quantified usi

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Di Pasquale, G., G. Pinelli, P. Grazi, A. Andreoli, C. Corbelli, G. L. Manini, S. Urbinati, and G. C. Carini. "Incidence of silent myocardial ischaemia in patients with cerebral ischaemia." European Heart Journal 9, suppl N (December 2, 1988): 104–7. http://dx.doi.org/10.1093/eurheartj/9.suppl_n.104.

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