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Journal articles on the topic 'Cerebral ischemia'
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1
Zhao, Ling, Qiwei Liao, Yueting Zhang, Shufen Tan, Shuqing Li, and Tingyu Ke. "Ischemic Postconditioning Mitigates Retinopathy in Tree Shrews with Diabetic Cerebral Ischemia." Journal of Diabetes Research 2020 (February 12, 2020): 1–10. http://dx.doi.org/10.1155/2020/6286571.
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Ischemic postconditioning (PC) is proved to efficiently protect diabetic patients with acute myocardial infarction from ischemia-reperfusion injury. We aimed to explore the protective roles of ischemic PC on diabetic retinopathy in tree shrews with diabetic cerebral ischemia. A diabetic tree shrew model was established through high-fat diet feeding combined with streptozotocin (STZ) injection, while cortical thrombotic cerebral ischemia was induced photochemically. Tree shrews were divided into the normal control group, sham operation group, diabetes mellitus group, diabetes mellitus+cerebral ischemia group, and diabetes mellitus+cerebral ischemia+PC group (in which the tree shrews with diabetic cerebral ischemia were treated with ischemic PC). H&E staining was used to examine the pathological changes in the retina, and immunohistochemistry was performed to determine the retinal expression of VEGF (vascular endothelial growth factor). The modeling resulted in 77% tree shrews with diabetes. Ischemic PC reduced the blood glucose levels in the tree shrews with diabetic cerebral ischemia. Tree shrews with diabetes had thinned retina with disordered structures, and these pathological changes were aggravated after cerebral ischemia. The retinopathy was alleviated after ischemic PC. Retina expression of VEGF was mainly distributed in the ganglion cell layer in tree shrews. Diabetes and cerebral ischemia increased retinal VEGF expression in a step-wise manner, while additional ischemic PC reduced retinal VEGF expression. Therefore, ischemic PC effectively alleviates retinopathy in tree shrews with diabetic cerebral ischemia, and this effect is associated with reduced retinal VEGF expression.
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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, although initial signals appear within hours of ischemia onset. Components of the neurovascular unit, its participation in new vessel formation, and the nature of the core and penumbra responses to experimental focal cerebral ischemia, are considered here. The potential co-localization of vascular remodeling and axonal outgrowth following focal cerebral ischemia based on the definition of tissue remodeling and the processes that follow ischemic stroke are also considered. The region of angiogenesis in the ischemic core and its surrounding tissue (ischemic periphery) may be a novel target for treatment. We summarize issues that are relevant to model studies of focal cerebral ischemia looking ahead to potential treatments.
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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 transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.
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Danilova, T. V. "Features of epilepsy in acute and chronic cerebral ischemia." Kazan medical journal 98, no. 6 (December 15, 2017): 877–83. http://dx.doi.org/10.17750/kmj2017-877.
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Aim. To study clinical features, functional and neuroimaging characteristics of the brain of patients with ischemic brain disease and epileptic seizures. Methods. 772 patients with acute and chronic cerebral ischemia (265 stroke patients with epileptic seizures and 174 patients with seizures on the background of chronic cerebral ischemia, and 203 patients with stroke and 130 patients with chronic cerebral ischemia without seizures) were comprehensively examined. The clinical neurological examination, electroencephalography, magnetic resonance imaging, ultrasound duplex scanning of extra- and intracranial arteries with the assessment of the level and degree of stenosis and cerebrovascular reactivity were carried out. Results. Focal seizures prevailed in patients with cerebral ischemia. In patients with epileptic seizures on the background of both ischemic stroke and chronic cerebral ischemia cortical localization of ischemic foci prevailed. Early epileptic seizures in patients with ischemic stroke developed with significantly more frequent localization of ischemic focus in the right hemisphere with the orientation vector of neuroimaging formation of the ischemic lesion in the caudal direction. In patients with chronic cerebral ischemia with epileptic seizures, along with frequent lesion of the cortex, more frequent damage of white matter of the brain was observed. In patients with acute and chronic ischemia of the brain with epileptic seizures, a higher incidence of stenosis of major arteries and predominance of impaired cerebrovascular reactivity in posterior cerebral circulation system were established. Conclusion. Multimodal examination of patients with acute and chronic cerebral ischemia allowed forming risk groups for epileptic seizures.
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Yamamoto, Kazumi, Fumiharu Akai, Toshiki Yoshimine, and Takehiko Yanagihara. "Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils." Journal of Neurosurgery 67, no. 3 (September 1987): 414–20. http://dx.doi.org/10.3171/jns.1987.67.3.0414.
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✓ Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving the neuropil, neuronal perikarya, and dendrites. The earliest lesion in the caudoputamen evolved after 30 minutes of ischemia. After reestablishment of cerebral circulation, the immunohistochemical ischemic lesions in the neuronal structure disappeared if the ischemic period was 10 minutes or less and partially disappeared even after ischemia for 15 minutes in the cerebral cortex, while the postischemic lesion in the caudoputamen disappeared even after ischemia for 15 minutes. Reactive astrocytes were detected in the cerebral cortex and caudoputamen as early as 24 hours after reperfusion, both in the areas with and without the neuronal lesions. No lesion was identified in the hippocampus or thalamus. This experimental model is suitable for investigation of rapidly progressive regional ischemia in the cerebral cortex and for comparison with other regional or global cerebral ischemia in the gerbil or other animal species.
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Duarte, Sinésio Grace, Antônio Dorival Campos, and Benedicto Oscar Colli. "Functional evaluation of temporary focal cerebral ischemia: experimental model." Arquivos de Neuro-Psiquiatria 61, no. 3B (September 2003): 751–56. http://dx.doi.org/10.1590/s0004-282x2003000500009.
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OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESULTS: There was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. CONCLUSION: Compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.
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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-adrenaline-induced systemic intravascular thrombosis in mice, thrombosis of carotid artery-jugular vein blood flow in the bypass of rats, and hypoxia tolerance in mice) were used to investigate the mechanisms underlying the actions of PNS on cerebral ischemia. The results indicated that (1) PNS improved neurological function and reduced the cerebral ischemia infraction area in MCAO rats; (2) PNS improved motor coordination function in rats with complete cerebral ischemia (blockade of four arteries), decreased Ca2+ levels, and ameliorated energy metabolism in the brains of ischemia rats; (3) PNS reduced thrombosis in common carotid artery-jugular vein blood flow in the bypass of rats; (4) PNS provided significant promise in antistroke hemiplegia and hypoxia tolerance in mice. In conclusion, PNS showed antagonistic effects on ischemic stroke, and pharmacological mechanisms are likely to be associated with the reduction of cerebral pathological damage, thrombolysis, antihypoxia, and improvement in the intracellular Ca2+ overload and cerebral energy metabolism.
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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 expressions of EPO could be detected in survival and necrotic neurons, glia as well as vascular endothelial cells. Focal cerebral ischemia promoted the expression of EPO. Significant enhanced EPO level was found in the ischemic peripheral zone after acupuncture preconditioning (P < 0.05). Conclusion Our results demonstrated that acupuncture preconditioning enhanced the expression of EPO in neurons, glia and vascular endothelial cells the ischemic peripheral zone, suggesting the involvement of EPO in acupuncture preconditioning-induced neuroprotection following focal cerebral ischemia. EPO may exert neuroprotective effects through promoting neurotrophic support and angiogenesis.
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Zeng, Xian-Si, Wen-Shuo Geng, Lei Chen, and Jin-Jing Jia. "Thioredoxin as a Therapeutic Target in Cerebral Ischemia." Current Pharmaceutical Design 24, no. 25 (November 8, 2018): 2986–92. http://dx.doi.org/10.2174/1381612824666180820143853.
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Background: Cerebral ischemia is a common cause of disability and death. Ischemic brain injury results from complex pathological processes, including oxidative stress, inflammation, and apoptosis. Thioredoxin( Trx) is an important multifunctional protein, which regulates cellular redox status. Increasing studies have demonstrated that Trx provides a neuroprotective role against cerebral ischemia-induced injury. Methods: A systematic search of PMC and the PubMed Database was conducted to summarize the protective effects of Trx against cerebral ischemia. Results: This article reviews the understanding of potential effects and mechanisms of Trx against cerebral ischemia, including the anti-oxidant, anti-apoptotic and anti-inflammatory effects, as well as the activation of prosurvival pathway. We also summarize that some natural compounds induce the expression of Trx, which is involved in their anti-ischemic effects. Conclusion: In conclusion, Trx has a potential neuroprotection in cerebral ischemia and may be very promising for clinical therapy of ischemic stroke in the future.
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Lee, Choong-Hyun, Tae-Kyeong Lee, Dae Won Kim, Soon Sung Lim, Il Jun Kang, Ji Hyeon Ahn, Joon Ha Park, et al. "Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury." International Journal of Molecular Sciences 23, no. 9 (May 3, 2022): 5096. http://dx.doi.org/10.3390/ijms23095096.
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Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe transient forebrain ischemia induced by blocking the blood supply to the forebrain for five or 15 min. Significant ischemia tFI-induced neuronal death occurred in the deep layers (layers V and VI) of the motor cortex: neuronal death occurred earlier and more severely in gerbils with severe ischemia than in gerbils with mild ischemia. Distinct astrogliosis was detected in layers V and VI. It gradually increased with time after both ischemiae. The astrogliosis was significantly higher in severe ischemia than in mild ischemia. The ischemia-induced increase of glial fibrillary acidic protein (GFAP; a maker of astrocyte) expression in severe ischemia was significantly higher than that in mild ischemia. However, GFAP-immunoreactive astrocytes were apparently damaged two days after both ischemiae. At five days after ischemiae, astrocyte endfeet around capillary endothelial cells were severely ruptured. They were more severely ruptured by severe ischemia than by mild ischemia. However, the number of astrocytes stained with S100 was significantly higher in severe ischemia than in mild ischemia. These results indicate that the degree of astrogliosis, including the disruption (loss) of astrocyte endfeet following ischemia and reperfusion in the forebrain, might depend on the severity of ischemia and that the degree of ischemia-induced neuronal damage may be associated with the degree of astrogliosis.
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Rehni, Ashish K., Pradeep Bhateja, and Nirmal Singh. "Diethyl dithiocarbamic acid, a possible nuclear factor kappa B inhibitor, attenuates ischemic postconditioning-induced attenuation of cerebral ischemia–reperfusion injury in mice." Canadian Journal of Physiology and Pharmacology 87, no. 1 (January 2009): 63–68. http://dx.doi.org/10.1139/y08-100.
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The present study was designed to pharmacologically investigate the possible role of nuclear factor kappa B (NF-κB) in the reversal of global cerebral injury induced by ischemia and reperfusion after ischemic postconditioning. Bilateral carotid artery occlusion for 17 min followed by reperfusion for 24 h was employed to produce ischemia- and reperfusion-induced cerebral injury in mice. Cerebral infarct size was measured by using triphenyltetrazolium chloride staining. Memory was evaluated using the Morris water maze test. The rotarod test was employed to assess motor incoordination. Bilateral carotid artery occlusion followed by reperfusion produced a marked increase in cerebral infarct size, impairment of memory, and motor coordination. A set of 5 episodes of carotid artery occlusion for a period of 10 s and reperfusion of 10 s (ischemic postconditioning) significantly prevented ischemia–reperfusion-induced cerebral infarct size and behavioral deficits measured in terms of loss of memory and motor coordination. Diethyl dithiocarbamic acid sodium salt trihydrate (DDA) (100 mg/kg, i.p.), an inhibitor of NF-κB, given 30 min before ischemia attenuated the beneficial effects of ischemic postconditioning. It may be concluded that the beneficial effects of ischemic postconditioning on global cerebral ischemia- and reperfusion-induced cerebral injury and behavioral deficits may involve activation of the NF-κB-linked pathway.
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Briones, Tess L., and Barbara Therrien. "Behavioral Effects of Transient Cerebral Ischemia." Biological Research For Nursing 1, no. 4 (April 2000): 276–86. http://dx.doi.org/10.1177/109980040000100404.
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CA1 neurons in the hippocampus, a brain structure involved in learning and memory, are selectively vulnerable to ischemic effects. In this study, the authors examined if duration of ischemia is directly related to extent of CA1 damage and degree of spatial learning deficit. Adult female Wistar rats received either 5-min or 10-min ischemia or sham surgery. Following recovery, rats were tested in the Morris water maze. Histological analysis showed moderate cell loss in CA1 (31%) and CA3 (12%) and minimal cell loss in CA2 (4%) with 5-min ischemia. Increased cell loss was seen in CA1 (68%), CA2 (16%), and CA3 (23%) with 10-min ischemia. Behavioral testing revealed that animals with 10-min ischemia have greater spatial learning deficits and they remain impaired across the test days compared to the 5-min ischemic group. Furthermore, degree of CA1 cell loss accounted for approximately 45% of the variance in spatial learning deficits in the ischemic group. The authors conclude that cell loss is largely confined to CA1 region in rats who received 5 and 10 min of ischemia and that increased ischemic duration results in persistent learning deficits in female rats; also, the degree of behavioral impairment is related to extent of CA1 cell loss.
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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 phosphorylation increased 6 hours after ischemia; however, there was an approximately 90% decrease in eNOS-Ser1177 phosphorylation observed 24 hours after ischemia that continued until at least 7 days after ischemia. Endothelial nitric oxide synthase monomer formation also increased 24 and 48 hours after ischemia ( P<0.05), and protein nitration progressed in parallel with monomerization. To assess the effect of a neuroprotective agent on eNOS dysfunction, we evaluated the effect of fasudil, a Rho-kinase inhibitor, on eNOS phosphorylation and dimerization. Postischemic treatment with fasudil suppressed lesion expansion and dephosphorylation and monomer formation of eNOS. In conclusion, functional deterioration of eNOS progressed after cerebral ischemia. Rho-kinase inhibitors can reduce ischemic lesion expansion as well as eNOS dysfunction in the ischemic brain.
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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 apoptosis was determined by TUNEL staining; the expressions of proteins were measured by immunohistochemistry, immunofluorescent labeling, and Western blotting. ARMET was found to be extensively upregulated in ischemic regions in a time-dependent manner. The expression of ARMET was neuronal in all examined structures in response to the ischemic insult. We also found that ARMET expression is earlier and more sensitive to ischemic stimulation than C/EBP homologous protein (CHOP). ER stress agent tunicamycin induced ARMET and CHOP expressions in the primary cultured neurons. Treatment with recombinant human ARMET promoted neuron proliferation and prevented from neuron apoptosis induced by tunicamycin. These results suggest that cerebral ischemia-induced ARMET expression may be protective to the neurons.
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Kitagawa, Kazuo, Masayasu Matsumoto, Takuma Mabuchi, Yoshiki Yagita, Toshiho Ohtsuki, Masatsugu Hori, and Takehiko Yanagihara. "Deficiency of Intercellular Adhesion Molecule 1 Attenuates Microcirculatory Disturbance and Infarction Size in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 18, no. 12 (December 1998): 1336–45. http://dx.doi.org/10.1097/00004647-199812000-00008.
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Recent evidence has shown crucial roles for cell-adhesion molecules in inflammation-induced rolling, adhesion, and accumulation of neutrophils in tissue. Intercellular adhesion molecule-1 (ICAM-1) is one of these adhesion molecules. Previous studies have shown marked reduction in the size of infarction after focal cerebral ischemia by depletion of granulocytes and administration of the antibody against ICAM-1. In the present study we investigated the role of ICAM-1 in the size of ischemic lesions, accumulation of granulocytes, and microcirculatory compromise in focal cerebral ischemia by using ICAM-1–knockout mice. Ischemic lesions were significantly mitigated in knockout mice after permanent and transient focal ischemia, even though the number of granulocytes in the infarcted tissue was almost the same between knockout and wild-type mice. Depletion of granulocytes further decreased the size of ischemic lesions after transient focal ischemia in ICAM-1–knockout mice. Microcirculation was reduced after focal ischemia, but it was better preserved in the cerebral cortex of knockout mice than that of wild-type mice. The present study demonstrated that ICAM-1 played a role in microcirculatory failure and subsequent development and expansion of infarction after focal cerebral ischemia. However, it is highly unlikely that ICAM-1 played a key role in accumulation of granulocytes after focal cerebral ischemia.
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Shin, Tae Hwan, Da Yeon Lee, Shaherin Basith, Balachandran Manavalan, Man Jeong Paik, Igor Rybinnik, M. Maral Mouradian, Jung Hwan Ahn, and Gwang Lee. "Metabolome Changes in Cerebral Ischemia." Cells 9, no. 7 (July 7, 2020): 1630. http://dx.doi.org/10.3390/cells9071630.
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Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and proteins. Yet, the metabolic and cellular pathologies of ischemic brain injury remain not fully elucidated, and the relationships among various pathological mechanisms are difficult to establish due to the heterogeneity and complexity of the disease. Metabolome-based techniques can provide clues about the cellular pathologic status of a condition as metabolic disturbances can represent an endpoint in biological phenomena. A number of investigations have analyzed metabolic changes in samples from cerebral ischemia patients and from various in vivo and in vitro models. We previously analyzed levels of amino acids and organic acids, as well as polyamine distribution in an in vivo rat model, and identified relationships between metabolic changes and cellular functions through bioinformatics tools. This review focuses on the metabolic and cellular changes in cerebral ischemia that offer a deeper understanding of the pathology underlying ischemic strokes and contribute to the development of new diagnostic and therapeutic approaches.
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Kinuta, Yuji, Haruhiko Kikuchi, Masatsune Ishikawa, Mieko Kimura, and Yoshinori Itokawa. "Lipid peroxidation in focal cerebral ischemia." Journal of Neurosurgery 71, no. 3 (September 1989): 421–29. http://dx.doi.org/10.3171/jns.1989.71.3.0421.
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✓ To verify whether lipid peroxidation is associated with focal cerebral ischemia, a unilateral middle cerebral artery occlusion was carried out in rats. The concentrations of various endogenous antioxidants in the ischemic center were measured, including α-tocopherol and ubiquinones as lipid-soluble antioxidants and ascorbate as a water-soluble antioxidant. At 30 minutes after ischemia, α-tocopherol decreased to 79% of baseline, reduced ubiquinone-9 to 73%, ubiquinone-10 to 66%, and reduced ascorbate to 76%. Six hours after ischemia, α-tocopherol decreased to 63% and reached a plateau, whereas reduced ubiquinones and reduced ascorbate declined further to 16% and 10%, respectively, 12 hours after ischemia and then reached plateau levels. These results suggest functional and durational differences between antioxidants and lipid peroxidation in this ischemic model. Although the reciprocal increase in oxidized ubiquinones during ischemia was not observed, that of oxidized ascorbate was noted. The complementary antioxidant system between cytoplasmic and membranous components, the combination α-tocopherol/ascorbate, was estimated from the calculated consumption ratio of these antioxidants on the basis that the loss of these reduced antioxidants is due to neutralization of free radicals. This system is suggested to play an important role in the early ischemic period. Urate also increased during ischemia. The possible involvement of the xanthine-xanthine oxidase system in initiating free radical reactions in cerebral ischemia is also discussed.
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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 cerebral microRNA levels, particularly those that target neuroprotective pathways. Therefore, we tested if resveratrol-mediated ischemic tolerance also alters microRNA expression with a goal to identify microRNAs that are amenable to manipulation to induce neuroprotection after cerebral ischemia. Hence, we tested the microRNA profiles in mouse brain following intraperitoneal administration of resveratrol that induced significant tolerance against transient focal ischemia. We analyzed microRNA profiles using microarrays from both Affymetrix and LC Sciences that contain probes for all known mouse microRNAs. The results show that there is no consistent change in any of the microRNAs tested between resveratrol and vehicle groups indicating that microRNAs play a minimal role in resveratrol-mediated cerebral ischemic tolerance.
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Liu, Zun-Jing, Wei Liu, Lei Liu, Cheng Xiao, Yu Wang, and Jing-Song Jiao. "Curcumin Protects Neuron against Cerebral Ischemia-Induced Inflammation through Improving PPAR-Gamma Function." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/470975.
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Cerebral ischemia is the most common cerebrovascular disease worldwide. Recent studies have demonstrated that curcumin had beneficial effect to attenuate cerebral ischemic injury. However, it is unclear how curcumin protects against cerebral ischemic injury. In the present study, using rat middle cerebral artery occlusion model, we found that curcumin was a potent PPARγagonist in that it upregulated PPARγexpression and PPARγ-PPRE binding activity. Administration of curcumin markedly decreased the infarct volume, improved neurological deficits, and reduced neuronal damage of rats. In addition, curcumin suppressed neuroinflammatory response by decreasing inflammatory mediators, such as IL-1β, TNF-α, PGE2, NO, COX-2, and iNOS induced by cerebral ischemia of rats. Furthermore, curcumin suppressed IκB degradation that was caused by cerebral ischemia. The present data also showed that PPARγinteracted with NF-κB-p65 and thus inhibited NF-κB activation. All the above protective effects of curcumin on cerebral ischemic injury were markedly attenuated by GW9662, an inhibitor of PPARγ. Our results as described above suggested that PPARγinduced by curcumin may play a critical role in protecting against brain injury through suppression of inflammatory response. It also highlights the potential of curcumin as a therapeutic agent against cerebral ischemia.
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Tranmer, Bruce I., Ted S. Keller, Glenn W. Kindt, and David Archer. "Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia." Journal of Neurosurgery 77, no. 2 (August 1992): 253–59. http://dx.doi.org/10.3171/jns.1992.77.2.0253.
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✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during the ischemic period. Local CBF in ischemic brain regions varied directly with CO, with a correlation coefficient of 0.89 (% change CBF/% change CO), while CBF in nonischemic brain was not affected by upward or downward manipulations of CO. The difference in these responses between ischemic and nonischemic brain was highly significant (p < 0.001). The results of this study show a profound loss of regulatory control in ischemic brain in response to alterations in CO, thereby suggesting that blood volume variations may cause significant changes in the intensity of ischemia. It is proposed that CO monitoring and manipulation may be vital for optimum care of patients with acute cerebral ischemia.
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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 treatment goals for both arterial and venous ICDs include perfusion recovery, reduction of cerebral ischemic injury, and preservation of the neuronal integrity of the involved region as soon as possible; however, therapy based on the current guidelines for either acute ischemic events or chronic cerebral ischemia is not ideal because the recurrence rate of AIS or CVST is still very high. Therefore, this review discusses the neuroprotective effects of four novel potential ICD treatments with high translation rates, known as the BE COOL treatments (Batroxobin, oxygEn, Conditioning, and cOOLing), and subsequently analyzes how BE COOL treatments are used in clinical settings. The combination of batroxobin, oxygen, conditioning, and cooling may be a promising intervention for preserving ischemic tissues.
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Chen, Chunli, Haiyun Qin, Jieqiong Tan, Zhiping Hu, and Liuwang Zeng. "The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia." Oxidative Medicine and Cellular Longevity 2020 (February 1, 2020): 1–12. http://dx.doi.org/10.1155/2020/5457049.
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The ubiquitin-proteasome pathway and autophagy-lysosome pathway are two major routes for clearance of aberrant cellular components to maintain protein homeostasis and normal cellular functions. Accumulating evidence shows that these two pathways are impaired during cerebral ischemia, which contributes to ischemic-induced neuronal necrosis and apoptosis. This review aims to critically discuss current knowledge and controversies on these two pathways in response to cerebral ischemic stress. We also discuss molecular mechanisms underlying the impairments of these protein degradation pathways and how such impairments lead to neuronal damage after cerebral ischemia. Further, we review the recent advance on the understanding of the involvement of these two pathways in the pathological process during many therapeutic approaches against cerebral ischemia. Despite recent advances, the exact role and molecular mechanisms of these two pathways following cerebral ischemia are complex and not completely understood, of which better understanding will provide avenues to develop novel therapeutic strategies for ischemic stroke.
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Bon, Elizabeth, Nataliya Maksimovich, Sergei Zimatkin, Oksana Ostrovskaya, and Nikita Kokhan. "Comparative Characteristics of the Ultrastructure of the Pyramidal Neurons of the Parietal Cortex in Cerebral Ischemia of Varying Severity." Annals of Clinical Cytology and Pathology 9, no. 1 (November 17, 2023): 1–6. http://dx.doi.org/10.47739/2475-9430.clinicalcytology.1147.
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Introduction: The ultra-structural characteristics of neuron organelles are important indicators of the degree of brain damage during ischemic exposure, which necessitates the study of changes in the ultrastructure of brain neurons. Methods: Models of subtotal, stepwise subtotal, partial and total cerebral ischemia were carried out on 24 outbred white male rats. Electron microscopy methods were used. Results: The data obtained indicate that with total cerebral ischemia the disturbances are more pronounced than with partial cerebral ischemia and stepwise subtotal cerebral ischemia. Conclusion: The data obtained, due to their novelty and relevance; represent a fundamental basis for further studies of neurons in various parts of the brain during cerebral ischemia, with subsequent implementation of the results into clinical practice.
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Peng, Cheng, Li-Ping Wang, Xia Tao, Xiao-Hui Dong, Chun-Fang Xu, Yu Jiang, Chun-Long Liu, et al. "Preventive Cold Acclimation Augments the Reparative Function of Endothelial Progenitor Cells in Mice." Cellular Physiology and Biochemistry 45, no. 1 (2018): 175–91. http://dx.doi.org/10.1159/000486356.
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Background/Aims: Chronic cold exposure may increase energy expenditure and contribute to counteracting obesity, an important risk factor for cerebrocardiovascular diseases. This study sought to evaluate whether preventive cold acclimation before ischemia onset might be a promising option for preventing cerebral ischemic injury. Methods: After a 14-day cold acclimation period, young and aged mice were subjected to permanent cerebral ischemia, and histological analyses and behavioral tests were performed. Mouse endothelial progenitor cells (EPCs) were isolated, their function and number were determined, and the effects of EPC transplantation on cerebral ischemic injury were investigated. Results: Preventive cold acclimation before ischemia onset increased EPC function, promoted ischemic brain angiogenesis, protected against cerebral ischemic injury, and improved long-term stroke outcomes in young mice. In addition, transplanted EPCs from cold-exposed mice had a greater ability to reduce cerebral ischemic injury and promote local angiogenesis compared to those from control mice, and EPCs from donor animals could integrate into the recipient ischemic murine brain. Furthermore, transplanted EPCs might exert paracrine effects on cerebral ischemic injury, which could be improved by preventive cold acclimation. Moreover, preventive cold acclimation could also enhance EPC function, promote local angiogenesis, and protect against cerebral ischemic injury in aged mice. Conclusions: Preventive cold acclimation before ischemia onset improved long-term stroke outcomes in mice at least in part via promoting the reparative function of EPC. Our findings imply that a variable indoor environment with frequent cold exposure might benefit individuals at high risk for stroke.
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Fisher, Wink S. "Cerebral Ischemia." Neurosurgery 30, no. 5 (May 1, 1992): 810. http://dx.doi.org/10.1097/00006123-199205000-00060.
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Westbrook, E. L. "Cerebral Ischemia." Neurology 42, no. 6 (June 1, 1992): 1259. http://dx.doi.org/10.1212/wnl.42.6.1259.
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Hacke, Werner, Michael Hennerici, Herman J. Gelmers, Gunter Kramer, and Alan T. Marty. "Cerebral Ischemia." Critical Care Medicine 20, no. 6 (June 1992): 910. http://dx.doi.org/10.1097/00003246-199206000-00043.
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Wintzen, A. R. "Cerebral ischemia." Clinical Neurology and Neurosurgery 93, no. 4 (January 1991): 358. http://dx.doi.org/10.1016/0303-8467(91)90127-b.
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Wintzen, A. R. "Cerebral ischemia." Journal of the Neurological Sciences 67, no. 2 (February 1985): 265. http://dx.doi.org/10.1016/0022-510x(85)90124-8.
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Wintzen, A. R. "Cerebral ischemia." Journal of the Neurological Sciences 104, no. 1 (July 1991): 118. http://dx.doi.org/10.1016/0022-510x(91)90230-5.
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Fisher, Wink S. "Cerebral Ischemia." Neurosurgery 30, no. 5 (May 1992): 810. http://dx.doi.org/10.1227/00006123-199205000-00060.
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Alger, J. R., A. Brunetti, G. Nagashima, and K. A. Hossmann. "Assessment of Postischemic Cerebral Energy Metabolism in Cat by 31P NMR: The Cumulative Effects of Secondary Hypoxia and Ischemia." Journal of Cerebral Blood Flow & Metabolism 9, no. 4 (August 1989): 506–14. http://dx.doi.org/10.1038/jcbfm.1989.74.
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The sensitivity of cerebral energy metabolism to ischemic and hypoxic stresses following global cerebral ischemia was evaluated in a cat model using 31P nuclear magnetic resonance (NMR) spectroscopic methods. Complete global cerebral ischemia of 5 to 10 min in length was produced at 1 h intervals by reversible arterial occlusion, permitting continuous monitoring of NMR and EEG. Ischemia appeared to produce slightly more severe energy failure in animals that had previously experienced an ischemic injury. Preischemic hypoxia (5% O2 for 5 min) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate, which were slightly amplified in animals that previously experienced ischemia.
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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 pathophysiological mechanisms of these ischemic conditions. It is important to understand the pathophysiology of cerebral ischemia in order to identify therapeutic strategies for prevention and treatment. Here, we review the neuropathologies that are caused by cerebral ischemia and discuss the mechanisms that occur in cerebral ischemia such as reduction of cerebral blood flow, hippocampal damage, white matter lesions, neuronal cell death, cholinergic dysfunction, excitotoxicity, calcium overload, cytotoxic oedema, a decline in adenosine triphosphate (ATP), malfunctioning of Na+/K+-ATPase, and the blood-brain barrier breakdown. Altogether, the information provided can be used to guide therapeutic strategies for cerebral ischemia.
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Lin, Ming-Cheng, Chien-Chi Liu, Yu-Chen Lin, and Ching-Wen Hsu. "Epigallocatechin Gallate Modulates Essential Elements, Zn/Cu Ratio, Hazardous Metal, Lipid Peroxidation, and Antioxidant Activity in the Brain Cortex during Cerebral Ischemia." Antioxidants 11, no. 2 (February 16, 2022): 396. http://dx.doi.org/10.3390/antiox11020396.
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Cerebral ischemia induces oxidative brain injury via increased oxidative stress. Epigallocatechin gallate (EGCG) exerts anti-oxidant, anti-inflammatory, and metal chelation effects through its active polyphenol constituent. This study investigates whether EGCG protection against cerebral ischemia-induced brain cortex injury occurs through modulating lipid peroxidation, antioxidant activity, the essential elements of selenium (Se), zinc (Zn), magnesium (Mg), copper (Cu), iron (Fe), and copper (Cu), Zn/Cu ratio, and the hazardous metal lead (Pb). Experimentally, assessment of the ligation group was performed by occlusion of the right common carotid artery and the right middle cerebral artery for 1 h. The prevention group was intraperitoneally injected with EGCG (50 mg/kg) once daily for 10 days before cerebral ischemia. The brain cortex tissues were homogenized and the supernatants were harvested for biochemical analysis. Results indicated that cerebral ischemia markedly decreased SOD, CAT, Mg, Zn, Se, and Zn/Cu ratio and increased malondialdehyde (MDA), Fe, Cu, and Pb in the ischemic brain cortex. Notably, pretreating rats with EGCG before ischemic injury significantly reversed these biochemical results. Our findings suggest that the neuroprotection of EGCG in the ischemic brain cortex during cerebral ischemia involves attenuating oxidative injury. Notably, this neuroprotective mechanism is associated with regulating lipid peroxidation, antioxidant activity, essential elements, Zn/Cu ratio, and hazardous metal Pb.
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Wang, Yang, Yongting Wang, and Guo-Yuan Yang. "MicroRNAs in Cerebral Ischemia." Stroke Research and Treatment 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/276540.
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The risk of ischemic stroke increases substantially with age, making it the third leading cause of death and the leading cause of long-term disability in the world. Numerous studies demonstrated that genes, RNAs, and proteins are involved in the occurrence and development of stroke. Current studies found that microRNAs (miRNAs or miRs) are also closely related to the pathological process of stroke. miRNAs are a group of short, noncoding RNA molecules playing important role in posttranscriptional regulation of gene expression and they have emerged as regulators of ischemic preconditioning and ischemic postconditioning. Here we give an overview of the expression and function of miRNAs in the brain, miRNAs as biomarkers during cerebral ischemia, and clinical applications and limitations of miRNAs. Future prospects of miRNAs are also discussed.
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Kim, Gyung W., Taku Sugawara, and Pak H. Chan. "Involvement of Oxidative Stress and Caspase-3 in Cortical Infarction after Photothrombotic Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (December 2000): 1690–701. http://dx.doi.org/10.1097/00004647-200012000-00008.
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Apoptosis-related cell death is linked to oxidative stress and caspases in experimental cerebral ischemia, However, the role of oxidative stress in caspase activation and subsequent apoptotic cell death after cerebral ischemia is unknown, The authors evaluated the role of oxidative stress in ischemic cerebral infarction after photothrombosis and the relation between oxidative stress and caspase-related cell death 6 and 24 hours after ischemia with and without U-74389G, a potent free radical scavenger (10 mg/kg, 30 minutes before and after ischemia induction). Reactive oxygen species, detected by hydroethidine oxidation, and cytosolic cytochrome c were detected in early ischemic lesions. Western blot analysis showed the cleaved form and the level of the proform of caspase-3 in the ischemic lesion 24 hours after ischemia. Decreased caspase-3 immunoreactivity was detected in the antioxidant-treated group after ischemia. Decreased DNA fragmentation and laddering were detected and the lesion was smaller in the treated group after ischemia compared with the untreated group. Oxidative stress and cytochrome c release occur in the ischemic lesion after photothrombotic ischemia. The free radical scavenger attenuated caspase-3 up-regulation, DNA fragmentation, and the final lesion. The authors concluded that oxidative stress may mediate caspase-related apoptotic cell death and subsequent cortical infarction after photothrombotic ischemia.
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Chen, Qun, Michael Chopp, Gordon Bodzin, and Hua Chen. "Temperature Modulation of Cerebral Depolarization during Focal Cerebral Ischemia in Rats: Correlation with Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (May 1993): 389–94. http://dx.doi.org/10.1038/jcbfm.1993.52.
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The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30°C, n = 4), normothermic (37°C, n = 4), and hyperthermic (40°C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes were measured using two active Ag–AgCl electrodes placed in the cortical lesion. Animals were killed 1 week after ischemia. The brains were sectioned and stained with hematoxylin and eosin, for evaluation of neuronal damage, and calculation of infarct volume. All animals exhibited an initial depolarization within 30 min of ischemia, followed by a single depolarization event in hypothermic animals, and multiple periodic depolarization events in both normothermic and hyperthermic animals. Hyperthermic animals exhibited significantly more (p < 0.05) DC potential deflections (n = 6.17 ± 0.67) than normothermic animals (n = 2.75 ± 0.96). The ischemic infarct volume (% of hemisphere) was significantly different for the various groups; hypothermic animals exhibited no measurable infarct volume, while the ischemic infarct volume was 10.2 ± 12.3% in normothermic animals and 36.5 ± 3.4% in hyperthermic animals (p < 0.05). A significant correlation was detected between the volume of infarct and number of depolarization events ( r = 0.90, p < 0.001). Our data indicate that body temperature has a profound effect on the number of ischemic depolarization events, and ischemic cell damage after transient MCA occlusion, and suggest a role for ischemic depolarizations in mediating ischemic cell damage.
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Pettigrew, L. Creed, Mary L. Holtz, Susan D. Craddock, Stephen L. Minger, Nathan Hall, and James W. Geddes. "Microtubular Proteolysis in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 16, no. 6 (November 1996): 1189–202. http://dx.doi.org/10.1097/00004647-199611000-00013.
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Calpain, a neutral protease activated by calcium, may promote microtubular proteolysis in ischemic brain. We tested this hypothesis in an animal model of focal cerebral ischemia without reperfusion. The earliest sign of tissue injury was observed after no more than 15 min of ischemia, with coiling of apical dendrites immunolabeled to show microtubule-associated protein 2 (MAP2). After 6 h of ischemia, MAP2 immunoreactivity was markedly diminished in the infarct zone. Quantitative Western analysis demonstrated that MAP2 was almost unmeasurable after 24 h of ischemia. An increase in calpain activity, shown by an antibody recognizing calpain-cleaved spectrin fragments, paralleled the loss of MAP2 immunostaining. Double-labeled immunofluorescent studies showed that intraneuronal calpain activity preceded evidence of MAP2 proteolysis. Perikaryal immunolabeling of τ protein became increasingly prominent between 1 and 6 h in neurons located within the transition zone between ischemic and unaffected tissue. Western blot experiments confirmed that dephosphorylation of τ protein occurred during 24 h of ischemia, but was not associated with significant loss of τ antigen. We conclude that focal cerebral ischemia is associated with early microtubular proteolysis caused by calpain.
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Rebel, Annette, John A. Ulatowski, Karena Joung, Enrico Bucci, Richard J. Traystman, and Raymond C. Koehler. "Regional cerebral blood flow in cats with cross-linked hemoglobin transfusion during focal cerebral ischemia." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 3 (March 1, 2002): H832—H841. http://dx.doi.org/10.1152/ajpheart.00880.2001.
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841, 2002. First published November 8, 2001; 10.1152/ajpheart. 00880.2001.—The beneficial effect of hemodilution on cerebral blood flow (CBF) during focal cerebral ischemia is mitigated by reduced arterial oxygen content (CaO2 ). In anesthetized cats subjected to permanent middle cerebral artery occlusion, the time course of regional CBF was evaluated after isovolemic exchange transfusion with either albumin or a tetrameric hemoglobin-based oxygen carrier. The transfusion started 30 min after arterial occlusion. We tested the hypothesis that bulk oxygen transport (CBF × CaO2 ) to ischemic tissue is increased by hemoglobin transfusion at a hematocrit of 18% compared with albumin-transfused cats at a hematocrit of 18% or control cats at a hematocrit of 30% and equivalent arterial pressure. In the nonischemic hemisphere, CBF increased selectively after albumin transfusion, and oxygen transport was similar among groups. In the ischemic cortex, albumin transfusion increased CBF, but oxygen transport was not increased above that of the control group. Hemoglobin transfusion increased both CBF and oxygen transport in the ischemic cortex above values in the control group, but the increase was delayed until 4 h of ischemia. Consequently, acute injury volume measured at 6 h of ischemia was not significantly attenuated. In contrast to the cortex, CBF in the ischemic caudate nucleus was not substantially increased by either albumin or hemoglobin transfusion. Therefore, in a large animal model of permanent focal ischemia in which transfusion starts 30 min after ischemia, tetrameric cross-linked hemoglobin transfusion can augment oxygen transport to the ischemic cortex, but the increase can be delayed and not necessarily provide protection. Moreover, an end-artery region such as the caudate nucleus is less likely to benefit from hemodilution.
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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 demonstrated that an imbalance in mitochondrial dynamics after cerebral ischemia, with or without reperfusion injury, plays an important role in the regulation of cell survival and infarct area size. Mitochondrial dysmorphology/dysfunction and inflammatory processes also occur after cerebral ischemia. Knowledge surrounding the mechanisms involved in the imbalance in mitochondrial dynamics following cerebral ischemia with or without reperfusion injury would help in the prevention or treatment of the adverse effects of cerebral injury. Therefore, this review aims to summarize and discuss the roles of mitochondrial dynamics, mitochondrial function, and inflammatory processes in cerebral ischemia with or without reperfusion injury from in vitro and in vivo studies. Any contradictory findings are incorporated and discussed.
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Hedayatpour, Azim, Maryam Shiasi, Peyman Modarresi, and Alieh Bashghareh. "Remote ischemic preconditioning combined with atorvastatin improves memory after global cerebral ischemia-reperfusion in male rats." Research Results in Pharmacology 8, no. 2 (June 14, 2022): 27–35. http://dx.doi.org/10.3897/rrpharmacology.8.75753.
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Introduction: Damage to hippocampus can occur through ischemia. Memory problems are among the most significant disabilities after stroke. Therefore, improving memory is of great interest in helping post-stroke patients. This study demonstrated that intraperitoneally injection of atorvastatin with a short cycle of ischemia-reperfusion in the left femoral artery improved hippocampal CA1 neurons injury and memory problems after global cerebral ischemia. Materials and methods: In this article survey, we used 64 animals. Rats were divided into 8 groups, (n=8). Group 1: control; group 2: sham; group 3: global cerebral ischemia (GCI) only; group 4: remote ischemic preconditioning (RIP) + GCI; group 5: GCI + atorvastatin (ATO); group 6: GCI + vehicle; group 7: RIP + GCI + ATO; group 8: RIP + GCI + vehicle. We created global cerebral ischemia (GCI) with 20 min occlusion of the Common carotid artery. Results and discussion: Remote ischemic preconditioning could improve rats performance in water maze tests along with a decrease in neuronal death. Also, atorvastatin combined with remote ischemic preconditioning was more effective for memory improvement and reduction of neuronal death. Inconsistent with our result, the function of the animals in the ischemia group was impaired. CA1 hippocampal neurons have an important role in memory and learning, and they can be damaged after cerebral ischemia. Therefore, ischemia can create memory problems. Remote ischemic preconditioning and atorvastatin had a neuroprotective effect and could improve rat performance in water maze test. Conclusion: This study showed that remote ischemic preconditioning with atorvastatin could improve CA1 neuronal injury and memory. Graphical abstract:
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Benveniste, Helene, and David S. Warner. "Glutamate, Microdialysis, and Cerebral Ischemia." Anesthesiology 110, no. 2 (February 1, 2009): 422–25. http://dx.doi.org/10.1097/aln.0b013e318194b620.
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Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis. By Helene Benveniste, Jørgen Drejer, Arne Schousboe, Nils H. Diemer. J Neurochem 1984; 43:1369-74. Reprinted with permission of Blackwell Publishing. Rats were implanted with 0.3-mm-diameter dialysis tubing through the hippocampus and subsequently perfused with Ringer's solution at a flow rate of 2 ml/min. Samples of the perfusate representing the extracellular fluid were collected over 5-min periods and subsequently analyzed for contents of the amino acids glutamate, aspartate, glutamine, taurine, alanine, and serine. Samples were collected before, during, and after a 10-min period of transient complete cerebral ischemia. The extracellular contents of glutamate and aspartate were increased, respectively, eight- and threefold during the ischemic period; the taurine concentration also was increased 2.6-fold. During the same period the extracellular content of glutamine was significantly decreased (to 68% of the control value), whereas the concentrations of alanine and serine did not change significantly during the ischemic period. The concentrations of gamma-aminobutyric acid (GABA) were too low to be measured reliably. It is suggested that the large increase in the content of extracellular glutamate and aspartate in the hippocampus induced by the ischemia may be one of the causal factors in the damage to certain neurons observed after ischemia.
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Hong, Pu, Feng-Xian Li, Ruo-Nan Gu, Ying-Ying Fang, Lu-Ying Lai, Yong-Wei Wang, Tao Tao, Shi-Yuan Xu, Zhi-Jian You, and Hong-Fei Zhang. "Inhibition of NLRP3 Inflammasome Ameliorates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice." Neural Plasticity 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/9163521.
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Sustained activation of NLRP3 inflammasome is closely related to diabetes and stroke. However, it is unknown whether NLRP3 inflammasome plays an essential role in stroke in diabetes. We aim to investigate the effect and the potential mechanism of NLRP3 inflammasome in diabetic mice with cerebral ischemia-reperfusion injury. A type 2 diabetic mouse model was induced by a high-fat diet and streptozotocin (STZ). Diabetic mice received MCC950 (the specific molecule NLRP3 inhibitor) or vehicle 60 minutes before the middle cerebral artery occlusion (MCAO) and reperfusion. MCC950 reduced the neurological deficit score of 24 h after cerebral ischemia reperfusion and improved the 28-day survival rate of cerebral ischemia-reperfusion injury in diabetic mice. Furthermore, we found that the mRNA transcription levels of NLRP3, IL-1β, and caspase-1 in the core ischemic area were remarkably amplified in diabetic mice with cerebral ischemia-reperfusion injury, whereas this phenomenon was obviously attenuated by MCC950 pretreatment. In conclusion, the NLRP3 inflammasome was involved in the complex diseases of diabetic stroke. MCC950, the NLRP3 specific inhibitor, ameliorated diabetic mice with cerebral ischemia-reperfusion injury and improved the 28-day survival rate during the recovery stage of ischemic stroke.
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Loddick, Sarah A., Andrew V. Turnbull, and Nancy J. Rothwell. "Cerebral Interleukin-6 is Neuroprotective during Permanent Focal Cerebral Ischemia in the Rat." Journal of Cerebral Blood Flow & Metabolism 18, no. 2 (February 1998): 176–79. http://dx.doi.org/10.1097/00004647-199802000-00008.
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Interleukin-6 (IL-6) is a neurotrophic cytokine expressed in both neurons and glia. The present study shows that cerebral ischemia produced by permanent occlusion of the middle cerebral artery (MCAO) produces a dramatic increase in IL-6 bioactivity in the ischemic hemisphere within 2 hours of MCAO (167 ± 55 IU versus sham: 50 ± 35 IU), with further increases at 8 hours (3,456 ± 1,162 IU) and 24 hours (6,088 ± 1,772 IU). In a separate series of experiments, intracerebroventricular injection of recombinant IL-6 (3,100 or 31,000 IU) significantly reduced ischemic brain damage after MCAO (to 52% and 65% of controls, respectively). The large increase in endogenous IL-6 bioactivity in response to ischemia, together with the marked neuroprotection produced by exogenous IL-6 suggest that this cytokine is an important endogenous inhibitor of neuronal death during cerebral ischemia.
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Li, Wangxiao, and Wei Zhang. "UTAC-Net: A Semantic Segmentation Model for Computer-Aided Diagnosis for Ischemic Region Based on Nuclear Medicine Cerebral Perfusion Imaging." Electronics 13, no. 8 (April 12, 2024): 1466. http://dx.doi.org/10.3390/electronics13081466.
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Cerebral ischemia has a high morbidity and disability rate. Clinical diagnosis is mainly made by radiologists manually reviewing cerebral perfusion images to determine whether cerebral ischemia is present. The number of patients with cerebral ischemia has risen dramatically in recent years, which has brought a huge workload for radiologists. In order to improve the efficiency of diagnosis, we develop a neural network for segmenting cerebral ischemia regions in perfusion images. Combining deep learning with medical imaging technology, we propose a segmentation network, UTAC-Net, based on U-Net and Transformer, which includes a contour-aware module and an attention branching fusion module, to achieve accurate segmentation of cerebral ischemic regions and correct identification of ischemic locations. Cerebral ischemia datasets are scarce, so we built a relevant dataset. The results on the self-built dataset show that UTAC-Net is superior to other networks, with the mDice of UTAC-Net increasing by 9.16% and mIoU increasing by 14.06% compared with U-Net. The output results meet the needs of aided diagnosis as judged by radiologists. Experiments have demonstrated that our algorithm has higher segmentation accuracy than other algorithms and better assists radiologists in the initial diagnosis, thereby reducing radiologists’ workload and improving diagnostic efficiency.
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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 VEGF, in the acute phase of cerebral ischemia. The effect of these angiogenic factors on the ischemic lesion volume was evaluated by magnetic resonance imaging. We observed that timely administration of VEGF exacerbates ischemic damage. In contrast, Ang2 decreases the ischemic volume and this beneficial effect is maintained in the presence of VEGF. This investigation reports, for the first time, a protective role of Ang2 following cerebral ischemia, an action associated with a reduced BBB permeability. We propose that Ang2 represents a pertinent molecular target for the treatment of cerebral ischemia since acute brain damage may be limited by a pharmacological protection of the vascular compartment.
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Juvela, Seppo, Matti Hillbom, and Markku Kaste. "Platelet thromboxane release and delayed cerebral ischemia in patients with subarachnoid hemorrhage." Journal of Neurosurgery 74, no. 3 (March 1991): 386–92. http://dx.doi.org/10.3171/jns.1991.74.3.0386.
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✓ Adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release were studied in 52 patients with subarachnoid hemorrhage (SAH) in order to detect a possible association between altered platelet function and development of cerebral ischemic complications after SAH. Compared to the values on admission, the patients showed significantly increased platelet aggregability (p < 0.05) and thromboxane release (p < 0.001) 1 to 2 weeks after SAH. The highest values of thromboxane release were seen in patients who deteriorated due to delayed cerebral ischemia with a permanent neurological deficit. Thromboxane release was significantly higher (p < 0.05) before the onset of severe delayed ischemia in six patients with preoperative ischemia compared to the patients without delayed ischemia. In five others, both ischemic deterioration and elevated thromboxane release occurred after operation. These patients had preoperative values similar to the values in those without ischemic symptoms. The observations suggest that increased platelet aggregability and thromboxane release are associated with delayed cerebral ischemia both before and after surgery.
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Vechkanova, N., and N. Melnikova. "Study of ischemic depolarization in focal cerebral ischemia in rats." Genetics and breeding of animals, no. 2 (August 26, 2022): 70–75. http://dx.doi.org/10.31043/2410-2733-2022-2-70-75.
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Purpose: to study ischemic depolarization in focal cerebral ischemia in rats.Materials and methods. We conducted simulations of focal cerebral ischemia in 30 rats. The animals were divided into three groups: 1) normothermia (n = 10), 2) hypothermia (n = 10), 3) hyperthermia (n = 10). We identified a statistically significant correlation between the animal's body temperature and the number of episodes of depolarization. (r = 0,87, p<0,001). The average number of DC potential deviations in animals with hyperthermia was statistically significantly higher than in animals with normothermia. (p<0,05).Results. Tissue damage as a result of focal cerebral ischemia correlates with body temperature fluctuations. A decrease in body temperature in focal cerebral ischemia leads to a decrease in the size of the ischemia zone, and as a result of a cerebral infarction, and vice versa, a slight increase in body temperature leads to an increase in the area of cerebral infarction.Conclusion. On tissue, temperature fluctuations have physiological and biochemical effects, a statistically significant correlation between episodes of depolarization in cerebral ischemia and the percentage of brain damage after ischemia are not always in a cause-and-effect relationship.
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Zhang, Fangyi, Sherry Xu, and Costantino Iadecola. "Time Dependence of Effect of Nitric Oxide Synthase Inhibition on Cerebral Ischemic Damage." Journal of Cerebral Blood Flow & Metabolism 15, no. 4 (July 1995): 595–601. http://dx.doi.org/10.1038/jcbfm.1995.73.
Full textAbstract:
Nitric oxide, a potent vasodilator and an inhibitor of platelet aggregation, may be beneficial in the early stages of focal cerebral ischemia as it may facilitate collateral blood flow to the ischemic territory. Accordingly, the effect of inhibition of nitric oxide synthesis on cerebral ischemic damage may vary depending on the timing of the inhibition relative to the induction of ischemia. We therefore studied the time course of the effect of nitric oxide synthesis inhibition on focal cerebral ischemic damage. The middle cerebral artery was permanently occluded in spontaneously hypertensive rats and the nitric oxide synthase (NOS) inhibitor nitro-l-arginine methyl ester (l-NAME) was administered systemically (3 mg/kg) <5 min or 2, 3, or 6 h later. Arterial pressure, rectal temperature, plasma glucose, and hematocrit were monitored. Infarct volume was determined on thioninstained sections 24 h after induction of ischemia. NOS activity was determined in cerebellum from the conversion of l-[3H]arginine to l-[3H]citrulline. Administration of l-NAME <5 min after arterial occlusion increased the infarct volume by 23 ± 14% (mean ± SD; p < 0.05, analysis of variance), while administration of l-NAME at 2 or 6 h did not affect the size of the infarct (p > 0.05). l-NAME administration 3 h after induction of ischemia reduced neocortical infarct size by 14 ± 11% (p < 0.05). l-NAME decreased cerebellar NOS activity comparably in all groups (range 16–25%). We conclude that the effects of inhibition of nitric oxide synthesis on focal cerebral ischemic damage are time dependent. Thus, inhibition of nitric oxide synthesis worsens ischemic damage when instituted shortly after induction of ischemia and does not affect or reduces damage at later times. The results support the hypothesis that the vascular actions of nitric oxide are beneficial only in the early stages of permanent focal cerebral ischemia.
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Bon, Lizaveta I., and Nataliya Y. Maksimovich. "Histological disorders of neurons of phylogenetically different parts of the cerebral cortex in partial, subtotal, stepwise subtotal, and total cerebral ischemia." Journal of Medical Science 90, no. 1 (March 24, 2021): e493. http://dx.doi.org/10.20883/medical.e493.
Full textAbstract:
Aim. Measure of the histological changes in neurons in the parietal cortex and hippocampus of rats with partial, subtotal, stepwise subtotal, and total cerebral ischemia. Material and Methods. Studies were performed on 84 rats. Partial cerebral ischemia was modelled by ligation of one common carotid artery. Subtotal cerebral ischemia was modelled by ligation of both common carotid arteries. Stepwise subtotal cerebral ischemia was performed by sequential ligation of both common carotid artery with 7-day, 3-day or 1-day intervals. Total cerebral ischemia (CI) was modelled by decapitation. Results. When comparing the morphological changes of neurons in the parietal cortex and hippocampus, we observed that, with the aggravation of the severity of cerebral ischemia, there was a progressive increase in the number of hyperchromic shrivelled neurons and neurons with pericellular oedema. Modelling of more severe types of ischemic damage lead to pronounced morphological changes in neurons – a decrease in size, deformation of the perikaryon, and increase in the degree of neuronal chromatophilia with their wrinkling. Conclusions. The smallest morphological changes in neurons were noted in the partial cerebral ischemia groups and subgroup 1 of stepwise subtotal cerebral ischemia, with an interval between common carotid artery dressings of 7 days. The most obvious morphological changes were observed in the conditions of total cerebral ischemia after 1 day. Changes in the parietal cortex and hippocampus were unidirectional, but in the parietal cortex, which is most sensitive to oxygen deficiency, they were more pronounced.