AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Reperfusion InjuryBrain IschemiaInfarction, Middle Cerebral ArteryNeuroprotective AgentsReperfusionIschemic Attack, TransientCerebral InfarctionMyocardial Reperfusion InjuryErigeronIschemiaRats, Sprague-DawleyBrain EdemaBrainGerbillinaeRats, WistarDisease Models, AnimalMyocardial IschemiaMyocardial ReperfusionBrain InfarctionBlood-Brain BarrierMalondialdehydeCerebral ArteriesCerebrovascular CirculationTime FactorsNeuronsIschemic PreconditioningCaspase 3HippocampusApoptosisMice, KnockoutIschemic Preconditioning, MyocardialMiddle Cerebral ArteryMyocardiumMyocardial InfarctionIschemic PostconditioningConstrictionArterial Occlusive DiseasesCerebral AngiographyCardiotonic AgentsMice, Inbred C57BLPeroxidaseWarm IschemiaCerebral PalsyStrokeDogsHemodynamicsOxidative StressPerfusionCoronary OcclusionNecrosisCoronary CirculationRandom AllocationCell DeathCerebral HemorrhageHeartCold IschemiaProtective AgentsOxygenMicrocirculationHypothermia, InducedBalloon OcclusionBlood PressureMyocytes, CardiacRetinal Artery OcclusionL-Lactate DehydrogenaseCerebrovascular DisordersSubarachnoid HemorrhageIn Situ Nick-End LabelingSuperoxide DismutaseCerebral CortexCytoprotectionCerebral VeinsIntracranial Embolism and ThrombosisRetinal Vein OcclusionImmunohistochemistryRegional Blood FlowMagnetic Resonance ImagingCreatine KinaseBlood Flow VelocityMitochondria, HeartAntioxidantsNitric OxideSpinal Cord IschemiaKidneyReactive Oxygen SpeciesNeutrophil InfiltrationMesenteric Vascular OcclusionMyocardial ContractionLaser-Doppler FlowmetryCollateral CirculationRabbitsEnzyme InhibitorsBlotting, WesternMalaria, CerebralAcute DiseaseModels, AnimalFree Radical ScavengersAntipyrineRecovery of FunctionTreatment Outcome
MCAOFocal ischemiaStrokeCaused by middle cerebrEffects against cerebral ischemiaDamage after ceMiddleApoptosisNeuronsProtectsInduced by transientPathophysiologyHippocampusInfarctInjury inducedTherapeuticMethodsInflammationLeading to neuronalIschemic injuryArtery occlusionSuccessful reperfusionExerts neuroprotectiveCarotidModelBrain tissue damageMiceDeficitsOxidativeOnsetDysfunctionProtective effectsHippocampalCIRIHypothermiaVascularIpsilateral cerebralInfarction volumeBlood-brain bEmbolismOxygenPathogenesisAtherosclerosisTissueInflammatoryResponsesMetabolism
MCAO18
Focal ischemia6
  • Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (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)
  • Propofol improved the signs of injury in the cortical mitochondria that were exposed to reperfusion following 2 h of focal ischemia. (nih.gov)
  • Neuroprotection by estrogen in animal models of global and focal ischemia. (ac.ir)
  • We tested the hypothesis that prolonged, continuous administration of PPBP would provide further neuroprotection in a rat model of transient focal ischemia and reperfusion. (utmb.edu)
  • These data demonstrate that the σ 1 -receptor ligand PPBP attenuates ischemic injury when administration is initiated 60 min after the onset of focal ischemia but that prolonged continuous treatment with PPBP beyond 24 h provides no neuroprotection. (utmb.edu)
Stroke31
  • An ischemic stroke consists of two related pathological injury processes: Primary ischemia-induced brain injury and secondary ischemia reperfusion injury ( 3 ). (spandidos-publications.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)
  • 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)
  • 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)
  • It is caused by disrupted blood supply (ischemia) and restricted oxygen supply (hypoxia), most commonly due to thromboembolism, and manifests clinically as ischemic stroke. (wikipedia.org)
  • on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation). (wikipedia.org)
  • In people who die of cerebral infarction, an autopsy of stroke may give a clue about the duration from the infarction onset until the time of death. (wikipedia.org)
  • 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)
  • Zhang G, Li Q, Tao W, Qin P, Chen J, Yang H, Chen J, Liu H, Dai Q, Zhen X. Sigma-1 receptor-regulated efferocytosis by infiltrating circulating macrophages/microglial cells protects against neuronal impairments and promotes functional recovery in cerebral ischemic stroke. (thno.org)
  • The roles of Sig-1R in the efferocytosis activity of microglia/macrophages using bone marrow-derived macrophages (BMDMs) or using Sig-1R knockout mice subjected to transient middle artery occlusion (tMCAO)-induced stroke were investigated. (thno.org)
  • Primary cortical neurons were subjected to glucose deprivation (GD), oxygen-glucose deprivation (OGD) or simulated ischemia-reperfusion (I/R). Ischemic stroke was induced in C57BL/6J mice by middle cerebral artery occlusion, followed by reperfusion. (scienceopen.com)
  • Similarly, levels of NLRP1 and NLRP3 inflammasome proteins, IL-1 β and IL-18 were elevated in ipsilateral brain tissues of cerebral I/R mice and stroke patients. (scienceopen.com)
  • Temporal and spatial dynamics of cerebral immune cell accumulation in stroke. (scienceopen.com)
  • Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. (sciencegate.app)
  • Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice? (uni-wuerzburg.de)
  • Methods In C57Bl/6 (wildtype, WT), \(hcn2^{+/+}\) and \(hcn2^{-/-}\) mice we used an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of HCN2 in stroke formation. (uni-wuerzburg.de)
  • however, the role of the two distinct TNF-α receptors, TNFR1 and TNFR2, in mediating angiogenic signaling after cerebral ischemic stroke is relatively unknown. (biomedcentral.com)
  • Neuroprotective Potential of Hericium Erinaceus aqueous extract utilization in ischemia-reperfusion injury related middle cerebral artery occlusion stroke model. (ijehsr.com)
  • A deleterious consequence of cerebral ischemia is upregulation of vasoconstrictor receptors in cerebral arteries that exacerbate stroke injury. (lu.se)
  • Furthermore, we demonstrated that PT enhanced brain inflammation and aggravated stroke severity in middle cerebral artery occlusion mouse model. (bmj.com)
  • Ocular ischemia is often observed in cases of cerebral stroke and atherosclerosis of the ophthalmic or carotid arteries. (arvojournals.org)
  • Patients were enrolled if they had acute ischemic stroke with National Institutes of Health Stroke Scale score ≥8 due to large vessel occlusion within 8 hours of onset. (baptisthealth.net)
  • Diagnosis and management of a rare form of stroke, cerebral venous thrombosis (CVT), was the subject of a 2011 American Heart Association/American Stroke Association (AHA/ASA) statement for healthcare professionals. (medscape.com)
  • 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)
  • and proximal arterial stenosis with hypotension that decreases cerebral blood flow in arterial watershed zones (hemodynamic stroke). (msdmanuals.com)
  • Multicenter cohort study of patients with acute ischemic stroke who underwent a brain computed tomography perfusion and were scheduled to undergo reperfusion therapy. (medscape.com)
  • Migraine is likely to increase individual vulnerability to ischemic stroke during the process of acute brain ischemia and might represent, therefore, a potential new therapeutic target against occurrence and progression of the ischemic damage. (medscape.com)
  • [ 1 ] A recent hypothesis to explain the migraine-stroke association, based on experimental data obtained in mice expressing familial hemiplegic migraine type 1 mutations, is that the cerebral hyperexcitability phenotype associated with migraine might sensitize brain tissue to ischemia. (medscape.com)
  • Based on these premises, taking advantage of the reliability of computed tomography perfusion (CTP) imaging in the estimation of cerebral tissue viability in both clinical and research settings, [ 4 ] we conducted a case-control study comparing CTP maps of migraineurs and nonmigraineurs patients with acute ischemic stroke aimed at investigating whether a personal history of migraine is associated with vulnerability to brain ischemia. (medscape.com)
  • Monitoring of cerebral oxygen saturation can be used in the diagnosis of cerebral desaturations in stroke patients. (lu.se)
Caused by middle cerebr1
Effects against cerebral ischemia2
  • The results showed that puerarin derivative P1-EA and P2-EA were resulting in an increased lipophilicity that enabled the derivatives to pass more efficiently through the blood-brain barrier, thus, improving the protective effects against cerebral ischemia/reperfusion injury. (hindawi.com)
  • Abstract BACKGROUND: Several β-adrenergic receptor (βAR) antagonists have been shown to have neuroprotective effects against cerebral ischemia. (starrlifesciences.com)
Damage after ce1
Middle10
  • Middle Cerebral Artery Occlusion Allowing Reperfusion via Common Carotid Artery Repair in Mice JOVE-JOURNAL OF VISUALIZED EXPERIMENTS. (nottingham.ac.uk)
  • Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice. (scienceopen.com)
  • Therefore, we investigated the effect of VAC extract on ovariectomized mice after the induction of permanent middle cerebral artery occlusion (PMCAO) model. (ac.ir)
  • Loosen the loose knot of the internal carotid artery and continue inserting the thread bolt to the beginning of the middle cerebral artery marked with the suture and cut off the exposed thread bolt. (jove.com)
  • Sprague-Dawley rats were used as experimental animals, and middle cerebral artery occlusion was used to make cerebral ischemia/reperfusion model. (molecularhydrogenstudies.com)
  • Female rats with intact ovaries and ovariectomized (OVX) females treated with 17β-estradiol, progesterone, or placebo were subjected to transient, unilateral middle cerebral artery occlusion followed by reperfusion (I/R). The maximum contractile response, measured my wire myography, in response to the endothelin B receptor agonist sarafotoxin 6c was increased in female arteries after I/R, but the maximum response was significantly lower in arteries from OVX females. (lu.se)
  • Transient focal cerebral ischemia (90 min) was induced by occlusion of the left middle cerebral artery that followed by 24 h reperfusion periods. (ac.ir)
  • IMPLICATIONS: Brain injury is reduced and neurological outcome improved after middle cerebral artery occlusion in mice lacking the β2AR or in wild type mice pretreated with a selective β2AR antagonist. (starrlifesciences.com)
  • Under isoflurane anesthesia, a filament was inserted through an incision in the external carotid artery and slid into the internal carotid artery so that it blocked the right middle cerebral and ophthalmic arteries. (arvojournals.org)
  • Under controlled conditions of normoxia, normocarbia, and normothermia, halothane-anesthetized male Wistar rats were subjected to 2 h of middle cerebral artery occlusion by the intraluminal occlusion technique. (utmb.edu)
Apoptosis8
Neurons6
  • 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)
  • Adoptive transfer of Sig-1R intact bone marrow-derived macrophages (BMDMs) to Sig-1R knockout mice restored the clearance activity of dead/dying neurons, reduced infarct area and neuroinflammation, and improved long-term functional recovery after cerebral ischemia. (thno.org)
  • Ischemia-like conditions increased the levels of NLRP1 and NLRP3 inflammasome proteins, and IL-1 β and IL-18, in primary cortical neurons. (scienceopen.com)
  • In neurons, TASK channels carrying hyperpolarizing \(K^+\) leak currents, and the pacemaker channel HCN2, carrying depolarizing Background Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (uni-wuerzburg.de)
  • The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. (ewha.ac.kr)
Protects5
  • Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
  • Cerebral autoregulation protects the brain against sudden changes in systemic blood pressure. (medscape.com)
  • Another new study from China suggests that nicotinic acid protects memory function caused by the disruption of oxygen (cerebral ischemia) and the restoration of blood flow (reperfusion) into the brains of rats following disruption. (life-enhancement.com)
  • Our previous studies have demonstrated that EA protects cerebral neural cells against inflammatory injury after cerebral ischemia, which appears at 24 h to 14 days after treatment. (biomedcentral.com)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
Induced by transient2
  • Our results indicate that moderate hypothermia has a significant protective effect on the inflammatory injury induced by transient focal cerebral ischemia. (banglajol.info)
  • This study aimed to investigate the therapeutic potential of Ser on cognitive dysfunction induced by transient global cerebral ischemia/reperfusion (tGI/R) and its mechanism of action. (cjphysiology.org)
Pathophysiology2
  • This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. (nih.gov)
  • Reperfusion plays an important role in the pathophysiology of cerebral ischemia. (nih.gov)
Hippocampus5
  • 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)
  • 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)
  • The present study was designed to investigate the expression changes of PPAR-alpha, -beta, -gamma and NF-kappa B in the hippocampus of rats with global cerebral ischemia/reperfusion injury (GCIRI) after treatment with agonists or antagonists of PPAR-gamma. (biomedcentral.com)
  • Although steady-state conditions revealed no increase in primitive cell proliferation in p21-null mice, a significantly larger fraction of quiescent neural precursors was activated in the hippocampus and subventricular zone after brain ischemia. (rupress.org)
  • The immunoreactivity of synapsin I and GAP-43 was increased in the stratum lucidum in the CA3 subfield as well as in the inner and outer molecular layers of dentate gyrus in the hippocampus at reperfusion for 2 weeks. (ewha.ac.kr)
Infarct2
  • Cerebral infarction is the pathologic process that results in an area of necrotic tissue in the brain (cerebral infarct). (wikipedia.org)
  • Neurological score was determined at 24 h reperfusion and infarct size was determined by cresyl violet or 2,3,5-triphenyltetrazolium chloride staining. (starrlifesciences.com)
Injury induced1
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
Therapeutic2
  • Perhaps, the therapeutic effect was related to a reduction in releasing of cytotoxic products and improvement of the cerebral microcirculation. (banglajol.info)
  • These novel findings could form a platform for future therapeutic strategies aimed at stimulating angiogenesis following cerebral ischemia. (biomedcentral.com)
Methods1
  • The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative. (nih.gov)
Inflammation6
  • Global cerebral ischemia/reperfusion injury (GCIRI) occurs in patients who are successfully resuscitated from various clinical conditions such as cardiac arrest, asphyxia and shock, which are frequently accompanied by inflammation and can lead to serious neuronal injury, and further to neurodegeneration and learning and memory impairment [ 12 ]. (biomedcentral.com)
  • When cerebral ischemia-reperfusion injury happened in patients, multiple pathological processes occur, such as leukocyte infiltration, platelet, and complement activation, which would result in cognitive dysfunction and inflammation. (hindawi.com)
  • An UCCAO caused a slight cerebral ischemia (cerebral blood flow [CBF] 70%) without hypotension (MABP 85 mmHg), systemic inflammation, multiple organs injuries, or neurological injury. (medsci.org)
  • An HS caused a moderate cerebral ischemia (52% of the original CBF levels), a moderate hypotension (MABP downed to 22 mmHg), systemic inflammation, and peripheral organs injuries. (medsci.org)
  • However, combined an UCCAO and an HS caused a severe cerebral ischemia (18% of the original CBF levels), a moderate hypotension (MABP downed to 17 mmHg), systemic inflammation, peripheral organs damage, and neurological injury, which can be attenuated by whole body cooling. (medsci.org)
  • Water electrolysis-derived hydrogen inhalation had neuroprotective effects on cerebral ischemia/reperfusion injury in rats with the effect of suppressing oxidative stress and inflammation, and it is a possible new hydrogen resource to electrolyze water at the bedside clinically. (molecularhydrogenstudies.com)
Leading to neuronal1
  • Occlusion of a cerebral artery impairs blood flow leading to neuronal death. (edu.au)
Ischemic injury4
  • Studies have shown that puerarin reduced cerebral edema in rats with cerebral ischemia-reperfusion injury, removed lipid peroxidation products, enhanced antioxidant capacity, improved antioxidant activity of the brain tissue, and reduced the degree of focal cerebral ischemic injury [ 2 - 4 ]. (hindawi.com)
  • Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that the ischemic injury of brain leads to the injury of brain cells, and ischemic injury is further aggravated after the recovery of blood reperfusion. (sciencegate.app)
  • However, the P2X7R/P2Y1R related EA treatment with the development of cerebral ischemic injury is complex and unclear. (biomedcentral.com)
  • Along with the observation that migraine mutants had an elevated minimum cerebral blood flow threshold required for tissue survival and developed larger infarcts, these findings directly support the hypothesis that brain tissue in migraineurs is more susceptible to ischemic injury. (medscape.com)
Artery occlusion1
  • This study aimed to investigate whether resuscitation after a hemorrhagic shock (HS) and/or mild cerebral ischemia caused by a unilateral common carotid artery occlusion (UCCAO) can cause brain injury and concomitant neurological dysfunction, and explore the potential mechanisms. (medsci.org)
Successful reperfusion2
  • The primary efficacy end point was successful reperfusion, defined as core laboratory-adjudicated modified Thrombolysis in Cerebral Ischemia score 2b-3 within 3 passes of the Tigertriever. (baptisthealth.net)
  • Secondary efficacy end points included 3-month good clinical outcome (modified Rankin Scale score 0-2) and first-pass successful reperfusion. (baptisthealth.net)
Exerts neuroprotective2
  • Here we investigated whether remifentanil postconditioning exerts neuroprotective effects against global cerebral ischemia/reperfusion injury in rats and its potential mechanisms. (springer.com)
  • Genistein exerts neuroprotective effect on focal cerebral ischemia injury in rats. (ac.ir)
Carotid3
  • A rat GCIRI model was established by occlusion of bilateral common carotid arteries and cervical vena retransfusion. (biomedcentral.com)
  • Cerebral reperfusion, or hyperperfusion, syndrome is a rare but serious complication that can occur following rapid revascularization of a partially or completely occluded artery with successful thrombolytic therapy, successful thrombectomy, carotid enterectomy (CEA), or carotid artery stenting (CAS). (medscape.com)
  • The scientists then induced a brief occlusion of the carotid artery, the main vessel carrying blood to the brain. (life-enhancement.com)
Model6
  • 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)
  • 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)
  • The mouse model of cerebral artery ischemia/reperfusion injury was established to test the anticerebral ischemia-reperfusion injury activity of the puerarin derivatives. (hindawi.com)
  • The objectives of this study were to define the temporal and spatial infiltration of immune cell populations and their activation patterns in a murine cerebral ischemia-reperfusion injury model. (scienceopen.com)
  • In a previous study using a mouse model of focal cerebral ischemia, we demonstrated the presence of proliferating endothelial cells in the ischemic penumbra and found that this correlated with increased vessel density [ 5 ]. (biomedcentral.com)
  • This study uses an established animal model to research the recovery and the sequelae stages of brain ischemia. (jove.com)
Brain tissue damage1
  • Proinflammatory cytokines, such as interleukin (IL)-1β, IL-6 and tissue necrosis factor (TNF)-α, have been implicated as important mediators of injury following cerebral ischemia [ 13 ] and contribute to pathogenesis, exacerbating brain tissue damage following ischemia/reperfusion (I/R) injury [ 14 ]. (biomedcentral.com)
Mice4
  • Results After 60 min of tMCAO induction in WT mice, we collected tissue samples at 6, 12, and 24 h after reperfusion. (uni-wuerzburg.de)
  • Vascular remodeling and α5β1 and αVβ3 integrin expression were then examined in the brains of these mice after 4, 7, and 14 days post-ischemia. (biomedcentral.com)
  • We used β2AR knockout mice and a β2selective antagonist to test the effect of loss of β2ARs on outcome from transient focal cerebral ischemia. (starrlifesciences.com)
  • After cerebral ischemia, total levels of Hsp72 and the number of Hsp72 immunopositive cells were greater in mice lacking β2 AR. (starrlifesciences.com)
Deficits5
  • Morris water maze task was used to quantify spatial learning and memory deficits after reperfusion. (springer.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)
  • Background Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (uni-wuerzburg.de)
  • Induction of cerebral ischemia in the control group produced severe neurological sensorimotor deficits in conjunction with considerable cerebral infarctions. (ac.ir)
Oxidative1
  • However, it decreased the production of the mitochondrial reactive oxidative species, which are generated during reperfusion. (nih.gov)
Onset1
  • Sixty minutes after the onset of ischemia, rats were randomly assigned to six treatment groups to receive a continuous IV infusion of PPBP (1 μmol · kg -1 · h -1 ) for 1, 2, 3, or 4 days or saline for 1 or 4 days. (utmb.edu)
Dysfunction4
  • 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)
  • 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)
  • However, it is not known whether resuscitation after a [ 10 - 12 ] HS can cause cerebral injury and concomitant neurological dysfunction, and its potential mechanisms. (medsci.org)
  • Transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction that results from focal cerebral, spinal cord, or retinal ischemia and is not associated with acute tissue infarction. (medscape.com)
Protective effects2
  • 2. Zhang X, Zhang B-Z, Yang X-P, Zhang W-W. Protective effects of nicotinic acid on disturbance of memory retrial induced by cerebral ischemia-reperfusion in rats. (life-enhancement.com)
  • Isosteviol has been demonstrated to have protective effects against ischemia-reperfusion (IR) injury in the rat heart and the current study was undertaken to determine whether it is also effective in preventing IR injury in the brain. (edu.au)
Hippocampal1
  • Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling positive cells and expression of Bcl-2 and Bax in the hippocampal CA1 region were assessed after reperfusion. (springer.com)
CIRI1
Hypothermia1
  • The effect of moderate whole body hypothermia (300 C) on transient focal cerebral ischemia induced inflammatory injury was investigated. (banglajol.info)
Vascular2
  • More recently, we described that in response to cerebral ischemia, vascular expression of fibronectin (Fn), and its two receptors, α5β1 and αVβ3 integrins, were all noticeably increased by day 4, peaked at day 7, then declined at day 14. (biomedcentral.com)
  • To understand the mechanism of intracerebroventricular transplantation of vascular endothelial growth factor (VEGF) genemodified bone mesenchymal stem cells (BMSCs) in rats after cerebral infarction. (dergisi.org)
Ipsilateral cerebral1
  • [ 11 , 12 ] Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue. (medscape.com)
Infarction volume2
  • Our findings demonstrate that PI3K/AKT/GSK3β pathway could reduce reactive gliosis, ameliorate neurological deficit, diminish the percentage of cerebral infarction volume in rats, and facilitate angiogenesis. (dergisi.org)
  • The infarction volume was assessed by triphenyltetrazolium chloride (TTC) staining on Day 4 after ischemia in all rats. (utmb.edu)
Blood-brain b3
  • The original phenolic hydroxyl in the puerarin molecules was substituted in order to change the blood-brain barrier permeability and thus enhance the efficacy for preventing cerebral ischemia/reperfusion injury. (hindawi.com)
  • In addition, we tested the anticerebral ischemia-reperfusion injury activity of these puerarin derivatives in order to determine their permeability through the blood-brain barrier and pharmacological activity. (hindawi.com)
  • 17β-Estradiol attenuates blood-brain barrier disruption induced by cerebral ischemia-reperfusion injury in female rats. (ac.ir)
Embolism1
  • The disruption to blood supply can come from many causes, including: Thrombosis (obstruction of a blood vessel by a blood clot forming locally) Embolism (obstruction due to an embolus from elsewhere in the body), Systemic hypoperfusion (general decrease in blood supply, e.g., in shock) Cerebral venous sinus thrombosis. (wikipedia.org)
Oxygen1
  • In our studies, the feasibility of using PAI for estimating the spatial distribution of oxygen saturation is examined, in models of occlusion reperfusion and adrenalin-dependent vasoconstriction in humans. (lu.se)
Pathogenesis1
Atherosclerosis1
Tissue4
  • Cerebral infarction is caused by a disruption to blood supply that is severe enough and long enough in duration to result in tissue death. (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)
  • Examining both retina and cerebral responses to disease provides an opportunity to expand our knowledge of mechanisms of disease, to translate treatments from one tissue to the other, and to optimize treatments effective for both tissues. (arvojournals.org)
  • Cerebral hyperexcitability in migraine experiencers might sensitize brain tissue to ischemia. (medscape.com)
Inflammatory3
  • 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)
  • Early reperfusion strategies remain the treatment of choice but can initiate and augment an inflammatory response causing secondary brain damage. (scienceopen.com)
  • It is well-documented that extracellular ATP triggers surrounding glial purinergic receptors signaling pathway and pro-inflammatory cytokines release to aggravate neural injury in cerebral ischemia [ 8 , 9 ]. (biomedcentral.com)
Responses1
  • Our results suggest that TNFR1-mediated signaling plays a critical role in triggering angiogenic integrins and subsequent angiogenic responses following cerebral ischemia. (biomedcentral.com)
Metabolism2