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Journal articles on the topic 'Cerebral ischemia – Treatment'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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1

Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata, and Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (March 6, 2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.

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The ischemic penumbra is both a concept in understanding the evolution of cerebral tissue injury outcome of focal ischemia and a potential therapeutic target for ischemic stroke. In this review, we examine the evidence that angiogenesis can contribute to beneficial outcomes following focal ischemia in model systems. Several studies have shown that, following cerebral ischemia, endothelial proliferation and subsequent angiogenesis can be detected beginning four days after cerebral ischemia in the border of the ischemic core, or in the ischemic periphery, in rodent and non-human primate models,

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Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia." Journal of Neurosurgery 77, no. 3 (September 1992): 337–54. http://dx.doi.org/10.3171/jns.1992.77.3.0337.

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✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The

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3

Wang, Lei, Xu Zhang, Xiaoxing Xiong, Hua Zhu, Ran Chen, Shudi Zhang, Gang Chen, and Zhihong Jian. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke." Antioxidants 11, no. 12 (November 30, 2022): 2377. http://dx.doi.org/10.3390/antiox11122377.

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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcript

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4

Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia." Journal of Neurosurgery 108, no. 3 (March 2008): 616–31. http://dx.doi.org/10.3171/jns/2008/108/3/0616.

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✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk,” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably inc

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Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia." Journal of Neurosurgery 77, no. 2 (August 1992): 169–84. http://dx.doi.org/10.3171/jns.1992.77.2.0169.

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✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk.” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably inc

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6

Han, Xue Mei, Hong Tao Wei, and Song Yan Liu. "Involvement of Erythropoietin Expression in Acupuncture Preconditioning-Induced Ischemic Tolerance." Advanced Materials Research 554-556 (July 2012): 1650–55. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1650.

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Abstract Objective To investigate the expression of erythropoietin (EPO) after acupuncture preconditioning plus focal cerebral ischemia treatment. Methods Rat focal cerebral ischemia model and acupuncture preconditioning model were established. Animals were randomly assigned into different groups: control (focal cerebral ischemia) and acupuncture preconditioning plus focal cerebral ischemia, with 8 rats for each group. The expression of EPO after different treatments was determined by histological examination, immunohistochemistry and in situ hybridization. Results The mRNA and protein express

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Song, Siying, Hao Wu, Xunming Ji, and Ran Meng. "The BE COOL Treatments (Batroxobin, oxygEn, Conditioning, and cOOLing): Emerging Adjunct Therapies for Ischemic Cerebrovascular Disease." Journal of Clinical Medicine 11, no. 20 (October 20, 2022): 6193. http://dx.doi.org/10.3390/jcm11206193.

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Ischemic cerebrovascular disease (ICD), the most common neurological disease worldwide, can be classified based on the onset time (acute/chronic) and the type of cerebral blood vessel involved (artery or venous sinus). Classifications include acute ischemic stroke (AIS)/transient ischemic attack (TIA), chronic cerebral circulation insufficiency (CCCI), acute cerebral venous sinus thrombosis (CVST), and chronic cerebrospinal venous insufficiency (CCSVI). The pathogenesis of cerebral arterial ischemia may be correlated with cerebral venous ischemia through decreased cerebral perfusion. The core

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Spetzler, Robert F. "Treatment of chronic cerebral ischemia." Surgical Neurology 23, no. 2 (February 1985): 201. http://dx.doi.org/10.1016/0090-3019(85)90350-7.

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9

Ghosh, Nilanjan, Rituparna Ghosh, Zulfiqar A. Bhat, Vivekananda Mandal, Sitesh C. Bachar, Namsa D. Nima, Otimenyin O. Sunday, and Subhash C. Mandal. "Advances in Herbal Medicine for Treatment of Ischemic Brain Injury." Natural Product Communications 9, no. 7 (July 2014): 1934578X1400900. http://dx.doi.org/10.1177/1934578x1400900739.

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Ischemic brain injury is one of the leading causes of death worldwide and has attracted a lot of attention in the field of drug discovery. Cerebral ischemia is a complex pathological process involving a series of mechanisms, including generation of free radicals, oxidative stress, disruption of the membrane function, release of neurotransmitters and apoptosis. Thrombolytic therapy is the most effective therapeutic strategy, but the benefits are far from being absolute. Increased attention in the field of drug discovery has been focused on using natural compounds from traditional medicinal herb

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10

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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Dong, Chao, Jiawei Li, Ming Zhao, Lin Chen, Xiaochen Zhai, Lingling Song, Jin Zhao, Qiang Sun, Jie Wu, and Xiaolu Xie. "Pharmacological Effect of Panax notoginseng Saponins on Cerebral Ischemia in Animal Models." BioMed Research International 2022 (August 4, 2022): 1–12. http://dx.doi.org/10.1155/2022/4281483.

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Panax notoginseng saponins (PNS), bioactive compounds, are commonly used to treat ischemic heart and cerebral diseases in China and other Asian countries. Most previous studies of PNS have focused on the mechanisms underlying their treatment of ischemic cardiovascular diseases but not cerebral ischemic diseases. This study sought to explore the pharmacological mechanisms underlying the effectiveness of PNS in treating cerebral ischemic diseases. Different experimental cerebral ischemia models (including middle cerebral artery occlusion (MCAO) and the blockade of four arteries in rats, collagen

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Ye, Hui, Zaiming Liu, Long Zhou, and Qiang Cai. "Dynamic Observation of the Effect of L-Theanine on Cerebral Ischemia-Reperfusion Injury Using Magnetic Resonance Imaging under Mathematical Model Analysis." Journal of Healthcare Engineering 2021 (October 26, 2021): 1–7. http://dx.doi.org/10.1155/2021/5679665.

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This study was to use the partial differential mathematical model to analyze the magnetic resonance imaging (MRI) images of cerebral ischemia-reperfusion injury (CIRI) and to dynamically observe the role of L-theanine in CIRI based on this. 30 patients with cerebral ischemia in a hospital in a certain area were selected and divided into a cerebral ischemia group and a L-theanine treatment group. The two groups of patients were examined by MRI within 48 hours, and the relative apparent diffusion coefficient (rADC) of the cerebral ischemic part of the patients was determined. The partial differe

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13

Lopez, Mary S., Robert J. Dempsey, and Raghu Vemuganti. "Resveratrol preconditioning induces cerebral ischemic tolerance but has minimal effect on cerebral microRNA profiles." Journal of Cerebral Blood Flow & Metabolism 36, no. 9 (July 21, 2016): 1644–50. http://dx.doi.org/10.1177/0271678x16656202.

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The health benefits of the plant-derived polyphenol resveratrol were established in multiple disease systems. Notably, pre-treatment with resveratrol was shown to be neuroprotective in several models of cerebral ischemia. Mechanisms of resveratrol-mediated neuroprotection have been explored in the context of canonical resveratrol targets, but epigenetic and non-coding RNA processes have not yet been evaluated. Resveratrol was shown to alter microRNAs in cancer and cardiac ischemia. Previous studies also showed that ischemic preconditioning that induces ischemic tolerance significantly alters c

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Li, Jin-hui, Jing Lu, and Hong Zhang. "Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with18F-Fluorodeoxyglucose MicroPET." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/507091.

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Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of18F-fluorodeoxyglucose (18F-FDG) micro positron emission tomography (microPET).Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit

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15

Yano, Toshiyuki, Sakiko Anraku, Ryosuke Nakayama, and Kazuo Ushijima. "Neuroprotective Effect of Urinary Trypsin Inhibitor against Focal Cerebral Ischemia–Reperfusion Injury in Rats." Anesthesiology 98, no. 2 (February 1, 2003): 465–73. http://dx.doi.org/10.1097/00000542-200302000-00028.

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Background Acute inflammatory reactions cause neuronal damage in cerebral ischemia-reperfusion. Urinary trypsin inhibitor (UTI), a serine protease inhibitor, is cytoprotective against ischemia-reperfusion injury in the liver, intestine, kidney, heart, and lung through its antiinflammatory activity. Neuroprotective action of UTI on transient global cerebral ischemia has been documented. This is the first study to determine whether UTI is neuroprotective against transient focal cerebral ischemia. Methods Adult male Wistar rats were randomly assigned to the following treatment groups: 0.9% saline

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Yagita, Yoshiki, Kazuo Kitagawa, Naoki Oyama, Toshiro Yukami, Akihiro Watanabe, Tsutomu Sasaki, and Hideki Mochizuki. "Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (July 3, 2013): 1532–39. http://dx.doi.org/10.1038/jcbfm.2013.112.

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Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ~ 8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177

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Pikis, Stylianos, Georgios Mantziaris, Vasileios Mamalis, Konstantinos Barkas, Antonios Tsanis, Stavroula Lyra, Kuriakos Karkoulias, Tigran Petrosyan, and Eftychios Archontakis. "Diffusion weighted image documented cerebral ischemia in the postprocedural period following pipeline embolization device with shield technology treatment of unruptured intracranial aneurysms: a prospective, single center study." Journal of NeuroInterventional Surgery 12, no. 4 (September 26, 2019): 407–11. http://dx.doi.org/10.1136/neurintsurg-2019-015363.

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ObjectiveAcute ischemic stroke and silent cerebral infarctions following pipeline embolization device (PED) treatment of intracranial aneurysms have been estimated to occur in 3–6% and in 50.9–90% of patients respectively. The PED with Shield technology (PED-Shield) incorporates a surface phosphorylcholine polymer to reduce the thrombogenicity of the implant. We sought to determine the incidence of diffusion weighted image (DWI) documented cerebral ischemia after PED-Shield treatment of unruptured intracranial aneurysms.MethodsThis prospective study involved a single center series of consecuti

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Yu, Yong-Qiang, Lian-Cheng Liu, Fa-Cai Wang, Yan Liang, Da-Qin Cha, Jing-Jing Zhang, Yu-Jun Shen, Hai-Ping Wang, Shengyun Fang, and Yu-Xian Shen. "Induction Profile of MANF/ARMET by Cerebral Ischemia and its Implication for Neuron Protection." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (September 23, 2009): 79–91. http://dx.doi.org/10.1038/jcbfm.2009.181.

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Cerebral ischemia-induced accumulation of unfolded proteins in vulnerable neurons triggers endoplasmic reticulum (ER) stress. Arginine-rich, mutated in early stage tumors (ARMET) is an ER stress-inducible protein and upregulated in the early stage of cerebral ischemia. The purposes of this study were to investigate the characteristics and implications of ARMET expression induced by focal cerebral ischemia. Focal cerebral ischemia in rats was induced by right middle cerebral artery occlusion with a suture; ischemic lesions were assessed by magnetic resonance imaging and histology; neuronal apop

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Savić, Tanja, Giuseppe Gambino, Vahid S. Bokharaie, Hamid R. Noori, Nikos K. Logothetis, and Goran Angelovski. "Early detection and monitoring of cerebral ischemia using calcium-responsive MRI probes." Proceedings of the National Academy of Sciences 116, no. 41 (September 23, 2019): 20666–71. http://dx.doi.org/10.1073/pnas.1908503116.

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Cerebral ischemia is one of the leading causes of mortality and disability in infants and adults and its timely diagnosis is essential for an efficient treatment. We present a methodology for fast detection and real-time monitoring of fluctuations of calcium ions associated with focal ischemia using a molecular functional MRI approach. We used a dinuclear paramagnetic gadolinium(III) complex chelate that changes MR image contrast through its reversible interaction with extracellular calcium ions, while applying a remote transient middle cerebral artery occlusion as a model for ischemic stroke.

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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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Jacewicz, Michael, Steve Brint, Jody Tanabe, Xing-Je Wang, and William A. Pulsinelli. "Nimodipine Pretreatment Improves Cerebral Blood Flow and Reduces Brain Edema in Conscious Rats Subjected to Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 10, no. 6 (November 1990): 903–13. http://dx.doi.org/10.1038/jcbfm.1990.147.

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The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 μg/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment i

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Jacewicz, Michael, Steve Brint, Jody Tanabe, and William A. Pulsinelli. "Continuous Nimodipine Treatment Attenuates Cortical Infarction in Rats Subjected to 24 Hours of Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 10, no. 1 (January 1990): 89–96. http://dx.doi.org/10.1038/jcbfm.1990.11.

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Focal cerebral infarction and edema were measured in rats (Wistar, Fisher 344, and spontaneously hypertensive strains) pretreated with nimodipine (2 μg/kg/min i.v.) or its vehicle and subjected to the tandem occlusion of the middle cerebral and common carotid arteries. Animals awoke from anesthesia 10–15 min after onset of ischemia and continued to receive treatment over a 24-h survival period. Cortical infarction and edema were quantified by image analysis of frozen brain sections processed for histology. Nimodipine-treated rats developed 20–60% smaller cortical infarct volumes than controls

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Sun, Jui-Ming, Ting-Lin Yen, Jing-Shiun Jan, Pharaoh Fellow Mwale, Ruei-Dun Teng, Rajeev Taliyan, Cheng-Ta Hsieh, and Chih-Hao Yang. "Advances in Antibody-Based Therapeutics for Cerebral Ischemia." Pharmaceutics 15, no. 1 (December 31, 2022): 145. http://dx.doi.org/10.3390/pharmaceutics15010145.

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Cerebral ischemia is an acute disorder characterized by an abrupt reduction in blood flow that results in immediate deprivation of both glucose and oxygen. The main types of cerebral ischemia are ischemic and hemorrhagic stroke. When a stroke occurs, several signaling pathways are activated, comprising necrosis, apoptosis, and autophagy as well as glial activation and white matter injury, which leads to neuronal cell death. Current treatments for strokes include challenging mechanical thrombectomy or tissue plasminogen activator, which increase the danger of cerebral bleeding, brain edema, and

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Vongsfak, Jirapong, Wasana Pratchayasakul, Nattayaporn Apaijai, Tanat Vaniyapong, Nipon Chattipakorn, and Siriporn C. Chattipakorn. "The Alterations in Mitochondrial Dynamics Following Cerebral Ischemia/Reperfusion Injury." Antioxidants 10, no. 9 (August 30, 2021): 1384. http://dx.doi.org/10.3390/antiox10091384.

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Cerebral ischemia results in a poor oxygen supply and cerebral infarction. Reperfusion to the ischemic area is the best therapeutic approach. Although reperfusion after ischemia has beneficial effects, it also causes ischemia/reperfusion (I/R) injury. Increases in oxidative stress, mitochondrial dysfunction, and cell death in the brain, resulting in brain infarction, have also been observed following cerebral I/R injury. Mitochondria are dynamic organelles, including mitochondrial fusion and fission. Both processes are essential for mitochondrial homeostasis and cell survival. Several studies

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Packard, Amy E. B., Jason C. Hedges, Frances R. Bahjat, Susan L. Stevens, Michael J. Conlin, Andres M. Salazar, and Mary P. Stenzel-Poore. "Poly-IC Preconditioning Protects against Cerebral and Renal Ischemia-Reperfusion Injury." Journal of Cerebral Blood Flow & Metabolism 32, no. 2 (November 16, 2011): 242–47. http://dx.doi.org/10.1038/jcbfm.2011.160.

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Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is

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Smirnov, Ivan E., A. A. Stepanov, L. D. Shakina, I. A. Belyaeva, E. P. Bombardirova, and A. G. Kucherenko. "Neurologic manifestations of cerebral ischemia in infants at 1 year of age." Russian Pediatric Journal 19, no. 5 (April 30, 2019): 274–82. http://dx.doi.org/10.18821/1560-9561-2016-19-5-274-282.

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Hypoxic-ischemic brain damage of the newborn infant to date is the one of the major problems in neonatology. The comprehensive clinical, laboratory and neurological examination of newborns of different gestational ages with perinatal CNS disorder was executed with the use of informative diagnostic technologies. Structural and functional disorders caused by cerebral ischemia, were established to be accompanied by significant changes in brain activity, the severity of which increases with decreasing gestational age of newborns. Certain concentrations of plasma factors of hemostasis in newborns w

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Zhang, Chan, Luming Zhen, Zongping Fang, Liang Yu, Yuanyuan Zhang, Haidong Wei, Junfeng Jia та Shiquan Wang. "Adiponectin Treatment Attenuates Cerebral Ischemia-Reperfusion Injury through HIF-1α-Mediated Antioxidation in Mice". Oxidative Medicine and Cellular Longevity 2021 (14 липня 2021): 1–16. http://dx.doi.org/10.1155/2021/5531048.

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Adiponectin (ADPN) plays an important role in cerebral ischemia-reperfusion injury. Although previous studies have confirmed that ADPN pretreatment has a protective effect on ischemic stroke, the therapeutic effect of ADPN on ischemic stroke and the underlying mechanism are still unclear. In order to clarify these questions, focal transient cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice and ADPN was administered for three times at 6 h, 24 h, and 48 h after reperfusion. Meanwhile, a virus-delivered HIF-1α siRNA was used before ADPN administration. The infarct v

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Marteau, Léna, Samuel Valable, Didier Divoux, Simon A. Roussel, Omar Touzani, Eric T. MacKenzie, Myriam Bernaudin, and Edwige Petit. "Angiopoietin-2 is Vasoprotective in the Acute Phase of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 3 (December 5, 2012): 389–95. http://dx.doi.org/10.1038/jcbfm.2012.178.

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Most forms of cerebral ischemia are characterized by damage to the entire neurovascular unit, which leads to an increase in the permeability of the blood–brain barrier (BBB). In response to permanent focal cerebral ischemia in mice, we detected an early concomitant increase in the expression of the vascular endothelial growth factor (VEGF), a key inducer of vascular leakage and pathological blood vessel growth, and of angiopoietin-2 (Ang2), which is closely associated with VEGF in vascular remodeling. Thus, the aim of this study was to evaluate the role of Ang2 alone, or in combination with VE

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Armstrong, SL. "Cerebral vasospasm: early detection and intervention." Critical Care Nurse 14, no. 4 (August 1, 1994): 33–37. http://dx.doi.org/10.4037/ccn1994.14.4.33.

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Many patients survive SAH with minimal neurologic deficits but are at risk for developing further neurologic insult from ischemia resulting from cerebral vasospasm. Nursing care of the patient experiencing vasospasm is challenging. The nurse who is knowledgeable about the signs and symptoms of cerebral ischemia and necessity for continually reviewing the patient's neurologic status can initiate prompt treatment to prevent further ischemic damage. Recognition of this critical problem is the first step toward combating its ominous effects.

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Du, Fang, Tao Tang, Qingzhu Li, and Jiaxin Liu. "Fyn Signaling in Ischemia-Reperfusion Injury: Potential and Therapeutic Implications." Mediators of Inflammation 2022 (September 15, 2022): 1–10. http://dx.doi.org/10.1155/2022/9112127.

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Ischemic stroke caused by arterial occlusion is the most common type of stroke and is one of the leading causes of disability and death, with the incidence increasing each year. Fyn is a nonreceptor tyrosine kinase belonging to the Src family of kinases (SFKs), which is related to many normal and pathological processes of the nervous system, including neurodevelopment and disease progression. In recent years, more and more evidence suggests that Fyn may be closely related to cerebral ischemia-reperfusion, including energy metabolism disorders, excitatory neurotoxicity, intracellular calcium ho

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Lim, Songhyun, Tae Jung Kim, Young-Ju Kim, Cheesue Kim, Sang-Bae Ko, and Byung-Soo Kim. "Senolytic Therapy for Cerebral Ischemia-Reperfusion Injury." International Journal of Molecular Sciences 22, no. 21 (November 4, 2021): 11967. http://dx.doi.org/10.3390/ijms222111967.

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Ischemic stroke is one of the leading causes of death, and even timely treatment can result in severe disabilities. Reperfusion of the ischemic stroke region and restoration of the blood supply often lead to a series of cellular and biochemical consequences, including generation of reactive oxygen species (ROS), expression of inflammatory cytokines, inflammation, and cerebral cell damage, which is collectively called cerebral ischemia-reperfusion (IR) injury. Since ROS and inflammatory cytokines are involved in cerebral IR injury, injury could involve cellular senescence. Thus, we investigated

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Pu, Fengling, Kenichi Mishima, Nobuaki Egashira, Yuki Akiyoshi, An-Xin Liu, Kazunori Sano, Keiichi Irie, et al. "Post-ischemic Treatment with Toki-Shakuyaku-San (Tang-Gui-Shao-Yao-San) Prevents the Impairment of Spatial Memory Induced by Repeated Cerebral Ischemia in Rats." American Journal of Chinese Medicine 33, no. 03 (January 2005): 475–89. http://dx.doi.org/10.1142/s0192415x05003077.

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Previously we have reported that Toki-shakuyaku-san (TSS) ameliorated the impairment of spatial memory induced by single cerebral ischemia (1 × 10 minutes ) and scopolamine, a muscarinic receptor antagonist. In this experiment, we studied the effect of TSS on repeated cerebral ischemia (2 × 10 minutes , 1-hour interval) induced impairment of spatial memory and neuronal injury in rats. The 8-day post-ischemic treatment with TSS (30–300 mg/kg) was administered p.o. once per day. TSS dose-dependently prevented the impairment of spatial memory, neuronal death and TUNEL positive cells induced by re

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Godínez-Rubí, Marisol, Argelia E. Rojas-Mayorquín, and Daniel Ortuño-Sahagún. "Nitric Oxide Donors as Neuroprotective Agents after an Ischemic Stroke-Related Inflammatory Reaction." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/297357.

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Cerebral ischemia initiates a cascade of detrimental events including glutamate-associated excitotoxicity, intracellular calcium accumulation, formation of Reactive oxygen species (ROS), membrane lipid degradation, and DNA damage, which lead to the disruption of cellular homeostasis and structural damage of ischemic brain tissue. Cerebral ischemia also triggers acute inflammation, which exacerbates primary brain damage. Therefore, reducing oxidative stress (OS) and downregulating the inflammatory response are options that merit consideration as potential therapeutic targets for ischemic stroke

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Liang, Jia, Zhifeng Qi, Wenlan Liu, Peng Wang, Wenjuan Shi, Wen Dong, Xunming Ji, Yumin Luo, and Ke Jian Liu. "Normobaric Hyperoxia Slows Blood–Brain Barrier Damage and Expands the Therapeutic Time Window for Tissue-Type Plasminogen Activator Treatment in Cerebral Ischemia." Stroke 46, no. 5 (May 2015): 1344–51. http://dx.doi.org/10.1161/strokeaha.114.008599.

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Background and Purpose— Prolonged ischemia causes blood–brain barrier (BBB) damage and increases the incidence of neurovasculature complications secondary to reperfusion. Therefore, targeting ischemic BBB damage pathogenesis is critical to reducing neurovasculature complications and expanding the therapeutic time window of tissue-type plasminogen activator (tPA) thrombolysis. This study investigates whether increasing cerebral tissue P O 2 through normobaric hyperoxia (NBO) treatment will slow the progression of BBB damage and, thus, improve the outcome of delayed tPA treatment after cerebral

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Lu, Hongwei, Yaqin Meng, Xinrui Han, and Wei Zhang. "ADAM8 Activates NLRP3 Inflammasome to Promote Cerebral Ischemia-Reperfusion Injury." Journal of Healthcare Engineering 2021 (December 16, 2021): 1–14. http://dx.doi.org/10.1155/2021/3097432.

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Stroke is the leading cause of death and disability in humans. Strokes are classified as either ischemic or hemorrhagic. Ischemic stroke accounts for 70–80% of the cases. Inflammation is a key factor in ischemic brain injury. Studies have shown that inflammatory response induced by NLRP3 inflammasome is one of the root causes of brain damage in mice with cerebral ischemia. However, its specific mechanism in cerebral ischemia is still unclear. ADAM8 (a disintegrin and metalloproteases 8) is a transmembrane protein with different functions. It plays an important role in tumors and neuroinflammat

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36

Bullock, R., D. I. Graham, S. Swanson, and J. McCulloch. "Neuroprotective Effect of the AMPA Receptor Antagonist LY-293558 in Focal Cerebral Ischemia in the Cat." Journal of Cerebral Blood Flow & Metabolism 14, no. 3 (May 1994): 466–71. http://dx.doi.org/10.1038/jcbfm.1994.57.

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The effects of the glutamate α-amino-3-hydroxy 5-methyl-4-isoxazole propionate (AMPA) receptor antagonist LY-293558 in reducing ischemic brain damage have been assessed in halothane-anesthetized cats. Focal cerebral ischemia was produced by permanent occlusion of one middle cerebral artery, and the animals were killed 6 h later. The amount of early irreversible ischemic damage was assessed at 16 predetermined stereotactic planes by an observer blinded to treatment paradigm employed. Treatment with LY-293558 (15 mg/kg i.v., plus infusion of 7 mg/kg/h) initiated 30 min prior to middle cerebral a

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37

Fan, Yan-Ying, Zhe Shen, Ping He, Lei Jiang, Wei-wei Hou, Yao Shen, Xiang-Nan Zhang, Wei-Wei Hu, and Zhong Chen. "A Novel Neuroprotective Strategy for Ischemic Stroke: Transient Mild Acidosis Treatment by CO2 Inhalation at Reperfusion." Journal of Cerebral Blood Flow & Metabolism 34, no. 2 (November 6, 2013): 275–83. http://dx.doi.org/10.1038/jcbfm.2013.193.

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Acidosis is one of the key components in cerebral ischemic postconditioning that has emerged recently as an endogenous strategy for neuroprotection. We set out to test whether acidosis treatment at reperfusion can protect against cerebral ischemia/reperfusion injury. Adult male C57BL/6 J mice were subjected to 60-minute middle cerebral arterial occlusion followed by 24-hour reperfusion. Acidosis treatment by inhaling 10%, 20%, or 30% CO2 for 5 or 10 minutes at 5, 50, or 100 minutes after reperfusion was applied. Our results showed that inhaling 20% CO2 for 5 minutes at 5 minutes after reperfus

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Regli, Luca, Mark C. Held, Robert E. Anderson, and Fredric B. Meyer. "Nitric Oxide Synthase Inhibition by L-NAME Prevents Brain Acidosis during Focal Cerebral Ischemia in Rabbits." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 988–95. http://dx.doi.org/10.1097/00004647-199609000-00024.

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This experiment examined the effects of nitric oxide (NO) synthase inhibition on brain intracellular pH, regional cortical blood flow, and NADH fluorescence before and during 3 h of focal cerebral ischemia using in vivo fluorescence imaging. Thirty fasted rabbits under 1% halothane were divided into four treatment groups receiving Nω-nitro-L-arginine methyl ester (L-NAME) intravenously at 20 min prior to ischemia (0.1, I, and 10 mg/kg and 1 mg/kg + 5 mg/kg L-arginine) and two control groups (nonischemic and ischemic). In ischemic controls, brain pHi declined to 6.73 ± 0.03 at 30 min and remain

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Schulz, Mette K., Lars Peter Wang, Mogens Tange, and Per Bjerre. "Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage." Journal of Neurosurgery 93, no. 5 (November 2000): 808–14. http://dx.doi.org/10.3171/jns.2000.93.5.0808.

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Object. The success of treatment for delayed cerebral ischemia is time dependent, and neuronal monitoring methods that can detect early subclinical levels of cerebral ischemia may improve overall treatment results. Cerebral microdialysis may represent such a method. The authors' goal was to characterize patterns of markers of energy metabolism (glucose, pyruvate, and lactate) and neuronal injury (glutamate and glycerol) in patients with subarachnoid hemorrhage (SAH), in whom ischemia was or was not suspected.Methods. By using low-flow intracerebral microdialysis monitoring, central nervous sys

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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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Iwata, Naohiro, Hiroko Takayama, Meiyan Xuan, Shinya Kamiuchi, Hirokazu Matsuzaki, Mari Okazaki, and Yasuhide Hibino. "Effects of Etanercept against Transient Cerebral Ischemia in Diabetic Rats." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/189292.

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Diabetes mellitus is known to exacerbate acute cerebral ischemic injury. Previous studies have demonstrated that infarction volumes caused by transient cerebral ischemia were greater in diabetic rats than in nondiabetic rats. Tumor necrosis factor-α(TNF-α) is a proinflammatory protein produced in the brain in response to cerebral ischemia that promotes apoptosis. Etanercept (ETN), a recombinant TNF receptor (p75)-Fc fusion protein, competitively inhibits TNF-α. Therefore, we evaluated the neuroprotective effects of chronic or acute treatment with ETN on cerebral injury caused by middle cerebra

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Zakharov, V. V., V. V. Grinyuk, N. V. Vakhnina, and E. Yu Kalimeeva. "Treatment of comorbid patients with chronic brain ischemia and vertebrogenic pain syndromes." Medical Council, no. 9 (June 12, 2019): 15–20. http://dx.doi.org/10.21518/2079-701x-2019-9-15-20.

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Chronic brain ischemia and chronic pain both appear to be an extremely wide-spread disease. The reasons of widespread comorbidity of ischemic brain disease and chronic pain are common risk factors: old age, decrease of physical activity, syndrome of systemic inflammation and emotional disturbances. Treatment of patients with cerebrovascular diseases and chronic pain should influence common mechanisms of these disorders. Correction of microcirculatory disturbances pays particular important role, because this is the mechanism not only of chronic cerebral ischemia but compressive-ischemic radicul

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ISHIKAWA, Tatsuya. "Advancement in Treatment for Ischemic Cerebral Ischemia in the Acute Stage." Surgery for Cerebral Stroke 33, no. 2 (2005): 85–88. http://dx.doi.org/10.2335/scs.33.85.

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Koerner, Ines P., Matthias Gatting, Ruediger Noppens, Oliver Kempski, and Ansgar M. Brambrink. "Induction of Cerebral Ischemic Tolerance by Erythromycin Preconditioning Reprograms the Transcriptional Response to Ischemia and Suppresses Inflammation." Anesthesiology 106, no. 3 (March 1, 2007): 538–47. http://dx.doi.org/10.1097/00000542-200703000-00019.

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Background A single dose of the macrolide antibiotic erythromycin can induce tolerance against cerebral ischemia in vivo (pharmacologic preconditioning). This study identified potential mechanisms of tolerance induction by assessing effects of erythromycin preconditioning on the cerebral transcriptional response to transient global cerebral ischemia. Methods Preconditioned and nonpreconditioned rats were exposed to 15 min of global cerebral ischemia, and changes in cerebral gene expression were identified by complementary DNA expression array and quantified by real-time reverse-transcription p

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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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Chen, Jun, Roger P. Simon, Tesuya Nagayama, Raymond Zhu, J. Eric Loeffert, Simon C. Watkins, and Steven H. Graham. "Suppression of Endogenous bcl-2 Expression by Antisense Treatment Exacerbates Ischemic Neuronal Death." Journal of Cerebral Blood Flow & Metabolism 20, no. 7 (July 2000): 1033–39. http://dx.doi.org/10.1097/00004647-200007000-00002.

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Previous studies have shown that overexpression of bcl-2 in transgenic mice or by viral vectors protects the brain against cerebral ischemia. However, it is not known whether bcl-2, which is endogenously expressed in response to ischemia, exerts a protective effect. To address this question, the authors blocked the endogenous expression of bcl-2 after ischemia using antisense oligodeoxynucleotides (ODN). Antisense, sense, scrambled ODN, or vehicles were infused in the lateral ventricle of the rat for 24 hours after 30 minutes of temporary middle cerebral artery occlusion. Twenty-four hours lat

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Caraban, B. M., Aurelia Romila, L. T. Hangan, and Mihaela Lungu. "Cerebral Vasospasm in Subarachnoid Hemorrhage Through Aneurysm Rupture - Clinical Considerations and Case Report." ARS Medica Tomitana 22, no. 4 (November 1, 2016): 232–38. http://dx.doi.org/10.1515/arsm-2016-0040.

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Abstract Arterial aneurysm ruptures of the circle of Willis determine subarachnoid hemorrhage, which evolving due to the irritating effect of the blood in the subarachnoid space may lead to complications such as large arterial vasospasm in the origin of the large cerebral arteries, from the base of the brain. Cerebral vasospasm causes a downstream cerebral ischemia, that may lead to the establishment of an ischemic stroke which is life threatening. Early treatment against the vasospasm with calcium channels blockers should prevent occurrence of ischemia. However, the effectiveness of this trea

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Sharma, Shyam S., Shankar Munusamy, Meenakshisundaram Thiyagarajan, and Chaman L. Kaul. "Neuroprotective effect of peroxynitrite decomposition catalyst and poly(adenosine diphosphate—ribose) polymerase inhibitor alone and in combination in rats with focal ischemia." Journal of Neurosurgery 101, no. 4 (October 2004): 669–75. http://dx.doi.org/10.3171/jns.2004.101.4.0669.

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Object. The authors evaluated the neuroprotective effect of 5,10,15,20-tetrakis(N-methyl-4′-pyridyl)porphyrinatoiron(III) (FeTMPyP), a peroxynitrite decomposition catalyst, and 1,5-isoquinolinediol (ISO), a poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor, alone and in combination in rats with focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Methods. Male Sprague—Dawley rats were subjected to 2 hours of MCAO followed by 22 hours of reperfusion. Cerebral infarction and neurological deficits were estimated after ischemia. Intraperitoneal injections

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Fedin, A. I. "Diagnosis and treatment of chronic cerebral ischemia." Consilium Medicum 18, no. 2 (2016): 8–12. http://dx.doi.org/10.26442/2075-1753_2016.2.8-12.

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Zakharov, V. V., N. V. Vakhnina, A. G. Gogoleva, and S. K. Mezhmidinova. "Diagnostics and treatment of chronic cerebral ischemia." Meditsinskiy sovet = Medical Council, no. 8 (July 16, 2020): 36–45. http://dx.doi.org/10.21518/2079-701x-2020-8-36-45.

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5560 patients with the diagnosis “Other cerebral vascular diseases” per 100 000 of elderly population were registered in RF in 2017. Usually this is a code for chronic brain ischemia (CBI) – the most popular diagnosis in Russian neurological practice. However, diagnostic criteria of CBI are not well defined and need to be ascertained. Recent studies show that the most reliable clinical feature of CBI could be cognitive impairment. It is developed before other clinical signs and correlate with severity of vascular brain lesions. Typically, cognitive impairment is subcortical with prominent brad

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