We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25 micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n = 10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant. Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score = 4) compared with controls (median deficit ...
TY - JOUR. T1 - Treatment of acute focal cerebral ischemia with dimethyl sulfoxide. AU - Little, J. R.. AU - Cook, A.. AU - Lesser, Ronald P. PY - 1981. Y1 - 1981. N2 - The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 ± 10 ml/100 g/minute in the untreated group and 45 ± 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled ...
The effects of isosmolar loads of glucose and saline after onset of focal cerebral ischaemia (middle cerebral artery occlusion) were compared in cats. In cats given saline cerebral blood flow (CBF) fell and then rose slightly on the marginal gyrus (infarct penumbra). There was a sustained fall in CBF on the suprasylvian and ectosylvian gyri (infarct core). Reperfusion restored blood flow to preocclusion levels with no overall postischaemic hypoperfusion. Below ischaemic flows of 14 ml/100 g/min brain specific gravity was reduced in a smaller proportion of gyri by contrast with non reperfused cortex, suggesting that in some gyri resolution of cerebral oedema had taken place. GABA uptake was normal in the infarct core, but was reduced within the ischaemic penumbra. In animals given glucose after occlusion, CBF fell on the marginal gyrus during reperfusion. The degree of resolution of cerebral oedema was less than in saline infused cats. GABA uptake showed a pattern of abnormality similar to that ...
Interleukin-1 (IL-1) is a key regulator of inflammation and ischaemic brain injury, but the contribution of central and peripheral sources of IL-1 to brain injury is not well understood. Here we show that haematopoietic-derived IL-1 is a key driver of ischaemic brain injury. Wild type (WT) mice transplanted with IL-1αβ-deficient bone marrow displayed a significant (40%) reduction in brain injury induced by focal cerebral ischaemia compared to WT mice transplanted with WT bone marrow. This was paralleled by improved neurological outcome and the almost complete absence of splenic-derived, but not liver-derived, IL-1α after stroke in WT mice lacking haematopoietic-derived IL-1. IL-1αβ knockout (KO) mice transplanted with IL-1αβ-deficient bone marrow showed a 60% reduction in brain injury compared to WT mice receiving WT bone marrow. Transplantation of WT bone marrow in IL-1αβ KO mice resulted in a similar level of blood-brain-barrier injury to that observed in WT mice receiving ...
OBJECTIVES: Prolonged global cerebral ischaemia leads to irreversible injury, often with lethal outcome. Brain injuries are partly caused by the uncontrolled reperfusion that occurs once the circulation is re-established. Recent animal experiments suggest that controlled reperfusion following lengthy ischaemia might prevent severe brain injury. This study aimed at further exploring cerebral alterations and outcome following prolonged global cerebral ischaemia and mechanically manipulated reperfusion.. METHODS: Three groups of pigs were included; one sham operated (n = 3) and two that underwent 30-min global cerebral ischaemia. All vessels that supply the brain were isolated intrathoracically, after which they were occluded for 30 min in the ischaemic groups. In one of the ischaemic groups uncontrolled reperfusion was applied (URep, n = 6), i.e. normal circulation was restored 30 min after arrested cerebral circulation. The second ischaemic group received mechanical reperfusion (MRep, n = 6) with ...
TY - JOUR. T1 - Intraluminal suture occlusion of the middle cerebral artery in spontaneously hypertensive rats. AU - Dogan, Aclan. AU - Başkaya, Mustafa K.. AU - Rao, V. L Raghavendra. AU - Rao, A. Muralikrishna. AU - Dempsey, Robert J.. PY - 1998/4. Y1 - 1998/4. N2 - In models of middle cerebral artery occlusion using intraluminal suture, the size and the distribution of ischemic injury vary considerably among laboratories. In transcranial models of cerebral ischemia, a more consistent cerebral ischemic lesion is seen in Spontaneously Hypertensive rats (SHR). In the present study, we performed intraluminal suture occlusion of the MCA in SHR and compared its reproducibility with those in Sprague-Dawley (SD) rats. Male SHR and SD rats were anesthetized with halothane and subjected to 2 h of temporary middle cerebral artery occlusion by an intraluminal suture. Comparisons of regional cerebral blood flow figures taken throughout the experiment and lesion volume figures taken at 24 h after ...
Hypoxic-ischaemic brain injury at birth is associated with 1-3/1000 cases of moderate to severe encephalopathy. Previously, we have shown that connexin 43 hemichannel blockade, with a specific mimetic peptide, reduced the occurrence of seizures, improved recovery of EEG power and sleep state cycling, and improved cell survival following global cerebral ischaemia. In the present study, we examined the dose response for intracerebroventricular mimetic peptide infusion (50 µmol/kg/h for 1 h, followed by 50 µmol/kg/24 h (low dose) or 50 µmol/kg/h for 25 h (high dose) or vehicle only (control group), starting 90 min after the end of ischaemia), following global cerebral ischaemia, induced by 30 min bilateral carotid artery occlusion, in near-term fetal sheep (128 ± 1 days gestation). Both peptide infusion groups were associated with a transient significant increase in EEG power between 2-12 h after ischaemia. The ischaemia-low dose group showed a significant recovery of EEG power from day five compared
The present study shows that PC-SOD, the lecithinized form of SOD, decreased infarct volume and improved neurological outcomes at different time points after focal cerebral ischemic injury. PC-SOD decreased oxidative stress and provided neuronal protection through antiapoptotic mechanisms.. Previous studies have highlighted that unmodified SOD plays an important role in attenuating different forms of brain injury, including cerebral ischemia.1,2,3 However, its short in vivo half-life and low tissue affinity have hampered the practical use of unmodified SOD formulations.4 The enzymatic activity of PC-SOD is comparable to that of unmodified SOD. The in vitro activity of unmodified SOD by the xanthine-xanthine oxidase method was 3467 U/mg, whereas that of PC-SOD was 2876 U/mg. Therefore, the activity of PC-SOD was equivalent to 83% of unmodified SOD.15 PC-SOD, however, has many advantages, such as longer in vivo half-life, greater tissue affinity, and better drug delivery, resulting in ...
Brain ischemia (a.k.a. cerebral ischemia, cerebrovascular ischemia) is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage. Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis. There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, ...
TY - JOUR. T1 - Postischemic gene transfer of midkine, a neurotrophic factor, protects against focal brain ischemia. AU - Takada, J.. AU - Ooboshi, H.. AU - Ago, T.. AU - Kitazono, T.. AU - Yao, H.. AU - Kadomatsu, K.. AU - Muramatsu, T.. AU - Ibayashi, S.. AU - Iida, M.. PY - 2005/3/1. Y1 - 2005/3/1. N2 - Gene therapy may be a promising approach for treatment of brain ischemia. In this study, we examined the effect of postischemic gene transfer of midkine, a heparin-binding neurotrophic factor, using a focal brain ischemia model with the photothrombotic occlusion method. At 90 min after induction of brain ischemia in spontaneously hypertensive rats, a replication-deficient recombinant adenovirus encoding mouse midkine (AdMK, n = 7) or a control vector encoding β-galactosidase (Adβgal, n = 7) was injected into the lateral ventricle ipsilateral to ischemia. At 2 days after ischemia, we determined infarct volume by 2,3,5-triphenyltetrazolium chloride staining. There were no significant ...
Introduction: The aim of the study was to evaluate the endothelioprotective activity of 4-hydroxy-3,5-di-tret-butylcinnamic acid in conditions of experimental cerebral ischemia. Materials and methods: The brain ischemia was reproduced by the method of irreversible right-sided thermocoagulation of the middle cerebral artery. As comparative drugs, mexidol (30 mg/kg) and sulodexide (30 U/kg) were used. The vasodilating function of the vascular endothelium was assessed by the change in the rate of cerebral blood flow when the synthesis of nitric oxide was modified. Antithrombotic function was assessed by changes in the concentration of thromboxane A2, fibrinogen, von Willebrand factor activity and platelet aggregation activity. Serum concentration of C-reactive protein served as a marker of the state of anti-inflammatory endothelial function. To determine the potential mechanism of endothelioprotective activity of 4-4-hydroxy-3,5-di-tret-butylcinnamic acid, the anti-radical activity of
אינדוקציה כירורגי של נזק מוחי איסכמי בחולדה הוא מודל בשימוש נרחב עבור מחקר שבץ. כאן אנו מדגימים את האינדוקציה של איסכמיה מוחית המוקד על ...
Aging is a risk factor for stroke. Animal models of stroke have been widely used to study the pathophysiology of ischemic stroke, which in turn helped to develop numerous therapeutic strategies. Despite the considerable success of therapeutic strategies in animal models of ischemic stroke, almost all of them have been proved to be unsuccessful in the clinical trials. One of explanation is that data obtained from young animals may not fully resemble the effects of ischemic stroke in aged animals or elder patients, causing the discrepancy between animal experiments and clinical trials. To investigate these differences with regard to age, pathway specific gene arrays were used to identify and isolate differentially expressed genes in periinfarct following focal cerebral ischemia. The results from this study showed a persistent up-regulation of pro-apoptotic and inflammatory-related genes up to 14 days post stroke, a 50% reduction in the number of transcriptionally active stem cell-related genes and ...
TY - JOUR. T1 - Ablation of Neurogenesis Attenuates Recovery of Motor Function after Focal Cerebral Ischemia in Middle-Aged Mice. AU - Sun, Fen. AU - Wang, Xiaomei. AU - Mao, Xiao Ou. AU - Xie, Lin. AU - Jin, Kunlin. PY - 2012/10/26. Y1 - 2012/10/26. N2 - Depletion of neurogenesis worsens functional outcome in young-adult mice after focal cerebral ischemia, but whether a similar effect occurs in older mice is unknown. Using middle-aged (12-month-old) transgenic (DCX-TK(+)) mice that express herpes simplex virus thymidine kinase (HSV-TK) under control of the doublecortin (DCX) promoter, we conditionally depleted DCX-positive cells in the subventricular zone (SVZ) and hippocampus by treatment with ganciclovir (GCV) for 14 days. Focal cerebral ischemia was induced by permanent occlusion of the middle cerebral artery (MCAO) or occlusion of the distal segment of middle cerebral artery (dMCAO) on day 14 of vehicle or GCV treatment and mice were killed 24 hr or 12 weeks later. Increased infarct volume ...
ABSTRACT MECHANISMS OF PERSISTENT TRANSLATION ARREST FOLLOWING GLOBAL BRAIN ISCHEMIA and REPERFUSION by JILL T. JAMISON December 2011 Advisor: Donald J. DeGracia, Ph.D. Major: Physiology Degree: Doctor of Philosophy The information presented here studies the mechanisms that underlie persistent translation arrest (TA) following global brain ischemia and reperfusion (I/R). To summarize the main findings I have discovered a new mechanism for prolonged post-ischemic TA that correlated exactly with in vivo translation rates and correlated precisely with cell outcome. Through the extensive colocalization studies, my results indicate that the mRNA granules are ribonomic structures involved with mRNA regulation. This finding is significant because it shifts the focus onto mRNA metabolism and away from ribosomal molecular biology. I have identified new pathways to investigate for understanding why there is selective delayed death in post-ischemic neurons, however my work also gives insight into why resistant
It is crucial to establish an MCAO/R animal model according to the clinical characteristics of a human cerebral natural infarct. The model characteristics are as follows: i) single damage mechanism that is easy to study; ii) simple method, small wound, easy to control condition, stable infarct site, and distinct symptomatic reaction and high achievement ratio; iii) uniformity of cerebral infarction and good reproducibility; and iv) necrotic brain tissue following injury, with a similar pathophysiological process to clinical cerebral ischemia. In this study, a rat cerebral ischemia-reperfusion injury model was established according to the Zea-Longa method (4). Following cerebral ischemia for 1 h, the rats developed severe nervous and behavioral functional impairment symptoms, indicating the establishment of a successful model.. The Bederson (5) score method was employed for qualitative and semiquantitative evaluation, with particular emphasis on motor function evaluation. The balance beam walking ...
1. Li PA, He Q. Mechanisms of hyperglycemia-enhanced ischemic brain damage. Transl Med Res. 2013;3:1-11 2. Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC. Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke. 2001;32:2426-2432 3. Rajesh G, Ajay C, Frederick M, Paresh D. Hyperglycemia, insulin, and acute ischemic stroke: A mechanistic justification for a trial of insulin infusion therapy. Stroke. 2006;37:267-273 4. Balan IS, Fiskum G, Hazelton J, Cotto-Cumba C, Rosenthal RE. Oximetry-guided reoxygenation improves neurological outcome after experimental cardiac arrest. Stroke. 2006;37:3008-3013 5. Cipolla MJ, Godfrey JA. Effect of hyperglycemia on brain penetrating arterioles and cerebral blood flow before and after ischemia/reperfusion. Transl Stroke Res. 2010;1:127-134 6. Stead LG, Gilmore RM, Bellolio MF, Mishra S, Bhagra A, Vaidyanathan L, Decker WW, Brown RD Jr. Hyperglycemia as an independent predictor of worse outcome in ...
Increasing evidence suggests that toll-like receptors (TLRs) play an important role in cerebral ischemia-reperfusion injury. The endogenous ligands released from ischemic neurons activate the TLR signaling pathway, resulting in the production of a large number of inflammatory cytokines, thereby causing secondary inflammation damage following cerebral ischemia. However, the preconditioning for minor cerebral ischemia or the preconditioning with TLR ligands can reduce cerebral ischemic injury by regulating the TLR signaling pathway following ischemia in brain tissue (mainly, the inhibition of the TLR4/NF-κB signaling pathway and the enhancement of the interferon regulatory factor-dependent signaling), resulting in TLR ischemic tolerance. Additionally, recent studies found that postconditioning with TLR ligands after cerebral ischemia can also reduce ischemic damage through the regulation of the TLR signaling pathway, showing a significant therapeutic effect against cerebral ischemia. These studies
Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion.. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4).. In a stroke model rats were made hyperglycemic prior to transient ...
TroLucaM. Lemarchand E, Barrington J, Chenery A, Haley M, Coutts G, Allen JE, et al. Extent of Ischemic Brain Injury After Thrombotic Stroke Is Independent of the NLRP3 (NACHT, LRR and PYD Domains-Containing Protein 3) Inflammasome. Stroke. 2019;50:1232-1239.. Inflammation plays a key role in the fight against infection. However, following ischaemic brain injury, inflammation can play a very different role, exacerbating the severity of damage. Inflammation results in long lasting, ongoing damage from the onset of vessel blockage through to and during reperfusion of the ischaemic brain area. One possible player within the inflammation related post-stroke damage is the NLR family pyrin domain containing 3 (NLRP3) inflammasome. During ischaemic brain injury, NLRP3 senses multiple stroke-induced stimuli leading to the recruitment of the adaptor protein ASC (the apoptosis-associated speck-like pro-caspase-1) resulting in caspase 1 production leading to downstream IL-1β and IL-18 production and ...
phdthesis{e6a24cb9-3a1a-4b11-91f1-3152114bb8fb, abstract = {Enriched environment (EE) housing significantly ameliorates neurological deficits induced by cortical brain ischemia without changing infarction size, suggesting that EE-related functional benefits are associated with neuronal plasticity events in the remaining tissue. Brain-derived neurotrophic factor (BDNF), nerve growth factor-induced gene A (NGFI-A) and corticosteroid receptors (mineralocorticoid receptor, MR; glucocorticoid receptor, GR) have been demonstrated to be involved in brain plasticity. The purpose of this thesis was to determine if post-ischemic housing conditions had a significant effect on transcription and/or translation of BDNF, NGFI-A and corticosteroid receptors. We found that BDNF gene was down regulated in EE-housed rats when compared to the rats housed in standard cages at 2~12 days after cortical brain ischemia in peri-infarct cortex, contralateral cortex and bilateral hippocampus. The protein level of BDNF in ...
Female gender, which is abolished following ovariectomy and reproductive senescence, is associated with improved outcome following cerebral stroke. Estrogen replacement partially restores this benefit of the female gender but the effect of progesterone in hormone-deficient animals is currently unknown. We evaluated various outcomes following middle cerebral artery occlusion (MCAO) in ovariectomised female mice, with a physiologically relevant restoration of progesterone levels. Ovariectomised female mice had significantly elevated plasma (P=,0.05) and brain progesterone levels (P=,0.01) following implantation of a 21-day release pellet (50mg) compared with mice that received placebo implants 7 days prior to undergoing 60 min MCAO. Assessment of well-being (body weight recovery) and neurological score at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome compared with sham-operated mice but progesterone had no effect. MCAO resulted in a substantial lesion formation and a ...
Bilateral carotid occlusion coupled with systemic hypotension produces global brain ischemia in the rat, resulting in damage to the...
Older research outputs will score higher simply because theyve had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 222,049 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile - i.e., 1% of its contemporaries scored the same or lower than it ...
Reversible protein phosphorylation is under the control of opposing activities of protein kinases and protein phosphatases, and has a crucial role in the regulation of cellular signal transduction in a plethora of neural cell functions, including neurogenesis, differentiation, gene transcription and cell death signalling (Klumpp & Krieglstein, 2002b). During the symposium, expert reviews of research on reversible protein phosphorylation, examples from screening approaches for kinase functions in neurons and studies on particular signalling pathways highlighted the importance of this fast‐emerging topic for the understanding of neuronal cell death, and the development of novel neuroprotective strategies.. Protein kinases have been established as key regulators in many important cellular processes, such as proliferation, maintenance of cell shape, survival signalling and apoptosis. Approximately 500 genes encode members of the kinase family in the human genome, and the predicted human kinome ...
Diabetes is a major risk factor for ischemic stroke and is associated with increased mortality. Additionally, hyperglycemia, a common complication in acute stroke, is associated with poor outcome.In order to identify the correlation between blood glucose and early mortality, multiple logistic regression analyses were used and odds ratios calculated in a retrospective study of 447 stroke patients. Eighty-one patients (18%) had diabetes. The odds ratios for 30-day case-fatality and blood glucose were 1.9 and 1.6 in diabetic and non-diabetic patients respectively. Optimal blood glucose concentrations in respective group were 10.3 and 6.3 mmol/L, as determined by receiver operator characteristic (ROC) curves.Cerebral ischemia triggers different signaling pathways including mitogen-activated protein kinases (MAPK) which regulate fundamental cell functions. In an experimental rat model of combined hyperglycemia and transient middle cerebral artery occlusion (MCAO), the activation pattern of one such ...
Several experimental studies have indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox) exert detrimental effects on ischemic brain tissue; Nox-knockout mice generally exhibit resistance to damage due to experimental stroke following middle cerebral artery occlusion (MCAO). Furthermore, our previous MCAO study indicated that infarct size and blood-brain barrier breakdown are enhanced in mice with pericyte-specific overexpression of Nox4, relative to levels observed in controls. However, it remains unclear whether Nox affects the stroke outcome directly by increasing oxidative stress at the site of ischemia, or indirectly by modifying physiological variables such as blood pressure or cerebral blood flow (CBF ...
Cerebral hyperperfusion, or reperfusion syndrome, is a rare, but serious, complication following revascularization. Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue.
TY - CHAP. T1 - Histopathology of Cerebral Ischemia and Stroke. AU - Dalton Dietrich, W.. PY - 2017/3/7. Y1 - 2017/3/7. N2 - Ischemic stroke is a serious neurological problem and one of the leading causes of death and disability worldwide. The histopathological consequences of stroke are complex and may result in a variety of deficits including severe motor and cognitive disturbances. The histopathological consequences of severe focal ischemia are well described with characteristic structural changes occurring in both gray and white brain regions depending on the severity, location, and duration of the ischemic insult. Following focal ischemic injury, neuronal, astrocytic, vascular endothelial, and inflammatory cell changes occur. In white mater tracts, axonal injury with oligodendrocyte damage and subsequent demyelination are also commonly observed. In contrast, less severe or more transient ischemic insults can lead to patterns of selective neuronal injury whereby vulnerable neuronal ...
In our previous study, β-hydroxybutyrate (BHB) was found to prolong survival time and to inhibit cerebral edema by improving energy metabolism in the hypoxia, anoxia and global cerebral ischemia models. In this study, the cerebroprotective effect of BHB was examined in rats with permanent (p)-occlusion and transient (t)-occlusion of middle cerebral artery (MCA). BHB (30 mg · kg,sup,−,/sup,,sup,1,/sup, · h,sup,−,/sup,,sup,1,/sup,) was continuously administered through the femoral vein. In rats with p-MCA occlusion, BHB significantly reduced infarct area at 24 h after the occlusion, but not at 72 h after the occlusion. In rats with 2-h t-MCA occlusion followed by 22-h reperfusion, BHB significantly reduced cerebral infarct area, edema formation, lipid peroxidation and neurological deficits. Moreover, in the t-MCA occlusion model, delayed administration of BHB started at 1 h after the initiation of the MCA occlusion also significantly reduced cerebral infarct area. Taking together the ...
1. Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011;123:1428-35 2. Harukuni I, Bhardwaj A. Mechanisms of brain injury after global cerebral ischemia. Neurol Clin. 2006;24:1-21 3. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G. et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-63 4. Camara AK, Bienengraeber M, Stowe DF. Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury. Front Physiol. 2011;2:13 5. Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci. 2005;1047:248-58 6. Perez-Pinzon MA, Stetler RA, Fiskum G. Novel mitochondrial targets for neuroprotection. J Cereb Blood Flow Metab. 2012;32:1362-76 7. Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M. et al. Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest ...
If the entire ischemic region supplied by the occluded artery evolved into infarction within minutes or even 1 to 2 hours after onset, there would be little if any opportunity to successfully intervene to improve functional and neurologic outcome. Abundant experimental data suggest that brain injury, secondary to an arterial occlusion, is a dynamic process involving varying degrees of early ischemic injury related primarily to the severity of local cerebral blood flow (CBF) impairment. Ischemic regions with very low CBF (,10 mL/100 g/min) rapidly become irreversibly damaged and are referred to as the ischemic core. [14] In stroke models, surrounding or intermixed zones of less severely impaired CBF (approximately 15 to 40 mL/100 g/min) occur and likely also exist in many ischemic stroke patients. This zone of mild to moderately reduced CBF relates to the concept of the ischemic penumbra originally suggested by Astrup et al. [15] As initially defined, the ischemic penumbra encompasses that ...
The present study aimed to investigate the anti-inflammatory effect of 4-methylcyclopentadecanone (4-MCPC) in rats suffering from a cerebral ischemia/ reperfusion (I/R) injury. In this study, the focal cerebral ischemia in rats was induced by middle cerebral artery occlusion (MCAO) for 2 h, and the rats were treated with 4-MCPC (8 mg/kg) just 0.5 h before reperfusion. The ischemic infarct volume was recorded 24 h after the MCAO. In addition, myeloperoxidase (MPO) activity and TNF-α and IL-1β levels in the ischemic cerebral cortex were determined by ELISA, while nuclear translocation of NF-κB p65 subunit and expression of p-IκBα were investigated by western blotting ...
This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In …
The animal model of stroke that is most frequently used is a rat model of focal brain ischemia caused by middle cerebral artery occlusion (MCAO). Several studies have reported a link between levels of cell-free DNA (CFD) and neurologic outcome in human stroke. The purpose of this study was to assess brain injury and measure CFD levels in 2 models of MCAO in rats, and to determine whether brain injury correlates with CFD. A total of 60 rats were used for this study. Twenty rats underwent a sham procedure, 20 rats had MCAO using a monofilament, and 20 rats had MCAO with a silicon-coated filament. Groups were further divided into 2 subgroups. In 1 subgroup of 10 rats, neurologic performance [measured as a neurologic severity score, (NSS)] was measured at 1 and 24 hours after the procedure, and brain edema and infarct volume were determined at 24 hours. In the second subgroup of 10 rats, CFD was measured at 0, 1, 2, 4, 8, 12, and 24 hours and at 2, 3, 4, and 5 days. Neurologic performance (measured ...
The histologic description of cerebral ischemia is complex, and within most lesions there are regional variations in degrees of neuronal cell injury, edema, and neuropil disruption. These parameters of tissue injury were analyzed histopathologically in transient and permanent experimental cerebral ischemia in 15 rabbits and the results were spatially correlated with MR images of pre- and postmortem (formalin-fixed) brains. MR was performed at 1.5 T (eight animals) and at 0.38 T (seven animals). Areas of high signal on T2-weighted MR images were closely correlated with histologic signs of cytotoxic glial edema and with disruption of the neuropil (widening of the interstitial spaces in the background matrix of glial and neuronal cellular processes), but MR tended to underestimate the extent of ischemic neuronal injury, especially low-grade histologic changes (mild neuronal shrinkage and nuclear basophilia). Low-grade ischemic neuronal changes were often found in the penumbra zone of ischemic ...
Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to develop effective pharmacological treatments. However, the underlying molecular mechanisms are complex and not completely understood. One of the main problems is the fact that the ischemic damage is time-dependent and ranges from negligible to massive, involving different cell types such as neurons, astrocytes, microglia, endothelial cells, and some blood-derived cells (neutrophils, lymphocytes, etc.). Thus, approaching such a complicated cellular response generates a more complex combination of molecular mechanisms, in which cell death, cellular damage, stress and repair are intermixed. For this reason, animal and cellular model systems are needed in order to dissect and clarify which molecular mechanisms have to be promoted and/or blocked.Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage per se) and that of deprivation of
DESCRIPTION (provided by applicant): There is growing evidence that estrogen (E2) and SERMs may have beneficial effects upon the CNS in neurodegenerative diseases. This application would study the potential mechanisms of E2/SERM neuroprotection in cerebral ischemia, and would follow up on exciting preliminary work by our lab which suggests that E2/SERMs enhance neurogenesis following cerebral ischemia. With regards to neuroprotection, our preliminary studies suggest that E2 and the SERM, tamoxifen (TMX) inhibit activation of putative prodeath factors (ROS, ERKs, INK, c-Jun), with an increase in activation of the prosurvival factor, Akt. To confirm these preliminary findings and clarify the underlying mechanisms, Aim 1 would determine the temporal pattern and cell type of ERK/JNK/Akt activation following cerebral ischemia in female animals (which is currently lacking), establish the onset and duration of E2/SERM regulatory effects upon these key kinases, and determine the role of estrogen ...
During recent years neurotransmitters and neuromodulators have been recognized as important extracellular modulators of ischemic and hypoglycemic brain damage. Several investigations have...
Synonyms for Cerebral ischaemia in Free Thesaurus. Antonyms for Cerebral ischaemia. 54 synonyms for stroke: caress, rub, fondle, pat, pet, apoplexy, fit, seizure, attack, shock, collapse, mark, line, slash, movement, action, motion, chime.... What are synonyms for Cerebral ischaemia?
Looking for Cerebral ischemia? Find out information about Cerebral ischemia. Localized tissue anemia as a result of obstruction of the blood supply or to vasoconstriction. a local deficiency of blood; insufficient blood in an organ... Explanation of Cerebral ischemia
Intravenous Administration of Cilostazol Nanoparticles Ameliorates Acute Ischemic Stroke in a Cerebral Ischemia-Reperfusion-Induced Injury Model. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Intensive attention was recently payed to brain impairment due to acute cerebral ischemia and reperfusion, this paper reports on cortex somatosensory evoked potentials (SEPs), light microscope and electron microscope have been used to study the effect of calcium channel blocker I -65 on the brain impairment due to acute cerebral ischemia and reperfusion. The results suggest that 1-65 can protect electric activily of cerebral cortex neurons and ultrastructure of mitochondria and RER of neurons during acute cerebral ischemia and reperfusion. The mechanism may be blocking Ca2+ channel selectively so that preventing the increase of concentrations of Ca2+ within neurons.
Background Traumatic brain injury is a major medical problem globally and is one of the leading causes of death and disability. There is no known treatment for stroke or ischaemic brain injury. A stroke is a medical emergency and can cause permanent brain damage and death. Risk factors for stroke include old age, high blood pressure, previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, smoking and heart attack. Stroke is the second leading cause of death worldwide. The Technology This invention has arisen from our discovery of a novel isoform of the TRPC3 ...
This stock medical exhibit compares three coronal views of the head and brain to describe the Progression of Brain Ischemia. The following views are illustrated: 1- Initial infarct in the region of the left cerebral artery. 2- Generalized spread of hypoxia and swelling from the left to right side. 3- Involvement of the right cerebral artery with further brain damage.
What is Cerebral Ischemia? What are its causes? And how can Ischemia be treated effectively? ► Learn more about Cerebral Ischemia now
Interview with Shelagh B. Coutts, MD, FRCPC, author of Rate and Prognosis of Brain Ischemia in Patients With Lower-Risk Transient or Persistent Minor Neurologic
Ferrer Therapeutics has made available CerAxon Oral Solution, a medical food containing citicoline, for the dietary management of brain ischemia due to stroke or traumatic brain injury in patients who have difficulty swallowing.
Atif F, Yousuf S, Agrawal SK. S-allyl L-cysteine diminishes cerebral ischemia-induced mitochondrial dysfunctions in hippocampus ...