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Artigos de revistas sobre o tema "Global cerebral ischaemia"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 3 de fevereiro de 2022

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1

Kolvenbach, R., C. Figge, E. Godehardt e W. Sandmann. "Adenosine agonists and global cerebral ischaemia [letter]". British Journal of Clinical Pharmacology 36, n.º 2 (agosto de 1993): 134–35. http://dx.doi.org/10.1111/j.1365-2125.1993.tb04210.x.

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2

Picozzi, Piero, Nicholas V. Todd e 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, n.º 1 (março de 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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3

Spencer, Sarah J., Roland N. Auer e Quentin J. Pittman. "Rat Neonatal Immune Challenge Alters Adult Responses to Cerebral Ischaemia". Journal of Cerebral Blood Flow & Metabolism 26, n.º 4 (10 de agosto de 2005): 456–67. http://dx.doi.org/10.1038/sj.jcbfm.9600206.

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Infection, inflammation, and hyperthermia associated with cerebral ischaemia are known to contribute to enhanced neuronal cell loss and more severe behavioural deficits. Because neonatal exposure to an immune challenge has been shown to alter the severity of inflammatory and febrile responses to a further immune challenge experienced in adulthood, we hypothesised that this could also alter temperature responses and neuronal survival after ischaemia. Thus, male Sprague–Dawley rats were treated at postnatal day 14 with a single injection of the bacterial endotoxin lipopolysaccharide (LPS) and were examined as adults for temperature changes, behavioural deficits, and neuronal cell loss associated with global cerebral ischaemia after a two-vessel occlusion (2 VO). Neonatally LPS-treated rats showed behavioural differences in a novel object exploration paradigm, as well as altered temperature responses to the 2 VO compared with neonatally salinetreated controls. Interestingly, these neonatally LPS-treated rats also showed increased cell loss in the central nucleus of the amygdala, a region that is important in the processing of emotional responses, but that is not usually examined in animal models of cerebral ischaemia. No differences were seen in the CA1, CA3, or dentate gyrus regions of the hippocampus. This work shows the importance of examining brain regions other than the hippocampus in association with global ischaemia. We also highlight the importance of the early period of development in programming an animal's ability to deal with injury such as cerebral ischaemia in adulthood.

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4

O'Neill, Michael J., Caroline A. Hicks, Mark A. Ward, Geraldine P. Cardwell, Jean-Michel Reymann, Hervé Allain e Daniele Bentué-Ferrer. "Dopamine D2 receptor agonists protect against ischaemia-induced hippocampal neurodegeneration in global cerebral ischaemia". European Journal of Pharmacology 352, n.º 1 (julho de 1998): 37–46. http://dx.doi.org/10.1016/s0014-2999(98)00333-1.

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5

Abels, C., F. Röhrich, S. Corvin, R. Meyermann, A. Baethmann e L. Schürer. "Leukocyte-Endothelium-Interaction in Pial Vessels Following Global, Cerebral Ischaemia". Acta Neurochirurgica 142, n.º 3 (15 de março de 2000): 333–39. http://dx.doi.org/10.1007/s007010050043.

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6

Hodges, Helen, Alan Nelson, David Virley, Timothy R. Kershaw e John D. Sinden. "Cognitive Deficits Induced by Global Cerebral Ischaemia: Prospects for Transplant Therapy". Pharmacology Biochemistry and Behavior 56, n.º 4 (abril de 1997): 763–80. http://dx.doi.org/10.1016/s0091-3057(96)00424-8.

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7

Kil, H. Y., W. Sl Oh e T. H. Han. "Fentanyl alters cytokine level during global cerebral ischaemia/reperfusion in rats". European Journal of Anaesthesiology 17, Supplement 19 (2000): 90. http://dx.doi.org/10.1097/00003643-200000002-00291.

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8

Davidson, Joanne O., Caroline A. Yuill, Guido Wassink, Laura Bennet e Alistair J. Gunn. "Spontaneous Pre-Existing Hypoxia Does Not Affect Brain Damage after Global Cerebral Ischaemia in Late-Gestation Fetal Sheep". Developmental Neuroscience 37, n.º 1 (14 de novembro de 2014): 56–65. http://dx.doi.org/10.1159/000368306.

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There is considerable evidence that a mild, non-injurious insult can protect (precondition) against a subsequent injurious insult. Typically, protection is seen when the gap between insults is several days to a week. However, the effect of mild but persistent hypoxia is unknown. In this study we examined the hypothesis that mild pre-existing hypoxia (PaO2 <17 mm Hg) would reduce neural injury in chronically instrumented late-gestation (0.85 gestation) fetal sheep exposed to 30 min of global cerebral ischaemia induced by bilateral carotid artery occlusion (normoxia: n = 9 vs. pre-existing hypoxia: n = 9) or normoxia plus sham ischaemia (sham controls: n = 9). Histopathology was assessed after 7 days of recovery. Fetuses with pre-existing hypoxia had lower PaO2 values (16.1 ± 0.6 vs. 26.0 ± 1.1 mm Hg) and were lighter at post-mortem (4,033 ± 412 vs. 5,261 ± 238 g) compared to normoxic fetuses. Cerebral ischaemia was associated with secondary cortical oedema and seizures, reduced final EEG power, loss of sleep state cycling, and significant loss of neurons and oligodendrocytes, with no significant effect of pre-existing hypoxia. Pre-existing hypoxia was associated with a significantly attenuated rise in mean arterial pressure between 18 and 36 h and slower resolution of cortical oedema between 96 and 150 h after ischaemia. These data suggest that chronic hypoxia is not associated with a significant preconditioning effect.

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9

Von Lubitz, Dag K. J. E., R. C. S. Lin, Robert J. McKenzie, Thomas M. Devlin e R. Tyler McCabe. "A novel treatment of global cerebral ischaemia with a glycine partial agonist". European Journal of Pharmacology 219, n.º 1 (agosto de 1992): 153–58. http://dx.doi.org/10.1016/0014-2999(92)90594-t.

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10

Endo, H., A. Saito e P. H. Chan. "Mitochondrial translocation of p53 underlies the selective death of hippocampal CA1 neurons after global cerebral ischaemia". Biochemical Society Transactions 34, n.º 6 (25 de outubro de 2006): 1283–86. http://dx.doi.org/10.1042/bst0341283.

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p53, a tumour suppressor, is involved in DNA repair and cell death processes and mediates apoptosis in response to death stimuli by transcriptional activation of pro-apoptotic genes and by transcription-independent mechanisms. In the latter process, p53 induces permeabilization of the outer mitochondrial membrane by forming an inhibitory complex with a protective Bcl-2 family protein, resulting in cytochrome c release in several cell line systems. However, it is unclear how the mitochondrial p53 pathway mediates neuronal apoptosis after cerebral ischaemia. We examined interaction between the mitochondrial p53 pathway and vulnerable hippocampal CA1 neurons using a tGCI (transient global cerebral ischaemia) rat model. We showed mitochondrial translocation of p53 and its binding to Bcl-XL. Mitochondrial p53 translocation, interaction between p53 and Bcl-XL, and cytochrome c release from mitochondria and subsequent CA1 neuronal death were prevented by pifithrin-α, a p53-specific inhibitor. These results suggest that the mitochondrial p53 pathway plays a role in delayed CA1 neuronal death after tGCI.

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11

Hicks, Caroline A., Mark A. Ward, Nella Ragumoorthy, Samantha J. Ambler, Colin P. Dell, David Dobson e Michael J. O'Neill. "Evaluation of glycine site antagonists of the NMDA receptor in global cerebral ischaemia". Brain Research 819, n.º 1-2 (fevereiro de 1999): 65–74. http://dx.doi.org/10.1016/s0006-8993(98)01329-8.

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12

Frick, Tamara, Dirk Springe, Denis Grandgirard, Stephen L. Leib e Matthias Haenggi. "An improved simple rat model for global cerebral ischaemia by induced cardiac arrest". Neurological Research 38, n.º 4 (2 de abril de 2016): 373–80. http://dx.doi.org/10.1179/1743132815y.0000000090.

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13

O'Neill, Michael J., Ann Bond, Paul L. Ornstein, Mark A. Ward, Caroline A. Hicks, Ken Hoo, David Bleakman e David Lodge. "Decahydroisoquinolines: novel competitive AMPA/kainate antagonists with neuroprotective effects in global cerebral ischaemia". Neuropharmacology 37, n.º 10-11 (outubro de 1998): 1211–22. http://dx.doi.org/10.1016/s0028-3908(98)00134-8.

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14

Grewal, Amarjot Kaur, Amteshwar Singh Jaggi, Avtar Chand Rana e Nirmal Singh. "Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice". Korean Journal of Physiology & Pharmacology 17, n.º 6 (2013): 485. http://dx.doi.org/10.4196/kjpp.2013.17.6.485.

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15

Smith, Stuart E., Delphine Lekieffre, Peter Sowinski e Brian S. Meldrum. "Cerebroprotective effect of BW619C89 after focal or global cerebral ischaemia in the rat". NeuroReport 4, n.º 12 (setembro de 1993): 1339–42. http://dx.doi.org/10.1097/00001756-199309150-00013.

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16

Pratt, Jeremy, Jean Rataud, Florence Bardot, Michel Roux, Jean-Charles Blanchard, Pierre M. Laduron e Jean-Marie Stutzmann. "Neuroprotective actions of riluzole in rodent models of global and focal cerebral ischaemia". Neuroscience Letters 140, n.º 2 (junho de 1992): 225–30. http://dx.doi.org/10.1016/0304-3940(92)90108-j.

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17

O'Neill, Michael J., Caroline Hicks e Mark Ward. "Neuroprotective effects of 7-nitroindazole in the gerbil model of global cerebral ischaemia". European Journal of Pharmacology 310, n.º 2-3 (agosto de 1996): 115–22. http://dx.doi.org/10.1016/0014-2999(96)00387-1.

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18

O' Neill, Michael J., Caroline Hicks, Mark Ward e Jill A. Panetta. "Neuroprotective effects of the antioxidant LY231617 and NO synthase inhibitors in global cerebral ischaemia". Brain Research 760, n.º 1-2 (junho de 1997): 170–78. http://dx.doi.org/10.1016/s0006-8993(97)00293-x.

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19

Tanabe, M. "Hippocampal ischaemia in a patient who experienced transient global amnesia after undergoing cerebral angiography". Neurocase 6, n.º 3 (1 de junho de 2000): 227. http://dx.doi.org/10.1093/neucas/6.3.227.

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20

Kettunen, M. I., R. A. Kauppinen e O. H. J. Gröhn. "Dispersion of cerebral on-resonanceT 1 in the rotating frame (T 1ρ) in global ischaemia". Applied Magnetic Resonance 29, n.º 1 (março de 2005): 89–106. http://dx.doi.org/10.1007/bf03166957.

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21

Nunn, Julia, e Helen Hodges. "Cognitive deficits induced by global cerebral ischaemia: Relationship to brain damage and reversal by transplants". Behavioural Brain Research 65, n.º 1 (novembro de 1994): 1–31. http://dx.doi.org/10.1016/0166-4328(94)90069-8.

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22

Holder, D. S. "Effects of urethane, alphaxolone/alphadolone, or halothane with or without neuromuscular blockade on survival during repeated episodes of global cerebral ischaemia in the rat". Laboratory Animals 26, n.º 2 (1 de abril de 1992): 107–13. http://dx.doi.org/10.1258/002367792780745814.

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The effect of 4 anaesthetic regimes on blood pressure and survival was investigated during repeated episodes of cerebral ischaemia in the rat induced by diathermy of the vertebral arteries and reversible occlusion of the carotid arteries. The best results were obtained with inspired halothane with neuromuscular blockade and artificial ventilation, followed in order by halothane, intravenous alphaxolone/alphadolone, and intraperitoneal urethane with spontaneous ventilation.

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23

Spray, S., S. E. Johansson, A. Radziwon-Balicka, K. A. Haanes, K. Warfvinge, G. K. Povlsen, P. A. T. Kelly e L. Edvinsson. "Enhanced contractility of intraparenchymal arterioles after global cerebral ischaemia in rat - new insights into the development of delayed cerebral hypoperfusion". Acta Physiologica 220, n.º 4 (29 de janeiro de 2017): 417–31. http://dx.doi.org/10.1111/apha.12834.

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24

O'Neill, Michael J., Catherine P. Bath, Colin P. Dell, Caroline A. Hicks, Jeremy Gilmore, Samantha J. Ambler, Mark A. Ward e David Bleakman. "Effects of Ca2+ and Na+ channel inhibitors in vitro and in global cerebral ischaemia in vivo". European Journal of Pharmacology 332, n.º 2 (agosto de 1997): 121–31. http://dx.doi.org/10.1016/s0014-2999(97)01074-1.

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25

O'Neill, Michael J., Liesbeth Bogaert, Caroline A. Hicks, Ann Bond, Mark A. Ward, Guy Ebinger, Paul L. Ornstein, Yvette Michotte e David Lodge. "LY377770, a novel iGlu5 kainate receptor antagonist with neuroprotective effects in global and focal cerebral ischaemia". Neuropharmacology 39, n.º 9 (agosto de 2000): 1575–88. http://dx.doi.org/10.1016/s0028-3908(99)00250-6.

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26

Aggarwal, Raman, Bikash Medhi, Ashis Pathak, Veena Dhawan e Amitava Chakrabarti. "Neuroprotective effect of progesterone on acute phase changes induced by partial global cerebral ischaemia in mice". Journal of Pharmacy and Pharmacology 60, n.º 6 (junho de 2008): 731–37. http://dx.doi.org/10.1211/jpp.60.6.0008.

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27

Lee, Jung-Hyun, e Seong-Ryong Lee. "The Effect of Baicalein on Hippocampal Neuronal Damage and Metalloproteinase Activity Following Transient Global Cerebral Ischaemia". Phytotherapy Research 26, n.º 11 (17 de fevereiro de 2012): 1614–19. http://dx.doi.org/10.1002/ptr.4644.

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28

Holder, D. S. "Electrical impedance tomography with cortical or scalp electrodes during global cerebral ischaemia in the anaesthetised rat". Clinical Physics and Physiological Measurement 13, n.º 1 (fevereiro de 1992): 87–98. http://dx.doi.org/10.1088/0143-0815/13/1/008.

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29

Endo, H., A. Saito e P. H. Chan. "Mitochondrial translocation of p53 underlies the selective death of hippocampal CA1 neurons after global cerebral ischaemia". Biochemical Society Transactions 35, n.º 6 (23 de novembro de 2007): 1649. http://dx.doi.org/10.1042/bst0351649.

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30

Lenglet, Sébastien, Fabrizio Montecucco, François Mach, Karl Schaller, Yvan Gasche e Jean-Christophe Copin. "Analysis of the expression of nine secreted matrix metalloproteinases and their endogenous inhibitors in the brain of mice subjected to ischaemic stroke". Thrombosis and Haemostasis 112, n.º 08 (2014): 363–78. http://dx.doi.org/10.1160/th14-01-0007.

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SummaryMatrix metalloproteinases (MMPs) are a family of more than twenty secreted and cell-surface endopeptidases. Among them, MMP2, MMP3 and MMP9 are involved in blood-brain barrier injury and neuronal death after cerebral ischaemia. On the other hand, very little is known about the expression of the other secreted MMPs. Herein, we compared the global changes in MMP1, MMP2, MMP3, MMP7, MMP8, MMP9, MMP10, MMP12 and MMP13, and their endogenous inhibitors TIMP1 and TIMP2, both at the mRNA and protein levels, during the hyperacute (6 h), acute (24 h) and subacute (72 h) stages following transient focal cerebral ischaemia and treatment with recombinant tissue plasminogen activator (rtPA). We observed a significant increase in MMP1, MMP2, MMP9, MMP10, MMP13 and TIMP1 levels during the acute stage of reperfusion, which was further amplified during the subacute stage for MMP1, MMP2, MMP10 and TIMP1. In general, no change of MMP3, MMP7, MMP8, MMP12 and TIMP2 was observed. However, rtPA treatment induced a rapid increase in MMP1/TIMP2, MMP2/TIMP2, MMP8/TIMP2 and MMP9/TIMP2 ratios during the hyperacute stage of reperfusion compared to saline treatment, which may have potential implications in the early disruption of the blood-brain barrier after rtPA treatment.

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31

Mathews, Kusum S., Christopher C. Toner, Daniel P. McLaughlin e Jonathan A. Stamford. "Comparison of ketamine stereoisomers on tissue metabolic activity in an in vitro model of global cerebral ischaemia". Neurochemistry International 38, n.º 5 (abril de 2001): 367–72. http://dx.doi.org/10.1016/s0197-0186(00)00125-x.

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32

Seo, J. H., H. P. Park, Y. T. Jeon, Y. J. Lim, K. Nam e J. W. Hwang. "Combined treatment with celecoxib and sevoflurane after global cerebral ischaemia has no additive neuroprotective effects in rats". British Journal of Anaesthesia 110, n.º 6 (junho de 2013): 988–95. http://dx.doi.org/10.1093/bja/aet009.

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33

Ivanov, Alexander Vladimirovich, Valery Vasil’evich Alexandrin, Alexander Alexandrovich Paltsyn, Ksenya Alexandrovna Nikiforova, Edward Danielevich Virus, Boris Petrovich Luzyanin, Marina Yurievna Maksimova, Mikhail Aleksanrovich Piradov e Aslan Amirkhanovich Kubatiev. "Plasma low-molecular-weight thiol/disulphide homeostasis as an early indicator of global and focal cerebral ischaemia". Redox Report 22, n.º 6 (8 de abril de 2017): 460–66. http://dx.doi.org/10.1080/13510002.2017.1311464.

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34

Molnár, A. H., C. Varga, A. Berkó, I. Rojik, A. Párducz, F. László e F. A. László. "Inhibitory effect of vasopressin receptor antagonist OPC-31260 on experimental brain oedema induced by global cerebral ischaemia". Acta Neurochirurgica 150, n.º 3 (20 de fevereiro de 2008): 265–71. http://dx.doi.org/10.1007/s00701-007-1400-1.

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35

Bath, Catherine P., Louise N. Farrell, Jeremy Gilmore, Mark A. Ward, Caroline A. Hicks, Michael J. O'Neill e David Bleakman. "The effects of ifenprodil and eliprodil on voltage-dependent Ca2+ channels and in gerbil global cerebral ischaemia". European Journal of Pharmacology 299, n.º 1-3 (março de 1996): 103–12. http://dx.doi.org/10.1016/0014-2999(95)00846-2.

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36

Allen, Bradley S., Yoshihiro Ko, Gerald D. Buckberg e Zhong Tan. "Studies of isolated global brain ischaemia: III. Influence of pulsatile flow during cerebral perfusion and its link to consistent full neurological recovery with controlled reperfusion following 30 min of global brain ischaemia". European Journal of Cardio-Thoracic Surgery 41, n.º 5 (20 de março de 2012): 1155–63. http://dx.doi.org/10.1093/ejcts/ezr318.

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37

Weiser, Thomas, Marion Wienrich, Michael Brenner, René Kubiak, Gerhard Weckesser e Rainer Palluk. "The AMPA receptor/Na+ channel blocker BIIR 561 CL is protective in a model of global cerebral ischaemia". European Journal of Pharmacology 421, n.º 3 (junho de 2001): 165–70. http://dx.doi.org/10.1016/s0014-2999(01)01031-7.

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38

O'Neill, Michael, Maeve Caldwell, Bernadette Earley, Mark Canney, Ambrose O'Halloran, John Kelly, B. E. Leonard e J. L. Junien. "The σ receptor ligand JO 1784 (igmesine hydrochloride) is neuroprotective in the gerbil model of global cerebral ischaemia". European Journal of Pharmacology 283, n.º 1-3 (setembro de 1995): 217–25. http://dx.doi.org/10.1016/0014-2999(95)00356-p.

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39

Torregrosa, Germán, María D. Barberá, José M. Centeno, Marta Ortí, Juan B. Salom, Teresa Jover e Enrique Alborch. "Characterization of the cortical laser-Doppler flow and hippocampal degenerative patterns after global cerebral ischaemia in the goat". Pfl�gers Archiv European Journal of Physiology 435, n.º 5 (2 de março de 1998): 662–69. http://dx.doi.org/10.1007/s004240050567.

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40

Wassink, Guido, Joanne O. Davidson, Mhoyra Fraser, Caroline A. Yuill, Laura Bennet e Alistair J. Gunn. "Non‐additive effects of adjunct erythropoietin therapy with therapeutic hypothermia after global cerebral ischaemia in near‐term fetal sheep". Journal of Physiology 598, n.º 5 (11 de fevereiro de 2020): 999–1015. http://dx.doi.org/10.1113/jp279131.

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41

Horsburgh, Karen, James McCulloch, Margaret Nilsen, Allen D. Roses e James A. R. Nicoll. "Increased neuronal damage and apoE immunoreactivity in human apolipoprotein E, E4 isoform-specific, transgenic mice after global cerebral ischaemia". European Journal of Neuroscience 12, n.º 12 (dezembro de 2000): 4309–17. http://dx.doi.org/10.1046/j.1460-9568.2000.01339.x.

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42

Kurihara, Junichi, Nobuhiko Ochiai e Hitoshi Kato. "Protection by nicorandil against the dysfunction of the central vagal baroreflex system following transient global cerebral ischaemia in dogs". British Journal of Pharmacology 109, n.º 4 (agosto de 1993): 1263–67. http://dx.doi.org/10.1111/j.1476-5381.1993.tb13758.x.

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43

Dirnagl, Ulrich, Peter Thorén, Arno Villringe, Gabriele Sixt, Andreas Them e Karl M. Einhäupl. "Global forebrain ischaemia in the rat: Controlled reduction of cerebral blood flow by hypobaric hypotension and two-vessel occlusion". Neurological Research 15, n.º 2 (abril de 1993): 128–30. http://dx.doi.org/10.1080/01616412.1993.11740122.

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44

Horsburgh, Karen, James McCulloch, Margaret Nilsen, Allen D. Roses e James A. R. Nicoll. "Increased neuronal damage and apoE immunoreactivity in human apolipoprotein E, E4 isoform-specific, transgenic mice after global cerebral ischaemia". European Journal of Neuroscience 12, n.º 12 (dezembro de 2000): 4309–17. http://dx.doi.org/10.1111/j.1460-9568.2000.01339.x.

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45

Christensen, Thomas, Torben Bruhn, Torben Balchen e Nils H. Diemer. "Evidence for formation of hydroxyl radicals during reperfusion after global cerebral ischaemia in rats using salicylate trapping and microdialysis". Neurobiology of Disease 1, n.º 3 (dezembro de 1994): 131–38. http://dx.doi.org/10.1006/nbdi.1994.0016.

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46

O’Neill, Michael J., Tracey K. Murray, Deborah R. McCarty, Caroline A. Hicks, Colin P. Dell, Kelly E. Patrick, Mark A. Ward et al. "ARL 17477, a selective nitric oxide synthase inhibitor, with neuroprotective effects in animal models of global and focal cerebral ischaemia". Brain Research 871, n.º 2 (julho de 2000): 234–44. http://dx.doi.org/10.1016/s0006-8993(00)02471-9.

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47

Padosch, S. A., E. Popp, P. Teschendorf, J. J. Krumnikl, P. Vogel, J. Motsch, E. Martin e B. W. Böttiger. "Improved outcome after global cerebral ischaemia due to cardiocirculatory arrest in transgenic rats expressing baculovirus broad spectrum caspase inhibitor p35". European Journal of Anaesthesiology 19, n.º 3 (março de 2002): 215. http://dx.doi.org/10.1097/00003643-200203000-00025.

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