Middle cerebral arteryRenal ischemia-reperfusion injuryApoptosisMCAOResult from Focal cerebralStrokeNeuronsOcclusionCerebral ischaemiaInjury in ratsIpsilateralGlobal ischemiaTherapeuticNeurologicalMetabolismExperimentalIntracerebral hemorrhageMicrovascular damageHypothermiaNeurologic deficitsBlood brain bDamageDeficitsDysfunctionMetabolicPathophysiologyRegulatesHypoxiaReactive OxygenPathophysiologicalCapillariesCorticalPostconditioningHydrogenVivoInflammationFemale ratsMitochondrialHippocampusPathogenesisInhibitsModelBrains
Middle cerebral artery5
- Experimental stroke (transient focal cerebral ischemia) was induced by a 2-hour middle cerebral artery occlusion (MCAO) with the use of a suture inserting into the lumen of the internal carotid artery (ICA) in male Wistar rats. (banglajol.info)
- Middle Cerebral Artery Occlusion Allowing Reperfusion via Common Carotid Artery Repair in Mice JOVE-JOURNAL OF VISUALIZED EXPERIMENTS. (nottingham.ac.uk)
- Adeno-associated viral (AAV)-NRP-1 was stereotaxically inoculated into the cortex and ipsilateral striatum posterior of adult male Sprague-Dawley (SD) rats before a 90-min transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion. (biomedcentral.com)
- The model used in this study was established by middle cerebral artery occlusion (MCAO) and reperfusion. (biomedcentral.com)
- Cerebral ischaemia is caused by middle cerebral artery occlusion, which leads to some brain tissue damage, accompanied by inflammation and immune response [ 2 ]. (biomedcentral.com)
Renal ischemia-reperfusion injury1
Apoptosis10
- Apoptosis is one of the major mechanisms that lead to neuronal death after cerebral ischemia and reperfusion. (springer.com)
- We found remifentanil postconditioning markedly improved the spatial learning and memory as well as attenuated neuronal apoptosis in hippocampus caused by cerebral ischemia/reperfusion injury. (springer.com)
- The results suggest that remifentanil postconditioning exhibits neuroprotective effects against global cerebral ischemia/reperfusion injury in rats, and its mechanisms might involve inhibition of neuronal apoptosis through the PI3K pathway. (springer.com)
- Ding ZM, Wu B, Zhang WQ et al (2012) Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the same effect on inhibition of apoptosis. (springer.com)
- Yuan Y, Guo Q, Ye Z et al (2011) Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (springer.com)
- Excitotoxic production of ROS elevates death-associated protein kinase (DAPK) activity, which provokes neuronal apoptosis in cerebral ischemia and seizure models 8 . (nature.com)
- A study has shown that neurons in the ischemic penumbra may undergo apoptosis hours or days after ischemia and alleviating ischemia reperfusion injury is an achievable therapeutic goal in the early intervention of ischemic stroke aimed at limiting the amount of infarction ( 4 ). (spandidos-publications.com)
- The cascade of events leading to neuronal injury and death in ischemia includes the release of cytokines and free radicals, and induction of inflammation, apoptosis, and excitotoxicity [ 1 ]. (biomedcentral.com)
- 6. Xing B, Chen H, Zhang M, Zhao D, Jiang R, Liu X, Zhang S. Ischemic postconditioning inhibits apoptosis after focal cerebral ischemia/reperfusion injury in the rat. (ac.ir)
- 7. Yuan Y, Guo Q, Ye Z, Pingping X, Wang N, Song Z. Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (ac.ir)
MCAO4
- A model of cerebral ischemia‑reperfusion was established using the MCAO method. (spandidos-publications.com)
- These results suggested that HSP90β is involved in the process of cerebral ischemia‑reperfusion injury in rats and that inhibition of HSP90β expression increases EAAT2 levels, conferring a neuroprotective effect in MCAO model rats. (spandidos-publications.com)
- The rats were subjected to MCAO for 2 h and killed after reperfusion 24 h. (cnki.net)
- Adequacy of MCAO and reperfusion was monitored with laser-Doppler flowmetry over the ipsilateral parietal cortex. (utmb.edu)
Result from Focal cerebral2
- Neuronal loss in the hippocampus, regarded as one of the basic pathological mechanisms underlying cognitive impairment, can result from Focal cerebral ischemia-reperfusion. (medindia.net)
- Ischemic stroke is sudden neurologic deficits that result from focal cerebral ischemia associated with permanent brain infarction (eg, positive results on diffusion-weighted MRI). (msdmanuals.com)
Stroke12
- The objective of the present study was to determine whether an alternate MMP activatable probe with a shorter optical imaging time, MMPSense ™ 750 FAST (MMPSense750), could be used for visualization of MMP activity in the early stages of ischemia reperfusion in a mouse model of stroke. (biomedcentral.com)
- Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage. (wikipedia.org)
- citation needed] Other pathological events that may result in brain ischemia include cardiorespiratory arrest, stroke, and severe irreversible brain damage. (wikipedia.org)
- Therefore, an effective therapeutic strategy is required to prevent the onset of acute stroke and manage the chronic symptoms associated with neural ischemia, i.e., long-term neuroinflammation and localized necrosis [ 8 , 9 ]. (hindawi.com)
- Graphical presentation of the various stages of cerebral ischemia stroke, i.e., acute phase, subacute phase, and chronic phase and their contributing factors. (hindawi.com)
- In stroke, the ischemic crisis activates a series of events, including the inflammatory reactions that are potentiated by reperfusion, eventually leading to neuronal damage. (banglajol.info)
- An ischemic stroke consists of two related pathological injury processes: Primary ischemia-induced brain injury and secondary ischemia reperfusion injury ( 3 ). (spandidos-publications.com)
- When ischemic stroke occurs, cerebral ischemia and hypoxia cause the release of excessive excitatory amino acids, mainly glutamic acid and aspartic acid, which exert excitotoxic effects on the central nervous system. (spandidos-publications.com)
- Pre-stroke surgery is not beneficial to normotensive rats undergoing sixty minutes of transient focal cerebral ischemia PLOS ONE. (nottingham.ac.uk)
- According to the theory of TCM, cerebral ischaemia, which is also called stroke, can be induced by hyperactivity of liver Yang, disordered diet, stagnation of blood, etc. (biomedcentral.com)
- Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
- Neuronally derived NO has been shown to be deleterious in the male but not in the female rodent model of focal ischemic stroke. (utmb.edu)
Neurons3
- Global cerebral ischemia followed by reperfusion, which leads to extensive neuronal damage, particularly the neurons in the hippocampal CA1 region. (springer.com)
- Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. (nih.gov)
- Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
Occlusion2
- Global cerebral ischemia was performed via 10 min of four-vessel occlusion. (springer.com)
- Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. (nih.gov)
Cerebral ischaemia3
- Burggraf D, Vosko MR, Schubert M, Stassen JM, Hamann GF Different therapy options protecting microvasculature after experimental cerebral ischaemia and reperfusion. (mpg.de)
- The abundance and diversity of the intestinal flora in rats decreased after cerebral ischaemia - reperfusion injury (CIRI). (biomedcentral.com)
- According to the World Health Organization, cerebral ischaemia is the second leading cause of death and the third leading cause of disability in the world [ 1 ]. (biomedcentral.com)
Injury in rats3
- Here we investigated whether remifentanil postconditioning exerts neuroprotective effects against global cerebral ischemia/reperfusion injury in rats and its potential mechanisms. (springer.com)
- Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
- 4. Ren C, Gao X, Niu G, Yan Z, Chen X, Zhao H. Delayed postconditioning protects against focal ischemic brain injury in rats. (ac.ir)
Ipsilateral3
- Images were acquired starting at 2 or 24 hours after reperfusion over the ipsilateral and contralateral cortex before and for 3 hours after, MMPSense750 was injected. (biomedcentral.com)
- The clinical presentation of cerebral reperfusion syndrome varies but generally includes components of the following triad: 1) ipsilateral headache, 2) contralateral focal neurologic deficits, and/or 3) seizures. (medscape.com)
- Cerebral reperfusion syndrome presents with ipsilateral headache, contralateral focal neurologic deficits, and/or seizures, but a complete triad is not required for diagnosis. (medscape.com)
Global ischemia2
- and global ischemia, which encompasses wide areas of brain tissue. (wikipedia.org)
- Charron C, Messier C, Plamondon H (2008) Neuroprotection and functional recovery conferred by administration of kappa- and delta 1-opioid agonists in a rat model of global ischemia. (springer.com)
Therapeutic1
- Background and Purpose - We demonstrated previously that treatment with selective κ-opioid receptor (KOR) agonist BRL 52537 hydrochloride [(±)-1-(3,4-dichlorophenyl) acetyl-2-(1-pyrrolidinyl) methylpiperidine] (1) has a long therapeutic window for providing ischemic neuroprotection, and (2) attenuates ischemia-evoked NO production in vivo in rats. (utmb.edu)
Neurological3
- Cerebrovascular diseases (CVDs) have become a global public health problem and ischemia‑reperfusion injury, the major cause of neurological impairment exacerbation, is closely related to excitotoxicity. (spandidos-publications.com)
- They were evaluated at 24 h after reperfusion for brain infarction, neurological deficit score, and the expression of 5-LOX. (biomedcentral.com)
- Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)
Metabolism1
- Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis. (wikipedia.org)
Experimental7
- Propofol has been shown to attenuate brain injury in experimental ischemia models, but few studies have focused on the direct effect of propofol on mitochondrial dysfunction. (nih.gov)
- Protection of cerebral microvasculature after moderate hypothermia following experimental focal cerebral ischemia in mice. (mpg.de)
- Burk J, Burggraf D, Vosko M, Dichgans M, Hamann G. Hypothermia strengths inhibitors of matrix degrading proteases following experimental focal cerebral ischemia in mice. (mpg.de)
- Increasing doses of rt-PA reduce MMP3-activity following experimental focal cerebral ischemia. (mpg.de)
- Microplasmin reduces dose-dependently microvascular basal lamina damage in experimental focal cerebral ischemia. (mpg.de)
- These experimental results suggest that complement Cordyceps sinensis extract is protective after cerebral ischemia in specific way. (biomedcentral.com)
- Conclusions - These data: (1) demonstrate that this dose of selective KOR agonist provides ischemic neuroprotection in male but not female rats, (2) demonstrate that the lack of protection by BRL is not attributable to circulating ovarian hormones, and (3) highlight the importance of using animal models of both sexes in preclinical studies of experimental ischemia. (utmb.edu)
Intracerebral hemorrhage1
- It also regulates angiogenic factors and vascular permeability after focal cerebral ischemia-reperfusion, and regulates matrix metalloproteinase-9 activity after intracerebral hemorrhage. (wikipedia.org)
Microvascular damage2
- Specifically, the gelatinases MMP-2 and MMP-9 have previously been considered to specifically injure the important components of the basal lamina around the cerebral blood vessels that precede microvascular damage in cerebral ischemia [ 1 ]. (biomedcentral.com)
- The mechanism for localized hypercoaguability in granulomatous sarcoidosis may be due to the localized increase in Tumor Necrosis Factor alpha (TNF alpha) and interleukin-6 (IL-6) which can cause " microvascular damage leading to thrombosis ," and " ischemia . (transcendingsquare.com)
Hypothermia3
- Burk J, Burggraf D, Vosko M, Dichgans M, Hamann G. Effects of hypothermia on focal cerebral ischemia in plasminogen knockout mice. (mpg.de)
- The effect of moderate whole body hypothermia (300 C) on transient focal cerebral ischemia induced inflammatory injury was investigated. (banglajol.info)
- Our results indicate that moderate hypothermia has a significant protective effect on the inflammatory injury induced by transient focal cerebral ischemia. (banglajol.info)
Neurologic deficits1
- Focal neurologic deficits are usually due to cortical injury or irritation and depend on the vascular territory involved. (medscape.com)
Blood brain b1
- These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.com)
Damage8
- Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible. (wikipedia.org)
- Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain damage or death, mediated by the ischemic cascade. (wikipedia.org)
- The extent of reperfusion injury likely depends on the extent of initial hypoperfusion, the time to collateral collapse, the volume of irreversible tissue damage, and the degree of autoregulatory and pro-inflammatory responses. (medscape.com)
- Liang HW, Qiu SF, Shen J et al (2008) Genistein attenuates oxidative stress and neuronal damage following transient global cerebral ischemia in rat hippocampus. (springer.com)
- The chief aim in this study was to investigate whether changing temperature during and after ischemia could minimize this damage by reducing the inflammatory injury. (banglajol.info)
- yet at the same time it can induce ischemia-reperfusion injury, which leads to brain damage both in the ischemic core and penumbra area. (spandidos-publications.com)
- Objective: To investigate the influence of gender on early cerebral damage of rats after focal ischemia reperfusion. (cnki.net)
- Reperfusion of ischemic areas could exacerbate ischemic brain damage through the generation of reactive oxygen species. (biomedcentral.com)
Deficits1
- Morris water maze task was used to quantify spatial learning and memory deficits after reperfusion. (springer.com)
Dysfunction2
- In this study, we observed the effects of propofol on multiple aspects of mitochondrial dysfunction by studying the mitochondria isolated from rat brains subjected to focal cerebral ischemia-reperfusion. (nih.gov)
- In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
Metabolic3
- Here, we assessed the metabolic alterations following subclinical focal ischemia-reperfusion injury with hyperpolarized [1- 13 C]pyruvate MRI in a porcine model. (au.dk)
- CONCLUSION: MRI with hyperpolarized [1- 13 C]pyruvate in a clinical setup is capable of detecting the acute, subtle, focal metabolic changes following ischemia. (au.dk)
- Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand. (wikipedia.org)
Pathophysiology2
Regulates1
- The present study aimed to investigate the effects of changes in heat shock protein (HSP)90β expression and verify whether HSP90β regulates EAAT2 expression in a cerebral ischemia‑reperfusion injury model. (spandidos-publications.com)
Hypoxia2
- In the present work, a hypoxia/reoxygenation (H/R) model in NRK-52E cells and ischemia-reperfusion model in rats were used. (mdpi.com)
- Hypoxia, viral infection, and traumatic injury are the most common environmental causes of DCMs, and are associated with the subsyndromes focal polymicrogyria and focal cortical dysplasia (FCD) Type IIId, both of which have a high incidence of epilepsy. (eneuro.org)
Reactive Oxygen2
- Intraoperative tissue hypoperfusion and re-reperfusion injury, which generate reactive oxygen species (ROS), are suggested to induce delirium. (mdpi.com)
- 16. Wang Q, Zhang X, Ding Q, Hu B, Xie Y, Li X, Yang Q, Xiong L. Limb Remote Postconditioning Alleviates Cerebral Reperfusion Injury Through Reactive Oxygen Species-Mediated Inhibition of Delta Protein Kinase C in Rats. (ac.ir)
Pathophysiological1
- Progress in pathophysiological mechanism of cerebral ischemia/reperfusion injury. (magtechjournal.com)
Capillaries1
- Vascular Integrin immunoreactivity is selectively lost on capillaries during rat focal cerebral ischemia and reperfusion. (mpg.de)
Cortical2
- Propofol improved the signs of injury in the cortical mitochondria that were exposed to reperfusion following 2 h of focal ischemia. (nih.gov)
- There are multiple DCM subsyndromes, including tuberous sclerosis, focal cortical dysplasia (FCD), and polymicrogyria. (eneuro.org)
Postconditioning6
- Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (springer.com)
- 2. Ren C, Yan Z, Wei D, Gao X, Chen X, Zhao H. Limb remote ischemic postconditioning protects against focal ischemia in rats. (ac.ir)
- Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. (ac.ir)
- Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats. (ac.ir)
- 13. Zhang W, Miao Y, Zhou S, Jiang J, Luo Q, Qiu Y. Neuroprotective effects of ischemic postconditioning on global brain ischemia in rats through upregulation of hippocampal glutamine synthetase. (ac.ir)
- Postconditioning in reperfusion injury: a status report. (ac.ir)
Hydrogen2
- In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. (molcells.org)
- The present study investigated the effects of intracerebral human-derived hair follicle stem cells (HFBSCs), whether alone or in combination with hydrogen sulfide (H2S) in a rat model of focal cerebral ischemia. (medipol.edu.tr)
Vivo3
- Matrix-metalloproteinase upregulation in ischemia reperfusion can be imaged acutely in-vivo with NIRF using MMPSense750. (biomedcentral.com)
- The IMPROVE Guidelines (Ischaemia Models: Procedural Refinements Of in Vivo Experiments). (nottingham.ac.uk)
- Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
Inflammation3
- Brain ischemia-reperfusion (IR) triggers a complex series of biochemical events including inflammation. (biomedcentral.com)
- Cerebral ischemia-reperfusion (IR) triggers lipid peroxidation and inflammation, which exacerbate injury. (biomedcentral.com)
- In ischemia, the p65 subunit is recognized to play an important role in regulation of inflammation [ 13 ]. (biomedcentral.com)
Female rats3
- 05). Conclusion: The reperfusion injury in female rats is less serious in the short term,whose mechanism may be related to estrogen in brain of female rats inhibiting oxygen free radical. (cnki.net)
- We tested the hypothesis that BRL provides significant neuroprotection from transient focal ischemia in male but not in female rats. (utmb.edu)
- In the first experiment, male and female rats were treated in a blinded randomized fashion with vehicle saline or 1 mg/kg per hour BRL infusion started at the onset of reperfusion and continued for 22 hours. (utmb.edu)
Mitochondrial3
- It did not affect the reperfusion-induced reduction in mitochondrial membrane potential. (nih.gov)
- However, it decreased the production of the mitochondrial reactive oxidative species, which are generated during reperfusion. (nih.gov)
- However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.com)
Hippocampus1
- Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6-12 hours) after ischemia. (nih.gov)
Pathogenesis3
- Several mechanisms have been proposed for the pathogenesis of cerebral reperfusion injury. (medscape.com)
- At the same time, supplementation of Cordyceps sinensis extract significantly boosted the defense mechanism against cerebral ischemia by increasing antioxidants activity related to lesion pathogenesis. (biomedcentral.com)
- The defense mechanism against cerebral ischemia was by increasing antioxidants activity related to lesion pathogenesis. (biomedcentral.com)
Inhibits1
Model2
- To test the neuroprotective efficacy of 5-LOX inhibition in a rat model of focal cerebral IR, ischemic animals were either pre- or post-treated with a potent selective 5-LOX inhibitor, (N- [3-[3-(-fluorophenoxy) phenyl]-1-methyl-2-propenyl]- N -hydroxyurea (BW-B 70C). (biomedcentral.com)
- In the present study, we used a 5-LOX inhibitor, N- [3-[3-(-fluorophenoxy) phenyl]-1-methyl-2-propenyl]- N -hydroxyurea (BW-B 70C), in a rat model of focal cerebral IR. (biomedcentral.com)
Brains1
- In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered. (wikipedia.org)