Journal articles: '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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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 reperfusion. Male Wistar rats were subjected to remote middle cerebral artery occlusion, where a long filament was advanced intraluminally through a guide cannula in the common carotid artery. Transcallosal stimulation evoked increases in blood flow, tissue oxygenation and neuronal activity, which were diminished by middle cerebral artery occlusion and partially restored during reperfusion. These evoked responses were not affected by administration of the thrombolytic alteplase at clinically used doses. Evoked cerebral blood flow responses were fully restored at 24 h post–middle cerebral artery occlusion indicating that neurovascular dysfunction was not sustained. These data show for the first time that the rat remote middle cerebral artery occlusion model coupled with transcallosal stimulation provides a novel method for continuous assessment of hyperacute neurovascular coupling changes during ischaemia and reperfusion, and offers unique insight into hyperacute ischaemic pathophysiology.

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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 was 1.58 ± 0.09 ml 100 g−1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 ± 0.24 ml 100 g−1) with a decrease during the period of hypoperfusion (1.33 ± 0.03 ml 100 g−1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability–surface area product at this time may be due to variations in surface area and not necessarily permeability.

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Schwaninger, M., I. Inta, and O. Herrmann. "NF-κB signalling in cerebral ischaemia." Biochemical Society Transactions 34, no. 6 (October 25, 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 factor κB) through the upstream kinase IKK [IκB (inhibitory κB) kinase]. In vivo, IKK is activated in neurons. Neuron-specific deletion of the subunit IKK2 or inhibition of IKK activity reduced the infarct size and neuronal cell loss. A pharmacological inhibitor of IKK also showed neuroprotective properties. IKK-dependent ischaemic brain damage is likely to be mediated by NF-κB, because neuron-specific inhibition of NF-κB through transgenic expression of the NF-κB superrepressor was found to reduce the infarct size. In summary, there is evidence that IKK/NF-κB signalling contributes to ischaemic brain damage and may provide suitable drug targets for the treatment of stroke.

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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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&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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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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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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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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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: Department of Radiology, CombinedMilitary Hospital Lahore, using Colour and Power Doppler Ultrasound machine ALOKA SSD-5500. Period: 14 October 2006 to 15 March 2007. Methodology: Total of 50 diagnosed patientsof either gender, aged 30 to 70 years with cerebral ischaemia and stroke were included in thestudy. Carotid Doppler examination was conducted in each patient and findings were recorded.Results: Among 50 patients who underwent carotid Doppler examination for diagnosis ofclinically significant carotid artery stenosis, 35 patients had carotid plaques. 08 patients werediagnosed to have more than 70 % stenosis, 07 patients with more than 50 % and 20 patientsless than 50 % carotid artery stenosis. 15 patients did not show any carotid artery disease.12 patients had bilateral stenosis while 23 had unilateral disease. Mean age of the patientswith and without carotid artery disease was 52 ± 7.87 years. Conclusion: Majority of patientswith Cerebral ischemia/stroke showed carotid artery stenosis on colour Doppler ultrasound.Common age group who developed cerebral ischemia/stroke was above 50years.

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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 volume and did not significantly affect heart rate, blood pressure, or body temperature. rhIL-1ra administered 30 min before, or at the time of ischaemia significantly reduced infarct volume in cortex (55 and 60%, respectively) and striatum (52 and 41%, respectively). rhIL-1ra administered 30 min after ischaemia significantly reduced total and cortical infarct volume (26 and 29%, respectively), but did not significantly protect striatal tissue. The effects of rhIL-1ra were still evident in both cortex and striatum 7 days after ischaemia. These results support the role of IL-1 in ischaemic brain damage, revealing potent, sustained, neuroprotective effects of rhIL-1ra in the cortex and striatum, which cannot be attributed directly to changes in physiological parameters.

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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 stroke fulfilled the inclusion criteria. Meta-analyses demonstrated that angiopoietin-1 upregulation significantly reduced cerebral infarction size (standardised mean difference: –3.02; 95% confidence intervals: –4.41, –1.63; p < 0.001; n = 171 animals) and improved blood–brain barrier integrity (standardized mean difference: –2.02; 95% confidence intervals: –3.27, –0.77; p = 0.002; n = 129 animals). Subgroup analyses demonstrated that angiopoietin-1 upregulation improved outcomes in models of transient, not permanent cerebral ischaemia. Six studies assessed the effect of angiopoietin-1 upregulation on neurological function; however, inter-study heterogeneity prevented meta-analysis. In conclusion, published rodent data suggest that angiopoietin-1 upregulation improves outcome following temporary cerebral ischaemia by reducing cerebral infarction size and improving blood–brain barrier integrity. Additional research is required to examine the effect of angiopoietin-1 upregulation on neurological function during stroke recovery and investigate the benefit and risks in patients.

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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 factor-κB (NF-κB) pathway from 6 hours to day 7. HSYA was injected intraperitoneally at a dose of 6 mg/kg per day, which activated TLR9 in microglia of ischaemic cortex at 6 hours after reperfusion and then obviously suppressed the NF-κB pathway from day 1 to day 7. Meanwhile, HSYA also activated the anti-inflammatory pathway through interferon regulatory factor 3 from day 1 to day 3. The anti-inflammatory effect of HSYA was partially reversed by TLR9-siRNA interference in primary microglia, which was stimulated by oxygen-glucose deprivation and reoxygenation treatment. The regulation of TLR9-mediated inflammation by HSYA was consistent with the recovery of neurological deficits in rats. Conclusion: Therefore, our findings support that HSYA exerts anti-inflammatory effects by reprogramming the TLR9 signalling pathway during treatment of acute cerebral ischaemia and reperfusion injury.

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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 the vessel occlusion. The blood-brain barrier (BBB) alterations were coincident with the onset of ischaemia—induced seizures that were accompanied by sudden “spikes” of systemic blood pressure. Epilepsy may play an important role in the development of BBB damage in this ischaemic model, and this factor must be considered in the interpretation of BBB damage data in gerbils.

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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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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 dizziness, fainting and walking instability, suddenly arising a few days prior to admission. Two years before, the left ICA reconstruction was done for kinking, after which there was no cerebral ischaemia symptoms. Symptoms have been present perpetually, enhanced when resting and with head movement. CT angiography (MSCT) showed haemodynamic significant right ICA kinking. The left ICA postoperative finding was regular. Computerized tomography (CT) of the endocranium was done and no novel lessions were verified than those seen two years earlier. Resection, shortening and reimplantation of the right ICA were performed. A few hours following surgical reconstruction, there was no cerebral ischaemia symptoms, neither when resting nor with head movement. On the third postoperative day, the patient was discharged for home treatment. Conclusion. Surgical repair for symptomatic ICA kinking contributes to cerebral ischaemia symptoms reduction, improves cerebral perfusion and significantly prevents carotid thrombosis and stroke. In this paper, we have seen that in case of acute cerebral ischaemia symptoms and ICA kinking, surgical ICA treatment appears to be justified.

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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 after middle cerebral artery occlusion. Genetic deletion and pharmacological inhibition of A-FABP alleviated cerebral ischaemia injury with reduced infarction volume, cerebral oedema, neurological deficits, and neuronal apoptosis; BBB disruption was attenuated and accompanied by reduced degradation of tight junction proteins and induction of matrix metalloproteinases-9 (MMP-9). In patients with acute IS, elevated circulating A-FABP levels positively correlated with those of MMP-9 and cerebral infarct volume. Mechanistically, ischaemia-induced elevation of A-FABP selectively in peripheral blood monocyte-derived macrophages and cerebral resident microglia promoted MMP-9 transactivation by potentiating JNK/c-Jun signalling, enhancing degradation of tight junction proteins and BBB leakage. The detrimental effects of A-FABP were prevented by pharmacological inhibition of MMP-9. Conclusion A-FABP is a key mediator of cerebral ischaemia injury promoting MMP-9-mediated BBB disruption. Inhibition of A-FABP is a potential strategy to improve IS outcome.

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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 improvements in vessel narrowing has failed to show improved functional outcomes. This has encouraged researchers to investigate other potential causes of delayed cerebral ischaemia, such as early brain injury, microthrombosis, and cortical spreading depolarisation. Adherence to a common definition of delayed cerebral ischaemia is needed in order to allow easier assessment of studies using multiple different terms. Furthermore, improved recognition of delayed cerebral ischaemia would not only allow for faster treatment but also better assessment of interventions. Finally, understanding nimodipine’s mechanism of action may allow us to develop similar agents with improved efficacy.

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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 resulted in excellent improvement of both his dysphasia and weakness from the left cerebral ischaemic stroke and reperfusion of the ischaemic bowel, without surgical intervention.

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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 treatment. In addition, brain regional ischaemic neuron loss was investigated by using immunofluorescent staining of neuronal nuclei (NeuN) and caspase-8/-9-dependent cell apoptosis was also examined by western blot analysis.ResultsBICAO-induced cerebral ischaemia resulted in decreased sucrose preference and increased immobility times, which were representative depressive-like behaviours of mice until 30 days after BICAO treatment compared with Sham-operated mice. This outcome was associated with significant neuron loss by using immunofluorescent staining and increased cleavage levels of pro-caspase-3/-8/-9, but not pro-caspase-12, by western blot analysis in hypothalamus, midbrain, prefrontal cortex and hippocampus of mice.ConclusionsThis study showed that BICAO-induced ischaemia caused depressive-like behaviours and caspase-8/-9-dependent neural cell apoptosis in several brain regions, including hypothalamus and midbrain of mice.

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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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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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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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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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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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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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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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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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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). Intravenous administration of PD156707 (3 μmol/kg bolus + 5 μmol/kg/h infusion) attenuated the vasoconstriction elicited by perivascular ET-1 (10 n M) in normal pial arterioles (ET-1 vasoconstriction: −37 ± 13% from preinjection baseline; after intravenous PD156707: 6 ± 10% from preinjection baseline). In the focal ischaemia studies, cerebral perfusion was measured in the suprasylvian and ectosylvian gyri (by laser Doppler flowmetry). Occlusion of the middle cerebral artery reduced cerebral perfusion in the suprasylvian and ectosylvian gyri by ∼50%. Intravenous administration of PD156707 (3 μmol/kg bolus + 5 μmol/kg/h infusion), initiated 30 min after middle cerebral artery occlusion, effected a progressive increase in cerebral perfusion up to preocclusion baseline levels, whereas cerebral perfusion in vehicle-treated animals did not vary from its postocclusion level. In these animals, the intravenous administration of PD156707 reduced the hemispheric volume of ischaemic damage by 45% (vehicle: 2,376 ± 1,107 mm3; PD156707: 1,307 ± 548 mm3; p < 0.05). Our investigations indicate that endothelin receptor antagonism may be a new therapeutic strategy for the amelioration of focal ischaemic damage.

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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 acute ischaemic stroke. Although there are no previous descriptions of its successful treatment with hyperbaric oxygen therapy following mechanical thrombectomy, this is likely to become more common as mechanical thrombectomy is increasingly used worldwide to treat acute ischaemic stroke.

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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 – 60 min, calcium balance was restored to the original pre-ischaemic level. It is postulated that (i) large increases in [Ca2+]i in cerebral neurones during ischaemia are related to the high density of pathways on neurones that allow calcium entry; (ii) differences in the amount of calcium accumulated during periods of oxygen deprivation between neurones of the CA1 and CA3 regions are linked to the level of glutamatergic input (and hence excitatory synapses) that the two areas receive; (iii) restitution of blood flow and consequent rapid restoration of ATP synthesis permit reactivation of calcium-eliminating mechanisms. These latter involve especially sequestration by the mitochondria and extrusion by the plasma membrane Ca pump, which restore the low cytoplasmic [Ca2+].Key words: brain ischemia, calcium homeostasis, microelectrodes.

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48

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 cerebral computed tomography imaging during extracorporeal membrane oxygenation, with no clinical evidence of cerebral pathology prior to cannulation. Cerebral complications were grouped by aetiology and the territories of the brain’s supplying arteries. Results: One hundred eighty-seven adult patients with a total of 190 veno-arterial extracorporeal membrane oxygenation treatments were included. A total of 16.3% (n = 31) had evidence of either cerebral ischaemia (11.1%) or haemorrhage (5.8%); one patient suffered from both. Cerebral computed tomography scans were performed early in median on the first day after extracorporeal membrane oxygenation cannulation; in-hospital mortality of intra-cranial ischaemia and haemorrhage was 71.4% and 45.5%, respectively. Associated with an increased risk for ischaemic lesions were cannulation of the ascending aorta, higher age, presence of an autoimmune disease and cardiac surgery prior to veno-arterial extracorporeal membrane oxygenation. An association with haemorrhagic lesions was found for a lower blood PaCO2 at 2 hours, lower blood flow through the extracorporeal membrane oxygenation device at 2 hours, higher international normalized ratio and constantly higher activated partial thromboplastin time values as well as higher mean arterial pressures until haemorrhagic lesions were evident. Conclusion: Cerebral complications are frequent in patients on veno-arterial extracorporeal membrane oxygenation and may be clinically silent events. Careful monitoring with routine neuroimaging seems to be the most appropriate diagnostic approach at present. Intra-cranial ischaemia occurs more frequent than haemorrhage and is associated with cannulation of the aorta ascendens.

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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 using a macroscopic haemorrhage score and haemoglobin spectrophotometry. Post-ischaemic blood-brain-barrier (BBB) damage was assessed using Evans blue. To increase the validity of findings, the duration of anticoagulation was prolonged in mice (5 x DE over 2 days), and the effect of DE after thrombolysis was also examined in thromboembolic MCAO in rats. Pretreatment with warfarin resulted in significantly more secondary haemorrhage (mean haemorrhage score 2.6 ± 0.2) compared to non-anticoagulated animals (1.7 ± 0.3) and DE (9 mg/kg, 1.6 ± 0.3) in 2 h ischaemia. Also after a 3 h period of ischaemia, haemorrhage was more severe in animals anticoagulated with warfarin compared to 9 mg/kg DE and non-anticoagulated control. Prolonged or enteral dabigatran pretreatment led to identical results. Also, thrombolysis after thromboembolic MCAO in rats did not induce more severe bleeding in DE-treated animals. Mice pretreated with warfarin had higher BBB permeability and increased activation of matrix-metalloproteinase 9. In conclusion, DE does not increase the risk of secondary haemorrhage after thrombolysis in various rodent models of ischaemia and reperfusion. The implications of this finding for stroke patients have to be determined in the clinical setting.

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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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Journal articles on the topic 'Cerebral ischaemia'

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