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Journal articles on the topic 'Global brain ischemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

WHITE, B., L. GROSSMAN, B. ONEIL, et al. "Global Brain Ischemia and Reperfusion." Annals of Emergency Medicine 27, no. 5 (1996): 588–94. http://dx.doi.org/10.1016/s0196-0644(96)70161-0.

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2

Littleton-Kearney, Marguerite T., Patricia D. Hurn, Thomas S. Kickler, and Richard J. Traystman. "Incomplete global cerebral ischemia alters platelet biology in neonatal and adult sheep." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (1998): H1293—H1300. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1293.

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Platelets are implicated as etiologic agents in cerebral ischemia and as modulators of neural injury following an ischemic insult. We examined the effects of severe, transient global ischemia on platelet aggregation during 45-min ischemia and 30-, 60-, and 120-min reperfusion in adult and neonatal lambs. We also examined postischemic platelet deposition in brain and other tissues (120-min reperfusion) using indium-111-labeled platelets. Ischemic cerebral blood flow fell to 5 ± 1 and 5 ± 2 ml ⋅ min−1⋅ 100 g−1in lambs and sheep, respectively. During ischemia, platelet counts fell to 47.5 ± 5.1%

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Li, Richard Changxun, Shang Zhi Guo, Seung Kwan Lee, and David Gozal. "Neuroglobin Protects Neurons against Oxidative Stress in Global Ischemia." Journal of Cerebral Blood Flow & Metabolism 30, no. 11 (2010): 1874–82. http://dx.doi.org/10.1038/jcbfm.2010.90.

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Neuroglobin (Ngb) is a recently discovered globin that affords protection against hypoxic/ischemic-induced cell injury in brain. Hypoxic/ischemic injury is associated with accumulation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS). In previous studies, we found that Ngb has antioxidative properties, and protects PC-12 cells against hypoxia- and β-amyloid-induced cell death. To further delineate the potential role of Ngb in protection against cerebral ischemia–reperfusion injury in vivo, we developed a transgenic mouse line that overexpresses Ngb. Hippocampal ischemia–

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Barone, F. C., M. Y. T. Globus, W. J. Price, et al. "Endothelin Levels Increase in Rat Focal and Global Ischemia." Journal of Cerebral Blood Flow & Metabolism 14, no. 2 (1994): 337–42. http://dx.doi.org/10.1038/jcbfm.1994.41.

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Endothelin-1, a peptide exhibiting extremely potent cerebral vasoactive properties, is elevated in the cerebrospinal fluid after hemorrhagic stroke and implicated in cerebral vasospasm. The purpose of this study was to determine changes in endothelin in ischemic rat brain by assaying endothelin tissue and extracellular levels. Immunoreactive endothelin levels in ischemic brain tissue following permanent or transient focal ischemia produced by middle cerebral artery occlusion was determined. In addition, endothelin levels were assayed in striatal extracellular fluid collected by microdialysis b

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Соколовская, А. А., Э. Д. Вирюс, В. В. Александрин, et al. "Platelets apoptosis in rats after global brain ischemia." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 1() (May 8, 2018): 27–35. http://dx.doi.org/10.25557/0031-2991.2018.01.27-35.

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Цель исследования. Ишемические повреждения головного мозга, являются одной из наиболее частой причин инвалидности и смертности во всем мире. Недавно была установлена роль апоптоза тромбоцитов в патофизиологии инсульта, однако его механизмы до сих пор остаются невыясненными. Несмотря на различные экспериментальные модели, направленные на мониторинг апоптоза тромбоцитов, результаты, относительно изучения и выявления апоптоза тромбоцитов при ишемии головного мозга у крыс, весьма немногочисленны. Цель исследования - анализ апоптоза тромбоцитов с помощью метода проточной цитофлуориметрии на модели

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Dietrich, W. Dalton, Raul Busto, Ofelia Alonso, Mordecai Y. T. Globus, and Myron D. Ginsberg. "Intraischemic but Not Postischemic Brain Hypothermia Protects Chronically following Global Forebrain Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 13, no. 4 (1993): 541–49. http://dx.doi.org/10.1038/jcbfm.1993.71.

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We investigated whether postischemic brain hypothermia (30°C) would permanently protect the hippocampus following global forebrain ischemia. Global ischemia was produced in anesthetized rats by bilateral carotid artery occlusion plus hypotension (50 mm Hg). In the postischemic hypothermic group, brain temperature was maintained at 37°C during the 10-min ischemic insult but reduced to 30°C starting 3 min into the recirculation period and maintained at 30°C for 3 h. In normothermic animals, intra- and postischemic brain temperature was maintained at 37°C. After recovery for 3 days, 7 days, or 2

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7

Lin, Baowan, Myron D. Ginsberg, Raul Busto, and Lin Li. "Hyperglycemic Transient Ischemia Induces Massive Neutrophil Deposition in Brain." Stroke 32, suppl_1 (2001): 353. http://dx.doi.org/10.1161/str.32.suppl_1.353-c.

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P80 Acute hyperglycemia worsens neurological signs and accentuates neuropathology after ischemia, but the mechanisms are poorly understood. In this study, we tested whether polymorphonuclear leukocytes (neutrophils) might be contributory. Anesthetized, physiologically monitored Wistar rats underwent global forebrain ischemia for 12.5 min by bilateral carotid artery occlusions plus hypotension (45 mm Hg). To induce hyperglycemia, rats received 2.5 ml of 25% dextrose i.p. 30 min prior to ischemia. Normoglycemic rats received saline. Plasma glucose levels were 340±66 and 133 ±21 mg/dl, respective

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8

Picone, Carmela M., James C. Grotta, Rosa Earls, Roger Strong, and John Dedman. "Immunohistochemical Determination of Calcium—Calmodulin Binding Predicts Neuronal Damage after Global Ischemia." Journal of Cerebral Blood Flow & Metabolism 9, no. 6 (1989): 805–11. http://dx.doi.org/10.1038/jcbfm.1989.114.

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Since ionic Ca2+ binds with intracellular calmodulin (CaM) before activating proteases, kinases, and phospholipases, demonstration of persistent Ca2+ –CaM binding in neurons destined to show ischemic cellular injury would support the concept that elevated intracellular Ca2+ plays a causative role in ischemic neuronal damage. In order to characterize Ca2+ –CaM binding, we used a sheep anti-CaM antibody (CaM-Ab) which recognizes CaM that is not bound to Ca2+ or brain target proteins. Therefore, immunohistochemical staining of brain sections by labeled CaM-Ab represented only unbound CaM. Six nor

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9

Gisvold, Sven Erik, and Peter Safar. "Systematic Studies of Cerebral Resuscitation Potentials after Global Brain Ischemia (GBI)." Prehospital and Disaster Medicine 1, S1 (1985): 255–60. http://dx.doi.org/10.1017/s1049023x00044678.

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Resuscitation of the brain after ischemic-anoxic brain injury remains a controversial topic. There is, however, presently a certain therapeutic optimism in this field. Ours is partly based on the recognition of a post-resuscitation disease, that is, treatable pathologic processes in all organsafterrestoration of adequate perfusion pressure and arterial oxygenation. Also, Hossmann has shown that neurons can survive longer periods of anoxia than previously assumed.There have been reports on experimentalfocalischemia indicating beneficial effects of barbiturates and moderate hemodilution before a

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Hossmann, Konstantin-Alexander. "REPERFUSION OF THE BRAIN AFTER GLOBAL ISCHEMIA." Shock 8, no. 2 (1997): 95–101. http://dx.doi.org/10.1097/00024382-199708000-00004.

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11

Johnson, Martha B., KunLin Jin, Manabu Minami, Dexi Chen, and Roger P. Simon. "Global Ischemia Induces Expression of Acid-Sensing Ion Channel 2a in Rat Brain." Journal of Cerebral Blood Flow & Metabolism 21, no. 6 (2001): 734–40. http://dx.doi.org/10.1097/00004647-200106000-00011.

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Acid-sensing ion channels (ASICs) are ligand-gated cation channels that respond to acidic stimuli. They are expressed throughout the mammalian nervous system. In the peripheral nervous system, ASICs act as nociceptors, responding to the tissue acidosis that accompanies ischemic and inflammatory conditions. The function of ASICs in the central nervous system is not known. In this article, the authors present evidence that transient global ischemia induces ASIC 2a protein expression in neurons that survive ischemia. Western blot analysis with an anti-ASIC 2a antibody revealed up-regulation of an

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12

Perasso, Luisa, Carla Emilia Cogo, Debora Giunti, et al. "Systemic Administration of Mesenchymal Stem Cells Increases Neuron Survival after Global Cerebral Ischemia In Vivo (2VO)." Neural Plasticity 2010 (2010): 1–5. http://dx.doi.org/10.1155/2010/534925.

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Although many studies have shown that administration of stem cells after focal cerebral ischemia improves brain damage, very little data are available concerning the damage induced by global cerebral ischemia. The latter causes neuronal death in selectively vulnerable areas, including the hippocampal CA1 region. We tested the hypothesis that intravenous infusion of bone marrowderived stromal cells (mesenchimal stem cells, MSC) reduce brain damage after transient global ischemia. In adult male Sprague-Dawley rats transient global ischemia was induced using bilateral common carotid artery occlus

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Dave, Kunjan R., Isabel Saul, Raul Busto, Myron D. Ginsberg, Thomas J. Sick, and Miguel A. Pérez-Pinzón. "Ischemic Preconditioning Preserves Mitochondrial Function after Global Cerebral Ischemia in Rat Hippocampus." Journal of Cerebral Blood Flow & Metabolism 21, no. 12 (2001): 1401–10. http://dx.doi.org/10.1097/00004647-200112000-00004.

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Ischemic tolerance in brain develops when sublethal ischemic insults occur before “lethal” cerebral ischemia. Two windows for the induction of tolerance by ischemic preconditioning (IPC) have been proposed: one that occurs within 1 hour after IPC, and another that occurs 1 or 2 days after IPC. The authors tested the hypotheses that IPC would reduce or prevent ischemia-induced mitochondrial dysfunction. IPC and ischemia were produced by bilateral carotid occlusions and systemic hypotension (50 mm Hg) for 2 and 10 minutes, respectively. Nonsynaptosomal mitochondria were harvested 24 hours after

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14

Sager, Thomas Nikolaj, Henning Laursen, and Anker Jon Hansen. "Changes in N-Acetyl-Aspartate Content during Focal and Global Brain Ischemia of the Rat." Journal of Cerebral Blood Flow & Metabolism 15, no. 4 (1995): 639–46. http://dx.doi.org/10.1038/jcbfm.1995.79.

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N-Acetyl-aspartate (NAA) is almost exclusively localized in neurons in the mature brain and might be used as a neuronal marker. It has been reported that the NAA content in human brain is decreased in neurodegenerative diseases and in stroke. Since the NAA content can be determined by nuclear magnetic resonance techniques, it has potential as a diagnostic and prognostic marker. The objective of this study was to examine the change of NAA content and related substances following cerebral ischemia and compare the results to the damage of the tissue. We used rats to study the changes of NAA, N-ac

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15

Hoehner, Paul J., Thomas J. J. Blanck, Rita Roy, Robert E. Rosenthal, and Gary Fiskum. "Alteration of Voltage-Dependent Calcium Channels in Canine Brain during Global Ischemia and Reperfusion." Journal of Cerebral Blood Flow & Metabolism 12, no. 3 (1992): 418–24. http://dx.doi.org/10.1038/jcbfm.1992.59.

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Elevated intracellular calcium (iCa2+) plays an important role in the pathophysiology of ischemic brain damage. The mechanisms by which iCa2+ increases are uncertain. Recent evidence implicates the voltage-dependent calcium channel (VDCC) as a likely site for the alteration in Ca2+ homeostasis during ischemia. The purpose of this study was to determine whether VDCCs are altered by global ischemia and reperfusion in a canine cardiac arrest, resuscitation model. We employed the radioligand, [3H]PN200-110, to quantitate the equilibrium binding characteristics of the VDCCs in the cerebral cortex.

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Handayani, Ety Sari, Rina Susilowati, Ismail Setyopranoto, and Ginus Partadiredja. "Transient Bilateral Common Carotid Artery Occlusion (tBCCAO) of Rats as a Model of Global Cerebral Ischemia." Bangladesh Journal of Medical Science 18, no. 3 (2019): 491–500. http://dx.doi.org/10.3329/bjms.v18i3.41616.

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Background: Transient bilateral common carotid artery occlusion (tBCCAO) has been performed in rats as a model of global ischemia. However, the technique varied between laboratories and produced difficulties in the comparison of results. Variations such as rat strain, age, ischemic and reperfusion duration could affect the results. This review aims to provide a general overview of the variation of animal strains, duration of tBCCAO, reported cerebral ischemic area produced by tBCCAO, use of TTC staining for measurement of volume of brain ischemia and functional neurological tests. Method

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17

Sabri, Mohammed, Elliot Lass, and R. Loch Macdonald. "Early Brain Injury: A Common Mechanism in Subarachnoid Hemorrhage and Global Cerebral Ischemia." Stroke Research and Treatment 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/394036.

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Early brain injury (EBI) has become an area of extreme interest in the recent years and seems to be a common denominator in the pathophysiology of global transient ischemia and subarachnoid hemorrhage (SAH). In this paper, we highlight the importance of cerebral hypoperfusion and other mechanisms that occur in tandem in both pathologies and underline their possible roles in triggering brain injury after hemorrhagic or ischemic strokes.

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Tsupykov, O., V. Kyryk, O. Rybachuk, et al. "Effect of neural stem cell transplantation on cognitive functions of mice after cerebral ischemia-reperfusion." Cell and Organ Transplantology 1, no. 1 (2013): 92–95. http://dx.doi.org/10.22494/cot.v1i1.51.

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This study is aimed to determine the effect of transplantation of neural progenitor cells (NPCs) isolated from fetal hippocampus on cognitive functions of experimental animals after short-term global cerebral ischemia. NPCs were isolated from hippocampus of FVB-Cg-Tg(GFPU)5Nagy/J mice, transgenic by the GFP. Ischemic brain injury in FVB “wild” type mice was modeled by bilateral occlusion of the common carotid arteries for 20 min. GFP-positive NPCs were stereotaxically transplanted into the hippocampus of experimental animals in 24 hours after ischemia-reperfusion. Cognitive functions were eval

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Gorshkova, O. P., M. V. Lensman, A. I. Artem'eva, and D. P. Dvoretsky. "Dynamics of pial vessels reactivity after brief cerebral ischemia." Regional blood circulation and microcirculation 14, no. 1 (2015): 74–78. http://dx.doi.org/10.24884/1682-6655-2015-14-1-74-78.

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Cerebral blood vessel reactivity is one of the main determinants of final outcome of brain ischemia. Most of studies on the vascular mechanisms of ischemic brain injury, however, focus on the acute changes within ischemic period or several hours after it. Dilatatory capacity of cerebral arterioles (perfusion reservoir) is considered as an important factor of brain perfusion elevation in critical situations.The aim of the present study was to examine the pial vessel reactivity in response to hypercapnia in rats, subjected to transient global cerebral ischemia, at 7, 14 and 21 days after ischemi

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Ko, Y., B. Allen, Z. Tan, S. Sakhai, and G. Buckberg. "Controlled reperfusion prevents neurologic injury after global brain ischemia in a novel ischemic brain model." Critical Care 13, Suppl 1 (2009): P70. http://dx.doi.org/10.1186/cc7234.

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Hayashi, Takeshi, Atsushi Saito, Shuzo Okuno, Michel Ferrand-Drake, Robert L. Dodd, and Pak H. Chan. "Damage to the Endoplasmic Reticulum and Activation of Apoptotic Machinery by Oxidative Stress in Ischemic Neurons." Journal of Cerebral Blood Flow & Metabolism 25, no. 1 (2005): 41–53. http://dx.doi.org/10.1038/sj.jcbfm.9600005.

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The endoplasmic reticulum (ER), which plays a role in apoptosis, is susceptible to oxidative stress. Because superoxide is produced in the brain after ischemia/reperfusion, oxidative injury to this organelle may be implicated in ischemic neuronal cell death. Activating transcription factor-4 (ATF-4) and C/EBP-homologous protein (CHOP), both of which are involved in apoptosis, are induced by severe ER stress. Using wild-type and human copper/zinc superoxide dismutase transgenic rats, we observed induction of these molecules in the brain after global cerebral ischemia and compared them with neur

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Shichita, Takashi, Hiroaki Ooboshi, Yasuhiro Kumai, et al. "Post-ischemic gene transfer of IL-10 protects against global brain ischemia." Journal of Cerebral Blood Flow & Metabolism 25, no. 1_suppl (2005): S507. http://dx.doi.org/10.1038/sj.jcbfm.9591524.0507.

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Harukuni, Izumi, and Anish Bhardwaj. "Mechanisms of Brain Injury after Global Cerebral Ischemia." Neurologic Clinics 24, no. 1 (2006): 1–21. http://dx.doi.org/10.1016/j.ncl.2005.10.004.

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Neumar, Robert W., Scott M. Hagle, Donald J. DeGracia, Gary S. Krause та Blaine C. White. "Brain μ-Calpain Autolysis During Global Cerebral Ischemia". Journal of Neurochemistry 66, № 1 (2002): 421–24. http://dx.doi.org/10.1046/j.1471-4159.1996.66010421.x.

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Setorki, Mahbubeh, and Zahra Hooshmandi. "Neuroprotective effect of Ziziphus spina-christi on brain injury induced by transient global cerebral ischemia and reperfusion in rat." Bangladesh Journal of Pharmacology 12, no. 1 (2017): 69. http://dx.doi.org/10.3329/bjp.v12i1.29964.

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<p class="Abstract">This study evaluated the protective effect of <em>Ziziphus </em>spina<em>-</em>christi on the cerebral oxidative stress and damage induced by ischemia. Male Wistar rats were divided randomly into six groups (seven in each group): Control group did not undergo surgery and received distilled water; shame group underwent surgery without ischemia; ischemic group underwent ischemia without any medication; extract-treated groups underwent ischemia and orally received 50, 100, 200 mg/kg/day doses <em>Z. </em>spina<em>-</em>chri

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Charriaut-Marlangue, C., I. Margaill, M. Plotkine, and Y. Ben-Ari. "Early Endonuclease Activation following Reversible Focal Ischemia in the Rat Brain." Journal of Cerebral Blood Flow & Metabolism 15, no. 3 (1995): 385–88. http://dx.doi.org/10.1038/jcbfm.1995.48.

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The structural changes that occur in chromatin DNA after ischemic brain injury are poorly understood. The presence of oligonucleosome fragments that are recognized as the characteristic DNA ladder has been demonstrated in global and focal ischemia, associated or not with random DNA fragmentation. Using pulsed-field gel electrophoresis, which improves DNA separation, we have now detected initial stages of DNA fragmentation that occur already 6 h after reversible focal cerebral ischemia in rats. This result confirms that internucleosomal DNA fragmentation precedes random DNA fragmentation in vul

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Bacher, Andreas, Jae Young Kwon, and Mark H. Zornow. "Effects of Temperature on Cerebral Tissue Oxygen Tension, Carbon Dioxide Tension, and pH during Transient Global Ischemia in Rabbits." Anesthesiology 88, no. 2 (1998): 403–9. http://dx.doi.org/10.1097/00000542-199802000-00019.

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Background A decrease in brain temperature (Tbrain) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (PO2 brain), carbon dioxide tension (PCO2 brain), and pH (pHbrain) were monitored during short episodes of global cerebral ischemia. Methods After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the

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Sieber, Frederick E., Richard J. Traystman, and Lee J. Martin. "Delayed Neuronal Death after Global Incomplete Ischemia in Dogs is Accompanied by Changes in Phospholipase C Protein Expression." Journal of Cerebral Blood Flow & Metabolism 17, no. 5 (1997): 527–33. http://dx.doi.org/10.1097/00004647-199705000-00006.

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Activation of phospholipase C (PLC) increases intracellular Ca++ and may play a role in delayed neuronal death after ischemia. Because changes in intracellular Ca++ are believed to participate in ischemic neuronal injury, we tested the hypothesis that PLCβ protein levels are temporally altered in brain regions that undergo neurodegeneration after global incomplete ischemia. Dogs (n = 12) were subjected to 20 minutes of global incomplete ischemia followed by recovery of either 1 (n = 5) or 7 days (n = 7). Six sham-operated animals were used as nonischemic controls. In hematoxylin and eosin-stai

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Chen, Jun, Steven H. Graham, Masaki Nakayama, et al. "Apoptosis Repressor Genes Bcl-2 and Bcl-x-Long are Expressed in the Rat Brain following Global Ischemia." Journal of Cerebral Blood Flow & Metabolism 17, no. 1 (1997): 2–10. http://dx.doi.org/10.1097/00004647-199701000-00002.

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The proto-oncogenes bcl-2 and bcl-x-long have been shown to suppress apoptotic cell death in a variety of in vitro systems and cell lines, including neurons. An alternatively spliced form of bcl-x, bcl-x-short, is a promoter of apoptotic death. Whether these genes are induced after ischemia or play any role in determining the fate of ischemic neurons is unknown. To begin to address this issue, we studied the expression of bcl-2, and bcl-x mRNA and protein after global ischemia in the rat. Ischemia was induced in isoflurane-anesthetized rats by the four-vessel occlusion method. mRNA expression

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Wang, Shu Yan, Ya Le Duan, Qing Wen Zeng, Zheng Zhao, and Xiang Rui Wang. "[D-Ala2, D-Leu5]-Enkephalin (Dadle) Reduces Inflammation Responses after Transient Global Ischemia." Advanced Materials Research 345 (September 2011): 343–48. http://dx.doi.org/10.4028/www.scientific.net/amr.345.343.

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[D-Ala2, D-Leu5]-Enkephalin (DADLE) is a δ-opioid receptor antagonist and has been shown to reduce neuronal loss in the selectively vulnerable brain regions after transient global ischemia. Here, we investigate whether this protection is mediated by the DADLE's modulation of the postischemia inflammation responses. After implanted with cannula at the right lateral ventricle, rats underwent 10 minutes of transient global ischemia by four vessel occlusion. Rats received a single infusion of DADLE (12.5 nmol) via the intracerebral cannula at the onset of reperfusion. At the time of 72 h after isc

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Le Roy, Lucas, Anne Letondor, Cloé Le Roux, Ahmed Amara, and Serge Timsit. "Cellular and Molecular Mechanisms of R/S-Roscovitine and CDKs Related Inhibition under Both Focal and Global Cerebral Ischemia: A Focus on Neurovascular Unit and Immune Cells." Cells 10, no. 1 (2021): 104. http://dx.doi.org/10.3390/cells10010104.

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Ischemic stroke is the second leading cause of death worldwide. Following ischemic stroke, Neurovascular Unit (NVU) inflammation and peripheral leucocytes infiltration are major contributors to the extension of brain lesions. For a long time restricted to neurons, the 10 past years have shown the emergence of an increasing number of studies focusing on the role of Cyclin-Dependent Kinases (CDKs) on the other cells of NVU, as well as on the leucocytes. The most widely used CDKs inhibitor, (R)-roscovitine, and its (S) isomer both decreased brain lesions in models of global and focal cerebral isc

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Le Roy, Lucas, Anne Letondor, Cloé Le Roux, Ahmed Amara, and Serge Timsit. "Cellular and Molecular Mechanisms of R/S-Roscovitine and CDKs Related Inhibition under Both Focal and Global Cerebral Ischemia: A Focus on Neurovascular Unit and Immune Cells." Cells 10, no. 1 (2021): 104. http://dx.doi.org/10.3390/cells10010104.

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Ischemic stroke is the second leading cause of death worldwide. Following ischemic stroke, Neurovascular Unit (NVU) inflammation and peripheral leucocytes infiltration are major contributors to the extension of brain lesions. For a long time restricted to neurons, the 10 past years have shown the emergence of an increasing number of studies focusing on the role of Cyclin-Dependent Kinases (CDKs) on the other cells of NVU, as well as on the leucocytes. The most widely used CDKs inhibitor, (R)-roscovitine, and its (S) isomer both decreased brain lesions in models of global and focal cerebral isc

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Mirzoyan, Narine R., Nelly G. Khostikyan, Vahe S. Meliksetyan, et al. "Neuroprotective and cerebrovascular effects of endogenous N-Arachidonoyl-GABA and its putative Cox-2 metabolite – GABA conjugate with Prostaglandin E2." Research Results in Pharmacology 7, no. 3 (2021): 49–61. http://dx.doi.org/10.3897/rrpharmacology.7.70974.

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Introduction: The aim of the study was to compare the neuroprotective and cerebrovascular effects of bioactive, endogenous lipid – N-arachidonoyl-GABA (AA-GABA) and GABA conjugate with prostaglandin E2 (PGE2-GABA) by evaluation of a morphological state of rat brain tissue and lipofuscin levels under the condition of permanent focal brain ischemia, as well as cerebral circulation under the condition of global transient ischemia. Materials and methods: The study has been implemented using the models of the left middle cerebral artery occlusion (MCAO) and global transient ischemia of the brain. A

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Espinosa-Garcia, Claudia, Fahim Atif, Seema Yousuf, Iqbal Sayeed, Gretchen N. Neigh, and Donald G. Stein. "Progesterone Attenuates Stress-Induced NLRP3 Inflammasome Activation and Enhances Autophagy Following Ischemic Brain Injury." International Journal of Molecular Sciences 21, no. 11 (2020): 3740. http://dx.doi.org/10.3390/ijms21113740.

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NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome inhibition and autophagy induction attenuate inflammation and improve outcome in rodent models of cerebral ischemia. However, the impact of chronic stress on NLRP3 inflammasome and autophagic response to ischemia remains unknown. Progesterone (PROG), a neuroprotective steroid, shows promise in reducing excessive inflammation associated with poor outcome in ischemic brain injury patients with comorbid conditions, including elevated stress. Stress primes microglia, mainly by the release of alarmins such as high-mobility group box-1

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Kuhmonen, Johanna, Jaroslav Pokorny, Riitta Miettinen, et al. "Neuroprotective Effects of Dexmedetomidine in the Gerbil Hippocampus after Transient Global Ischemia." Anesthesiology 87, no. 2 (1997): 371–77. http://dx.doi.org/10.1097/00000542-199708000-00025.

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Background Cerebral ischemia induces a massive release of norepinephrine associated with neuronal death in the brain. It has been demonstrated that alpha2-adrenoceptor agonists decrease the release and turnover of noradrenaline, and this might prove advantageous in counteracting the neurodegeneration in ischemic brain. Therefore, in the present study, the authors tested whether dexmedetomidine, a selective alpha2-receptor agonist, has neuroprotective effects in a gerbil transient global ischemia model. Methods Ischemia was induced by bilateral carotid occlusion for 5 min in diethylether-anesth

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Zhao, Heng. "Ischemic Postconditioning as a Novel Avenue to Protect against Brain Injury after Stroke." Journal of Cerebral Blood Flow & Metabolism 29, no. 5 (2009): 873–85. http://dx.doi.org/10.1038/jcbfm.2009.13.

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Ischemic postconditioning initially referred to a stuttering reperfusion performed immediately after reperfusion, for preventing ischemia/reperfusion injury in both myocardial and cerebral infarction. It has evolved into a concept that can be induced by a broad range of stimuli or triggers, and may even be performed as late as 6 h after focal ischemia and 2 days after transient global ischemia. The concept is thought to be derived from ischemic preconditioning or partial/gradual reperfusion, but in fact the first experiment for postconditioning was carried out much earlier than that of precond

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Pierpaoli, Carlo, Jeffry R. Alger, Andrea Righini, et al. "High Temporal Resolution Diffusion MRI of Global Cerebral Ischemia and Reperfusion." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (1996): 892–905. http://dx.doi.org/10.1097/00004647-199609000-00013.

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Although brain ischemia has been extensively studied using diffusion-weighted magnetic resonance imaging, most studies performed so far have not had adequate time resolution to follow the temporal changes in the water apparent diffusion coefficient (ADC) in hyperacute ischemia. Using diffusion echo planar imaging, we obtained ADC maps (calculated from measurements made with 8 b-values) with a time resolution of 43 s in a feline model of global brain ischemia and reperfusion. Different protocols were performed: 10-min hypoperfusion, 10- and 22-min ischemia followed by reperfusion, and cardiac a

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Handayani, Ety Sari, Zainuri Sabta Nugraha, Titis Nurmasitoh, Kuswati Kuswati, Dwi N. Ahsani, and Ajeng G. Nanda. "Black sugarcane decoction reduces rat brain ischemia." Universa Medicina 35, no. 1 (2016): 40. http://dx.doi.org/10.18051/univmed.2016.v35.40-45.

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Background<br />There are people in Yogyakarta, who use black sugarcane decoction (BSD) to prevent stroke. BSD contains policosanol and antioxidants. It has been proven that policosanol can reduce global ischemia in Mongolian gerbils. This study aims to evaluate the effect of BSD on brain ischemia in a rat stroke model. <br /><br />Methods<br />A laboratory experiment using eighteen 3-month old male Wistar rats without any defects, of 175-250 g body weight. Brain ischemia was produced by a 20-minute bilateral carotid communis artery oclusion (BCCAO). Using a rat stroke

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Miyazawa, T., and K. A. Hossmann. "Methodological Requirements for Accurate Measurements of Brain and Body Temperature during Global Forebrain Ischemia of Rat." Journal of Cerebral Blood Flow & Metabolism 12, no. 5 (1992): 817–22. http://dx.doi.org/10.1038/jcbfm.1992.113.

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The methodological requirements for accurate measurements of brain and body temperature during brain ischemia have been validated in Wistar rats submitted to 30 min of four-vessel occlusion. During ischemia, brains were exposed to three different temperature profiles: Spontaneous cooling from 36 to 31°C ( n = 10), constant hypothermia at 30°C ( n = 19), and constant normothermia at 36°C ( n = 21). Direct and indirect brain temperature recordings were carried out by placing fine thermocouples (200 μm diameter) into the striate nucleus, the temporal muscle, and the epidural space. Body temperatu

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Dimlich, R. V. W., and M. H. Biros. "Ultrastructure of neurons and astrocytes in cerebral cortex of fasted rats subjected to partial global ischemia." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 722–23. http://dx.doi.org/10.1017/s042482010012792x.

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Evidence exists that the morphoglogical expression of ischemic cell change in the central nervous system not only depends on the nutritional state of the animal, the adequacy of reperfusion and length of ischemia, but whether or not this ischemia was complete or incomplete. (1) In addition, changes that occur in neurons, associated glial cells, and adjacent neuropil are selective as well as progressive and need to be investigated by area and location within a specific region of the brain as well as over time. (2) In a model of incomplete ischemia in the rat, other investigators have examined c

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Miura, Yoshihide, Hilary P. Grocott, Robert D. Bart, Robert D. Pearlstein, Franklin Dexter, and David S. Warner. "Differential Effects of Anesthetic Agents on Outcome from Near-complete but Not Incomplete Global Ischemia in the Rat." Anesthesiology 89, no. 2 (1998): 391–400. http://dx.doi.org/10.1097/00000542-199808000-00016.

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Background It has been postulated that anesthetic agents that reduce cerebral metabolic rate will protect the brain against ischemia when electroencephalographic (EEG) activity is persistent, but will provide no protection when ischemia is severe enough to cause EEG isoelectricity. No outcome studies have addressed this issue. The authors studied anesthetic agents to determine if they provide differential effects on outcome from global cerebral ischemic insults that cause either an attenuated or isoelectric EEG. Methods Fasted rats were subjected to either (1) incomplete ischemia (attenuated E

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Sager, Thomas Nikolaj, Henning Laursen, Anders Fink-Jensen, et al. "N-Acetylaspartate Distribution in Rat Brain Striatum During Acute Brain Ischemia." Journal of Cerebral Blood Flow & Metabolism 19, no. 2 (1999): 164–72. http://dx.doi.org/10.1097/00004647-199902000-00008.

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Brain N-acetylaspartate (NAA) can be quantified by in vivo proton magnetic resonance spectroscopy (1H-MRS) and is used in clinical settings as a marker of neuronal density. It is, however, uncertain whether the change in brain NAA content in acute stroke is reliably measured by 1H-MRS and how NAA is distributed within the ischemic area. Rats were exposed to middle cerebral artery occlusion. Preischemic values of [NAA] in striatum were 11 mmol/L by 1H-MRS and 8 mmol/kg by HPLC. The methods showed a comparable reduction during the 8 hours of ischemia. The interstitial level of [NAA] ([NAA]e) was

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Takizawa, Shunya, Matthew J. Hogan, Alastair M. Buchan, and Antoine M. Hakim. "In vivo Binding of [3H]Nimodipine in Rat Brain after Transient Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 14, no. 3 (1994): 397–405. http://dx.doi.org/10.1038/jcbfm.1994.51.

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We report the regional variation in relative in vivo binding of the l-type voltage sensitive calcium channel (VSCC) antagonist [3H]nimodipine to brain following transient forebrain ischemia in the rat. At 30-min of reperfusion after 20 min of forebrain ischemia, [3H]nimodipine binding was significantly increased in striatum, CA3 and CA4, and dentate relative to binding in sham-operated rats, suggesting that VSCCs were responding to ischemic depolarization. Two h following ischemia, binding in all brain structures returned to normal levels indicating repolarization of cell membranes. At 24 h of

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Jin, Kunlin, Steven H. Graham, Tetsuya Nagayama, et al. "Altered Expression of the Neuropeptide-Processing Enzyme Carboxypeptidase E in the Rat Brain after Global Ischemia." Journal of Cerebral Blood Flow & Metabolism 21, no. 12 (2001): 1422–29. http://dx.doi.org/10.1097/00004647-200112000-00006.

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Carboxypeptidase E, an exoprotease involved in the processing of bioactive peptides released by a regulated secretory pathway, was identified in a subtractive complementary DNA library derived from an ischemic rat brain by differential screening. In situ hybridization and immunocytochemical analysis showed the presence of carboxypeptidase E messenger RNA and protein in the cerebral cortex, thalamus, striatum, and hippocampus of a healthy rat brain. After 15 minutes of transient global ischemia followed by 8 hours of reperfusion, increased levels of carboxypeptidase E messenger RNA and protein

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Cao, Guodong, Yumin Luo, Tetsuya Nagayama, et al. "Cloning and Characterization of Rat Caspase-9: Implications for a Role in Mediating Caspase-3 Activation and Hippocampal Cell Death after Transient Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 22, no. 5 (2002): 534–46. http://dx.doi.org/10.1097/00004647-200205000-00005.

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Delayed hippocampal neurodegeneration after transient global ischemia is mediated, at least in part, through the activation of terminal caspases, particularly caspase-3, and the subsequent proteolytic degradation of critical cellular proteins. Caspase-3 may be activated by the membrane receptor-initiated caspase-8–dependent extrinsic pathway and the mitochondria-initiated caspase-9–dependent intrinsic pathway; however, the precise role of these deduced apoptosis-signaling pathways in activating caspase-3 in ischemic neurons remains elusive. The authors cloned the caspase-9 gene from the rat br

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Zhao, Heng, Midori A. Yenari, Danye Cheng, Robert M. Sapolsky, and Gary K. Steinberg. "Biphasic Cytochrome c Release After Transient Global Ischemia and its Inhibition by Hypothermia." Journal of Cerebral Blood Flow & Metabolism 25, no. 9 (2005): 1119–29. http://dx.doi.org/10.1038/sj.jcbfm.9600111.

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Hypothermia is effective in preventing ischemic damage. A caspase-dependent apoptotic pathway is involved in ischemic damage, but how hypothermia inhibits this pathway after global cerebral ischemia has not been well explored. It was determined whether hypothermia protects the brain by altering cytochrome c release and caspase activity. Cerebral ischemia was produced by two-vessel occlusion plus hypotension for 10 mins. Body temperature in hypothermic animals was reduced to 33°C before ischemia onset and maintained for 3 h after reperfusion. Western blots of subcellular fractions revealed biph

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Maj, Hedtjärn, Carina Mallard, Saskia Eklind, Katarina Gustafson-Brywe, and Henrik Hagberg. "Global Gene Expression in the Immature Brain after Hypoxia-Ischemia." Journal of Cerebral Blood Flow & Metabolism 24, no. 12 (2004): 1317–32. http://dx.doi.org/10.1097/01.wcb.0000141558.40491.75.

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Ischemia induces a complex response of differentially expressed genes in the brain. In order to understand the specific mechanisms of injury in the developing brain, it is important to obtain information on global changes in the transcriptome after neonatal hypoxia-ischemia. In this study, oligonucleotide arrays were used to investigate genomic changes at 2, 8, 24, and 72 hours after neonatal hypoxia-ischemia, which was induced in 9-day-old mice by left carotid artery ligation followed by hypoxia (10% O2). In total, 343 genes were differentially expressed in cortex, hippocampus, thalamus, and

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Shcherbak, N. S., G. Yu Yukina, E. G. Sukhorukova, and V. V. Thomson. "Effect of ischemic postconditioining on reaction of neocortex microglia after global brain ischemia in rats." Regional blood circulation and microcirculation 19, no. 2 (2020): 59–66. http://dx.doi.org/10.24884/1682-6655-2020-19-2-59-66.

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Introduction. Ischemic postconditioning (IPostC) is a new concept in the brain protection strategy. Almost all researches in this area focus on the functioning and survival of neurons, while non-neuronal cells affected by IPostC remain unexplored. The aim is to study the IPostC effect on changes in microglia in the neocortex of Wistar rats after global brain ischemia during various periods of reperfusion. Materials and methods. Male Wistar rats were used as a model of a 10-minute global brain ischemia with a subsequent IPostC; the reperfusion-ischemia cycle was 15 s/15 s. In the early (2 days)

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Tuttolomondo, Antonino, Maria Grazia Puleo, Maria Chiara Velardo, Francesca Corpora, Mario Daidone, and Antonio Pinto. "Molecular Biology of Atherosclerotic Ischemic Strokes." International Journal of Molecular Sciences 21, no. 24 (2020): 9372. http://dx.doi.org/10.3390/ijms21249372.

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Among the causes of global death and disability, ischemic stroke (also known as cerebral ischemia) plays a pivotal role, by determining the highest number of worldwide mortality, behind cardiomyopathies, affecting 30 million people. The etiopathogenetic burden of a cerebrovascular accident could be brain ischemia (~80%) or intracranial hemorrhage (~20%). The most common site when ischemia occurs is the one is perfused by middle cerebral arteries. Worse prognosis and disablement consequent to brain damage occur in elderly patients or affected by neurological impairment, hypertension, dyslipidem

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Kinuta, Yuji, Mieko Kimura, Yoshinori Itokawa, Masatsune Ishikawa, and Haruhiko Kikuchi. "Changes in xanthine oxidase in ischemic rat brain." Journal of Neurosurgery 71, no. 3 (1989): 417–20. http://dx.doi.org/10.3171/jns.1989.71.3.0417.

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✓ Xanthine oxidase activity in the rat brain was measured by means of high-performance liquid chromatography with electrochemical detection of uric acid. Cerebral ischemia was produced by a four-vessel occlusion method. In the control rat, the enzyme activity was 0.87 ± 0.13 nmol/gm wet weight/min at 25°C (mean ± standard deviation), of which 92.4% was associated with the nicotinamide adenine dinucleotide (NAD)-dependent dehydrogenase form and only 7.6% with the oxygen-dependent superoxide-producing oxidase form. However, the ratio of the latter form increased to 43.7% after 30 minutes of glob

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