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Journal articles on the topic 'Cerebral ischemia – Animal models'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Umemura, Kazuo. "Experimental animal models of cerebral ischemia." Japanese Journal of Pharmacology 76 (1998): 39. http://dx.doi.org/10.1016/s0021-5198(19)40286-2.

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Takizawa, Shunya, and Antoine M. Hakim. "Animal Models of Cerebral Ischemia. 2. Rat Models." Cerebrovascular Diseases 1, no. 1 (1991): 16–21. http://dx.doi.org/10.1159/000108876.

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3

Ma, Rong, Qian Xie, Yong Li, Zhuoping Chen, Mihong Ren, Hai Chen, Hongyan Li, Jinxiu Li, and Jian Wang. "Animal models of cerebral ischemia: A review." Biomedicine & Pharmacotherapy 131 (November 2020): 110686. http://dx.doi.org/10.1016/j.biopha.2020.110686.

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Bacigaluppi, Marco. "Animal Models of Ischemic Stroke. Part Two: Modeling Cerebral Ischemia." Open Neurology Journal 4, no. 1 (August 31, 2010): 34–38. http://dx.doi.org/10.2174/1874205x01004010034.

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5

Traystman, R. J. "Animal Models of Focal and Global Cerebral Ischemia." ILAR Journal 44, no. 2 (January 1, 2003): 85–95. http://dx.doi.org/10.1093/ilar.44.2.85.

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6

O'Collins, Victoria E., Malcolm R. Macleod, Geoffrey A. Donnan, and David W. Howells. "Evaluation of Combination Therapy in Animal Models of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 32, no. 4 (February 1, 2012): 585–97. http://dx.doi.org/10.1038/jcbfm.2011.203.

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Combination therapy has been identified as a promising strategy to improve stroke management. We conducted a systematic review and meta-analysis of evidence from animal models of ischemic stroke to determine whether combining treatments improved efficacy. Multiple databases were searched and data were extracted from focal ischemia experiments comparing control groups, single treatments, and combination treatments. Of 11,430 papers identified, 142 met the inclusion criteria; these tested 126 treatments in 373 experiments using 8,037 animals ( I2 = 85 to 96%). Taken together, single treatments r

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7

Schweizer, Sophie, Andreas Meisel, and Stefanie Märschenz. "Epigenetic Mechanisms in Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 9 (June 12, 2013): 1335–46. http://dx.doi.org/10.1038/jcbfm.2013.93.

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Treatment efficacy for ischemic stroke represents a major challenge. Despite fundamental advances in the understanding of stroke etiology, therapeutic options to improve functional recovery remain limited. However, growing knowledge in the field of epigenetics has dramatically changed our understanding of gene regulation in the last few decades. According to the knowledge gained from animal models, the manipulation of epigenetic players emerges as a highly promising possibility to target diverse neurologic pathologies, including ischemia. By altering transcriptional regulation, epigenetic modi

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Handayani, Ety S., Titis Nurmasitoh, Syaefudin Ali Akhmad, Afifah Nur Fauziah, Rizky Rizani, Rika Yulita Rahmawati, and Angga Afriandi. "Effect of BCCAO Duration and Animal Models Sex on Brain Ischemic Volume After 24 Hours Reperfusion." Bangladesh Journal of Medical Science 17, no. 1 (January 11, 2018): 129–37. http://dx.doi.org/10.3329/bjms.v17i1.35293.

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Background: Literature study shows, there are several variations regarding BCCAO duration and duration of reperfusion after BCCAO that can cause cerebral ischemia. Duration of BCCAO techniques varies between 10 to 30 minutes, while the duration of reperfusion period ranging between 45 minutes to 72 hours. Differences in the duration of occlusion, duration of BCCAO reperfusion and the sex of animal model could lead to different responses to ischemia conditions.Objective. This study aims to determine whether the duration BCCAO and sex of the animal models influences the volume of cerebral ischem

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Cirillo, Carla, Nabila Brihmat, Evelyne Castel-Lacanal, Alice Le Friec, Marianne Barbieux-Guillot, Nicolas Raposo, Jérémie Pariente, et al. "Post-stroke remodeling processes in animal models and humans." Journal of Cerebral Blood Flow & Metabolism 40, no. 1 (October 23, 2019): 3–22. http://dx.doi.org/10.1177/0271678x19882788.

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After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understandin

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10

Hossmann, Konstantin-A. "Animal Models of Cerebral Ischemia. 1. Review of Literature." Cerebrovascular Diseases 1, no. 1 (1991): 2–15. http://dx.doi.org/10.1159/000108875.

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11

Wang, Peng-Fei, Yu Zhou, Huang Fang, Sen Lin, Yan-Chun Wang, Yong Liu, Jun Xia, Guy D. Eslick, and Qing-Wu Yang. "Treatment of acute cerebral ischemia using animal models: a meta-analysis." Translational Neuroscience 6, no. 1 (January 1, 2015): 47–58. http://dx.doi.org/10.1515/tnsci-2015-0006.

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AbstractBackground: There are numerous potential treatments assessed for acute cerebral ischemia using animal models. This study aimed to assess the effect of these treatments in terms of infarct size and neurobehavioral change. This meta-analysis was conducted to determine if any of these treatments provide a superior benefit so that they might be used on humans. Methods: A systematic search was conducted using several electronic databases for controlled animal studies using only nonsurgical interventions for acute cerebral ischemia. A random-effects model was used. Results: After an extensiv

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Meng, Wei, Xiaoying Wang, Minoru Asahi, Tsuneo Kano, Kazuko Asahi, Robert H. Ackerman, and Eng H. Lo. "Effects of Tissue Type Plasminogen Activator in Embolic versus Mechanical Models of Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 19, no. 12 (December 1999): 1316–21. http://dx.doi.org/10.1097/00004647-199912000-00004.

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Tissue type plasminogen activator (tPA) can be effective therapy for embolic stroke by restoring cerebral perfusion. However, a recent experimental study showed that tPA increased infarct size in a mouse model of transient focal ischemia, suggesting a possible adverse effect of tPA on ischemic tissue per se. In this report, the effects of tPA in two rat models of cerebral ischemia were compared. In experiment 1, rats were subjected to focal ischemia via injection of autologous clots into the middle cerebral artery territory. Two hours after clot injection, rats were treated with 10 mg/kg tPA o

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13

Bigdeli, Mohammad Reza. "Neuroprotection Caused by Hyperoxia Preconditioning in Animal Stroke Models." Scientific World JOURNAL 11 (2011): 403–21. http://dx.doi.org/10.1100/tsw.2011.23.

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Ischemic tolerance induced by hyperoxia (HO) can protect against brain injury and neurodegenerative diseases. Although multiple studies demonstrate neuroprotection by HO, the exact mechanism(s) of HO neuroprotection has not been elucidated. Here, I first review related mechanisms of brain ischemia and then data evaluating the neuroprotective effects of HO in focal and global ischemic animal models. I clearly establish that the cerebrovascular, extracellular matrix, plasma membrane, endoplasmic reticulum, mitochondrial, and lysosomal reactions are critical in neuroprotection induced by HO in fo

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14

Tamura, Akira. "Animal models of cerebral ischemia. How to select the model." Nosotchu 30, no. 6 (2008): 857–61. http://dx.doi.org/10.3995/jstroke.30.857.

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Hoehn, Mathias, Klaas Nicolay, Claudia Franke, and Boudewijn van der Sanden. "Application of magnetic resonance to animal models of cerebral ischemia." Journal of Magnetic Resonance Imaging 14, no. 5 (2001): 491–509. http://dx.doi.org/10.1002/jmri.1213.

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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 (May 30, 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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Kitagawa, Kazuo, Masayasu Matsumoto, Gongming Yang, Takuma Mabuchi, Yoshiki Yagita, Masatsugu Hori, and Takehiko Yanagihara. "Cerebral Ischemia after Bilateral Carotid Artery Occlusion and Intraluminal Suture Occlusion in Mice: Evaluation of the Patency of the Posterior Communicating Artery." Journal of Cerebral Blood Flow & Metabolism 18, no. 5 (May 1998): 570–79. http://dx.doi.org/10.1097/00004647-199805000-00012.

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Cerebral ischemia models using mice have drawn increasing attention, particularly because of the availability of transgenic animals. However, the variability of intracranial vasculature at the circle of Willis in mice can influence the degree of ischemia in both the bilateral common carotid artery (CCA) occlusion and intraluminal suture occlusion models. We have developed a method to predict the extent of the anastomosis between carotid and vertebrobasilar circulation in three mouse strains (C57BL/6, CBA, and DBA/2) by measuring cortical microperfusion with laser Doppler flowmetry during a 1-m

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Ahad, Mohamad Anuar, Kesevan Rajah Kumaran, Tiang Ning, Nur Izzati Mansor, Mohamad Azmeer Effendy, Thenmoly Damodaran, Kamilla Lingam, et al. "Insights into the neuropathology of cerebral ischemia and its mechanisms." Reviews in the Neurosciences 31, no. 5 (July 28, 2020): 521–38. http://dx.doi.org/10.1515/revneuro-2019-0099.

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AbstractCerebral ischemia is a result of insufficient blood flow to the brain. It leads to limited supply of oxygen and other nutrients to meet metabolic demands. These phenomena lead to brain damage. There are two types of cerebral ischemia: focal and global ischemia. This condition has significant impact on patient’s health and health care system requirements. Animal models such as transient occlusion of the middle cerebral artery and permanent occlusion of extracranial vessels have been established to mimic the conditions of the respective type of cerebral ischemia and to further understand

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Sysoev, Yuriy I., Veronika A. Prikhodko, Dmitry Y. Ivkin, and Sergey Okovity. "Rabbit models of ischemic stroke in biomedical research." Pharmacy Formulas 1, no. 1 (December 12, 2019): 10–21. http://dx.doi.org/10.17816/phf18514.

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The development of experimental models of ischemic stroke allowing for effective translation of results from animal studies to humans is an important task of modern neuropharmacology. Due to the fact that new drugs with neuroprotective properties that have shown activity in rodents most often turn out to be not effective enough in humans, the use of larger laboratory animals may become a viable solution. Among the latter, rabbits are the most accessible species for laboratories. Since they have gyrencephalic brains and a significant amount of white matter, they can be considered to be highly s

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Rosen, Charles L., Vincent A. Dinapoli, Tomoaki Nagamine, and Todd Crocco. "Influence of age on stroke outcome following transient focal ischemia." Journal of Neurosurgery 103, no. 4 (October 2005): 687–94. http://dx.doi.org/10.3171/jns.2005.103.4.0687.

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Object. More than 100 clinical trials based on animal models have failed to identify a clinically effective neuroprotectant for stroke. Current models of stroke do not account adequately for aging nor do they incorporate the use of female animals. The authors evaluated the pathological and physiological differences in stroke in young, adult, and elderly female rats. Methods. Three groups of female Sprague—Dawley rats were studied. Nine rats were divided into three groups: young (3 months); adult (9 months); and elderly (18 months). Intraluminal filament occlusion was performed for 120 minutes

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Barber, Philip A., Roland N. Auer, Alastair M. Buchan, and Garnette R. Sutherland. "Understanding and managing ischemic stroke." Canadian Journal of Physiology and Pharmacology 79, no. 3 (March 1, 2001): 283–96. http://dx.doi.org/10.1139/y00-125.

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Transient or permanent focal brain injury following acute thromboembolic occlusion develops from a complex cascade of pathophysiological events. The processes of excitotoxicity, peri-infarct depolarisation, inflammation, and apoptosis within the ischemic penumbra are proposed. While the translation of therapeutic agents from the animal models to human clinical trials have been disappointing, there remains an atmosphere of optimism as a result of the development of new diagnostic and therapeutic approaches, which include physiological, as opposed to pharmacological, intervention. This article p

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22

MAGGIONI, A. "Activity of ?-dihydroergocryptine in some animal models of cerebral anoxia and ischemia." Pharmacological Research 26 (September 1992): 69. http://dx.doi.org/10.1016/1043-6618(92)90848-6.

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23

Washida, Kazuo, Yorito Hattori, and Masafumi Ihara. "Animal Models of Chronic Cerebral Hypoperfusion: From Mouse to Primate." International Journal of Molecular Sciences 20, no. 24 (December 7, 2019): 6176. http://dx.doi.org/10.3390/ijms20246176.

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Vascular cognitive impairment (VCI) or vascular dementia occurs as a result of brain ischemia and represents the second most common type of dementia after Alzheimer’s disease. To explore the underlying mechanisms of VCI, several animal models of chronic cerebral hypoperfusion have been developed in rats, mice, and primates. We established a mouse model of chronic cerebral hypoperfusion by narrowing the bilateral common carotid arteries with microcoils, eventually resulting in hippocampal atrophy. In addition, a mouse model of white matter infarct-related damage with cognitive and motor dysfunc

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Han, Xue Mei, Hong Tao Wei та Song Yan Liu. "Functional Role of HIF-1α in Hypoxic Preconditioning-Induced Neuroprotection against Focal Cerebral Ischemia". Advanced Materials Research 554-556 (липень 2012): 1762–67. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1762.

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Objective To investigate the expression of HIF-1α after permenent focal cerebral ischemia and to explore the role of HIF-1α in hypoxic preconditioning-induced neuroprotection. Methods Rat focal cerebral ischemia model and hypoxic preconditioning models were established. Animals were randomly divided into four groups: healthy control, hypoxic preconditioning (3 h of 8% O2/92% N2 treatment), focal cerebral ischemia (6 h, 1 d, 3 d or 7 d) and hypoxic preconditioning + focal cerebral ischemia (6 h, 1 d, 3 d or 7 d). The expression of HIF-1α after different treatments was determined by histological

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Mages, Bianca, Thomas Fuhs, Susanne Aleithe, Alexandra Blietz, Constance Hobusch, Wolfgang Härtig, Stefan Schob, Martin Krueger, and Dominik Michalski. "The Cytoskeletal Elements MAP2 and NF-L Show Substantial Alterations in Different Stroke Models While Elevated Serum Levels Highlight Especially MAP2 as a Sensitive Biomarker in Stroke Patients." Molecular Neurobiology 58, no. 8 (May 1, 2021): 4051–69. http://dx.doi.org/10.1007/s12035-021-02372-3.

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AbstractIn the setting of ischemic stroke, the neurofilament subunit NF-L and the microtubule-associated protein MAP2 have proven to be exceptionally ischemia-sensitive elements of the neuronal cytoskeleton. Since alterations of the cytoskeleton have been linked to the transition from reversible to irreversible tissue damage, the present study investigates underlying time- and region-specific alterations of NF-L and MAP2 in different animal models of focal cerebral ischemia. Although NF-L is increasingly established as a clinical stroke biomarker, MAP2 serum measurements after stroke are still

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Zhou, An, Manabu Minami, Xiaoman Zhu, Sylvia Bae, John Minthorne, Jingquan Lan, Zhi-gang Xiong, and Roger P. Simon. "Altered Biosynthesis of Neuropeptide Processing Enzyme Carboxypeptidase E after Brain Ischemia: Molecular Mechanism and Implication." Journal of Cerebral Blood Flow & Metabolism 24, no. 6 (June 2004): 612–22. http://dx.doi.org/10.1097/01.wcb.0000118959.03453.17.

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In this study, using both in vivo and in vitro ischemia models, the authors investigated the impact of brain ischemia on the biosynthesis of a key neuropeptide-processing enzyme, carboxypeptidase E (CPE). The response to brain ischemia of animals that lacked an active CPE was also examined. Combined in situ hybridization and immunocytochemical analyses for CPE showed reciprocal changes of CPE mRNA and protein, respectively, in the same cortical cells in rat brains after focal cerebral ischemia. Western blot analysis revealed an accumulation of the precursor protein of CPE in the ischemic corte

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Lv, Xianli, Chen Li, and Weijian Jiang. "The intracranial vasculature of canines represents a model for neurovascular ischemia and training residents and fellows in endovascular neurosurgery." Neuroradiology Journal 33, no. 4 (May 5, 2020): 292–96. http://dx.doi.org/10.1177/1971400920920787.

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Background We describe use of a canine model to evaluate physiological effects and neuroprotective strategies in the setting of cerebral ischemia and endovascular neurosurgery training. Methods We performed transfemoral digital subtraction cerebral and cervical angiography on eight anesthetized dogs. Angiographic images of cerebral arteries were obtained following cannulation of the femoral artery. Cerebral ischemia models were made after angiography. Results The canine cerebral vasculature exhibited extensive tortuosity of the carotid and vertebral arteries. Conversely, the bilateral anterior

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Li, Le, and Creed M. Stary. "Targeting Glial Mitochondrial Function for Protection from Cerebral Ischemia: Relevance, Mechanisms, and the Role of MicroRNAs." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6032306.

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Astrocytes and microglia play crucial roles in the response to cerebral ischemia and are effective targets for stroke therapy in animal models. MicroRNAs (miRs) are important posttranscriptional regulators of gene expression that function by inhibiting the translation of select target genes. In astrocytes, miR expression patterns regulate mitochondrial function in response to oxidative stressviatargeting of Bcl2 and heat shock protein 70 family members. Mitochondria play an active role in microglial activation, and miRs regulate the microglial neuroinflammatory response. As endogenous miR expr

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Selakovic, V., Lj Arsenijevic, M. Jovanovic, S. Sivcev, N. Jovanovic, M. Leontijevic, M. Stojanovic, M. Radenkovic, P. Andjus, and L. Radenovic. "Functional and pharmacological analysis of agmatine administration in different cerebral ischemia animal models." Brain Research Bulletin 146 (March 2019): 201–12. http://dx.doi.org/10.1016/j.brainresbull.2019.01.005.

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Vinall, Phillip E., Michael S. Kramer, Lynn A. Heinel, and Robert H. Rosenwasser. "Temporal changes in sensitivity of rats to cerebral ischemic insult." Journal of Neurosurgery 93, no. 1 (July 2000): 82–89. http://dx.doi.org/10.3171/jns.2000.93.1.0082.

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Object. Experimental rat models are often used to study cerebral ischemia, yet rats are nocturnal animals that have activity cycles that are the opposite of those of humans. In the following study the authors examined the circadian rhythm of sensitivity to an ischemic insult in rats by using an intraluminal thread technique to produce reversible middle cerebral artery occlusion.Methods. Ischemia (2 hours of blockage followed by 22 hours of reperfusion) was induced in rats according to the 24-hour clock at either 100, 400, 700, 1000, 1300, 1600, 1900, or 2200 hours (11–14 rats per time period).

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Liu, Mengting, Liying Tang, Xin Liu, Jing Fang, Hao Zhan, Hongwei Wu, and Hongjun Yang. "An Evidence-Based Review of Related Metabolites and Metabolic Network Research on Cerebral Ischemia." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9162074.

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In recent years, metabolomics analyses have been widely applied to cerebral ischemia research. This paper introduces the latest proceedings of metabolomics research on cerebral ischemia. The main techniques, models, animals, and biomarkers of cerebral ischemia will be discussed. With analysis help from the MBRole website and the KEGG database, the altered metabolites in rat cerebral ischemia were used for metabolic pathway enrichment analyses. Our results identify the main metabolic pathways that are related to cerebral ischemia and further construct a metabolic network. These results will pro

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Yin, Bo, Yang Xu, Ruili Wei, and Benyan Luo. "Ginkgo biloba on Focal Cerebral Ischemia: A Systematic Review and Meta-Analysis." American Journal of Chinese Medicine 42, no. 04 (January 2014): 769–83. http://dx.doi.org/10.1142/s0192415x14500499.

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Gingko biloba extract (EGB) has been used in traditional medicines for centuries, and although its application to cerebral ischemia has been of great interest in recent years, high quality evidence-based clinical trials have not been carried out. This systematic review and meta-analysis aimed to examine the neuroprotective effect of EGB on focal cerebral ischemia in animal models. A systematic literature search was performed using five databases spanning January 1980–July 2013. The outcome was assessed using the effect size, which was based on infarct size and/or neurological score. A total of

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Fukuda, S., and G. J. del Zoppo. "Models of Focal Cerebral Ischemia in the Nonhuman Primate." ILAR Journal 44, no. 2 (January 1, 2003): 96–104. http://dx.doi.org/10.1093/ilar.44.2.96.

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Wei, Rui-li, Hai-juan Teng, Bo Yin, Yang Xu, Yue Du, Fang-pin He, Ke-tan Chu, Ben-yan Luo, and Guo-qing Zheng. "A Systematic Review and Meta-Analysis of Buyang Huanwu Decoction in Animal Model of Focal Cerebral Ischemia." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/138484.

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Buyang Huanwu Decoction (BHD) is a well-known Chinese herbal prescription for ischemic stroke. The objective of this systematic review and meta-analysis is to provide the current evidence for neuroprotective effects of BHD and its possible mechanisms in animal models of focal ischemia. A systematic literature search, through October 2012, was performed using six databases. The outcome measures assessed were infarct size and/or neurological score. Fifty-six studies with 1270 animals that met the inclusion criteria were identified. The median score for methodological quality was 3 with a range o

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Kirino, Takaaki. "Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 22, no. 11 (November 2002): 1283–96. http://dx.doi.org/10.1097/01.wcb.0000040942.89393.88.

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A brief period of cerebral ischemia confers transient tolerance to a subsequent ischemic challenge in the brain. This phenomenon of ischemic tolerance has been confirmed in various animal models of forebrain ischemia and focal cerebral ischemia. Since the ischemic tolerance afforded by preceding ischemia can bring about robust protection of the brain, the mechanism of tolerance induction has been extensively studied. It has been elucidated that ischemic tolerance protects neurons, and at the same time, it preserves brain function. Further experiments have shown that metabolic and physical stre

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Li, T. Q., Z. G. Chen, and T. Hindmarsh. "Diffusion-weighted MR imaging of acute cerebral ischemia." Acta Radiologica 39, no. 5 (September 1998): 460–73. http://dx.doi.org/10.1080/02841859809172209.

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Diffusion-weighted MR imaging has been used in studies on experimental animal models and on patients with acute cerebral ischemia. Compared with CT and conventional MR techniques, diffusion-weighted imaging can provide earlier and more precise detection of the location and the extent of an ischemic lesion during the critical first few hours after the onset of stroke Quantitative apparent diffusion coefficient (ADC) mapping of the brain water can also be carried out by recording a series of diffusion-weighted images with different amplitudes of the displacement encoding gradients. ADC maps can

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Howells, David W., Michelle J. Porritt, Sarah SJ Rewell, Victoria O'Collins, Emily S. Sena, H. Bart van der Worp, Richard J. Traystman, and Malcolm R. Macleod. "Different Strokes for Different Folks: The Rich Diversity of Animal Models of Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 30, no. 8 (May 19, 2010): 1412–31. http://dx.doi.org/10.1038/jcbfm.2010.66.

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No single animal model is able to encompass all of the variables known to affect human ischemic stroke. This review highlights the major strengths and weaknesses of the most commonly used animal models of acute ischemic stroke in the context of matching model and experimental aim. Particular emphasis is placed on the relationships between outcome and underlying vascular variability, physiologic control, and use of models of comorbidity. The aim is to provide, for novice and expert alike, an overview of the key controllable determinants of experimental stroke outcome to help ensure the most eff

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Boltze, Johannes, Annette Förschler, Björn Nitzsche, Daniela Waldmin, Anke Hoffmann, Christiane M. Boltze, Antje Y. Dreyer, et al. "Permanent Middle Cerebral Artery Occlusion in Sheep: A Novel Large Animal Model of Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 28, no. 12 (August 13, 2008): 1951–64. http://dx.doi.org/10.1038/jcbfm.2008.89.

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As effective stroke treatment by thrombolysis is bound to a narrow time window excluding most patients, numerous experimental treatment strategies have been developed to gain new options for stroke treatment. However, all approaches using neuroprotective agents that have been successfully evaluated in rodents have subsequently failed in clinical trials. Existing large animal models are of significant scientific value, but sometimes limited by ethical drawbacks and mostly do not allow for long-term observation. In this study, we are introducing a simple, but reliable stroke model using permanen

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Ma, Rong, Xiao Ma, Jianxia Wen, Jian Wang, Qian Xie, Nian Chen, and Taiwei Dong. "Preclinical Evidence and Mechanism of Xingnaojing Injection for Cerebral Ischemia: A Systematic Review and Meta-Analysis of Animal Studies." Evidence-Based Complementary and Alternative Medicine 2018 (November 15, 2018): 1–12. http://dx.doi.org/10.1155/2018/9624175.

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Objectives. Cerebral ischemia can cause severe harm to people’s health with the characteristics of high incidence, high disability, and high mortality. Xingnaojing injection (XNJI) is widely used in the treatment of cerebral ischemia. The aim of this review is to evaluate the efficacy and mechanism of XNJI in animal models of cerebral ischemia. Methods. Total seven electronic databases in English or Chinese (CNKI, Wanfang, VMIS, PubMed, MEDLINE, Embase, and the Cochrane Library) about most experiments and studies which came out before June 2018 of XNJI for cerebral ischemia have been searched.

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Felberg, Robert A., W. Scott Burgin, and James C. Grotta. "Neuroprotection and the Ischemic Cascade." CNS Spectrums 5, no. 3 (March 2000): 52–58. http://dx.doi.org/10.1017/s1092852900012967.

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AbstractBrain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the “ischemic cascade”) that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted.Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clini

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Kamp, Marcel A., Maxine Dibué, Toni Schneider, Hans-Jakob Steiger, and Daniel Hänggi. "Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia." Stroke Research and Treatment 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/382146.

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Healthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion channel expression and function is initiated, with acute and long-term effects differing from each other. Initial hypoperfusion after exposure of cerebral vessels to oxyhemoglobin correlates with a suppression of voltage-gated potassium channel activity, whereas delayed cerebral vasospasm involves chan

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Pike, Brian R., Jeremy Flint, Jitendra R. Dave, X. C. May Lu, Kevin K. K. Wang, Frank C. Tortella та Ronald L. Hayes. "Accumulation of Calpain and Caspase-3 Proteolytic Fragments of Brain-Derived αII-Spectrin in Cerebral Spinal Fluid after Middle Cerebral Artery Occlusion in Rats". Journal of Cerebral Blood Flow & Metabolism 24, № 1 (січень 2004): 98–106. http://dx.doi.org/10.1097/01.wcb.0000098520.11962.37.

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Preclinical studies have identified numerous neuroprotective drugs that attenuate brain damage and improve functional outcome after cerebral ischemia. Despite this success in animal models, neuroprotective therapies in the clinical setting have been unsuccessful. Identification of biochemical markers common to preclinical and clinical cerebral ischemia will provide a more sensitive and objective measure of injury severity and outcome to facilitate clinical management and treatment. However, there are currently no effective biomarkers available for assessment of stroke. Nonerythroid αII-spectri

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Ma, Di, Liangshu Feng, Fang Deng, and Jia-Chun Feng. "Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6891645.

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Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in

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Okami, Nobuya, Purnima Narasimhan, Hideyuki Yoshioka, Hiroyuki Sakata, Gab Seok Kim, Joo Eun Jung, Carolina M. Maier, and Pak H. Chan. "Prevention of JNK Phosphorylation as a Mechanism for Rosiglitazone in Neuroprotection after Transient Cerebral Ischemia: Activation of Dual Specificity Phosphatase." Journal of Cerebral Blood Flow & Metabolism 33, no. 1 (October 3, 2012): 106–14. http://dx.doi.org/10.1038/jcbfm.2012.138.

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Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-γ (PPARγ) agonist, prevents cell death after cerebral ischemia in animal models, but the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone protects neurons against ischemia. Mice treated with rosiglitazone were subjected to 60 minutes of focal ischemia followed by reperfusion. Rosiglitazone reduced infarct volume after ischemia and reperfusion. We show that this neuroprotective effect was reversed with a PPARgM antagonist. Western blot analysis showed a significant increase in expressi

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Cheng, Jian, Nabil J. Alkayed, and Patricia D. Hurn. "Deleterious Effects of Dihydrotestosterone on Cerebral Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 27, no. 9 (February 21, 2007): 1553–62. http://dx.doi.org/10.1038/sj.jcbfm.9600457.

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Outcome from cerebral ischemia is sexually dimorphic in many experimental models. Male animals display greater sensitivity to ischemic injury than do their female counterparts; however, the underlying mechanism is unclear. The present study determined if the potent and nonaromatizable androgen, dihydrotestosterone (DHT), exacerbates ischemic damage in the male rat and alters postischemic gene expression after middle cerebral artery occlusion. At 22 h reperfusion, removal of androgens by castration provided protection from ischemic injury in both cortex and striatum (2,3,5-triphenyltetrazolium

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Harston, George WJ, Brad A. Sutherland, James Kennedy, and Alastair M. Buchan. "The Contribution of L-Arginine to the Neurotoxicity of Recombinant Tissue Plasminogen Activator following Cerebral Ischemia: A Review of rtPA Neurotoxicity." Journal of Cerebral Blood Flow & Metabolism 30, no. 11 (August 25, 2010): 1804–16. http://dx.doi.org/10.1038/jcbfm.2010.149.

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Alteplase is the only drug licensed for acute ischemic stroke, and in this formulation, the thrombolytic agent recombinant tissue plasminogen activator (rtPA) is stabilized in a solution of L-arginine. Improved functional outcomes after alteplase administration have been shown in clinical trials, along with improved histological and behavioral measures in experimental models of embolic stroke. However, in animal models of mechanically induced ischemia, alteplase can exacerbate ischemic damage. We have systematically reviewed the literature of both rtPA and L-arginine administration in mechanic

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Bowes, Mark P., Steven Swanson, and Justin A. Zivin. "The AMPA Antagonist LY293558 Improves Functional Neurological Outcome following Reversible Spinal Cord Ischemia in Rabbits." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 967–72. http://dx.doi.org/10.1097/00004647-199609000-00021.

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Glutamate (Glu) neurotoxicity is an important element of a number of neurological disorders including central nervous system (CNS) ischemia. We evaluated the effects of the novel AMPA Glu antagonist LY293558 on functional neurological outcome in two rabbit stroke models. In the reversible spinal cord ischemia model, ischemia of the caudal lumbar spinal cord was produced by temporary occlusion of the abdominal aorta. LY293558 was administered 5 min after recirculation as a 16 mg/kg i.v. bolus followed by 2.2 mg/kg infused over 1 h. Control animals received saline. LY293558 significantly increas

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Koehler, Raymond C., Zeng-Jin Yang, Jennifer K. Lee, and Lee J. Martin. "Perinatal hypoxic-ischemic brain injury in large animal models: Relevance to human neonatal encephalopathy." Journal of Cerebral Blood Flow & Metabolism 38, no. 12 (August 28, 2018): 2092–111. http://dx.doi.org/10.1177/0271678x18797328.

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Perinatal hypoxia-ischemia resulting in death or lifelong disabilities remains a major clinical disorder. Neonatal models of hypoxia-ischemia in rodents have enhanced our understanding of cellular mechanisms of neural injury in developing brain, but have limitations in simulating the range, accuracy, and physiology of clinical hypoxia-ischemia and the relevant systems neuropathology that contribute to the human brain injury pattern. Large animal models of perinatal hypoxia-ischemia, such as partial or complete asphyxia at the time of delivery of fetal monkeys, umbilical cord occlusion and cere

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Khan, Mohd Muazzam, Badruddeen, Mohd Mujahid, Juber Akhtar, Mohammad Irfan Khan, and Usama Ahmad. "An Overview of Stroke: Mechanism, In vivo Experimental Models Thereof, and Neuroprotective Agents." Current Protein & Peptide Science 21, no. 9 (December 11, 2020): 860–77. http://dx.doi.org/10.2174/1389203721666200617133903.

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Background: Stroke is one of the causes of death and disability globally. Brain attack is because of the acute presentation of stroke, which highlights the requirement for decisive action to treat it. Objective: The mechanism and in-vivo experimental models of stroke with various neuroprotective agents are highlighted in this review. Method: The damaging mechanisms may proceed by rapid, nonspecific cell lysis (necrosis) or by the active form of cell death (apoptosis or necroptosis), depending upon the duration and severity and of the ischemic insult. Results: Identification of injury mediators

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Hao, Jiukuan, and Ulrich Bickel. "Transferrin Receptor Mediated Brain Uptake During Ischemia and Reperfusion." Journal of Pharmacy & Pharmaceutical Sciences 16, no. 4 (September 16, 2013): 541. http://dx.doi.org/10.18433/j3b303.

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Purpose. Drug delivery by transferrin receptor-mediated transport at the blood-brain barrier has shown beneficial effects in animal models of stroke, but it is unclear whether receptor mediated uptake remains functional in the ischemic tissue. The present study addressed that question in a mouse model of brain focal ischemia, permanent or transient middle cerebral artery occlusion (MCAO). Methods. Brain accumulation of 125I-labeled 8D3, a mouse-specific transferrin receptor antibody, or of the isotype control UPC-10 used as vascular marker, was measured autoradiographically by phosphorimaging

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