24 results match your criteria ischemia-induced fischer

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Absence of Cold-Inducible RNA-Binding Protein (CIRP) Promotes Angiogenesis and Regeneration of Ischemic Tissue by Inducing M2-Like Macrophage Polarization.

Biomedicines 2021 Apr 7;9(4). Epub 2021 Apr 7.

Walter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.

Cold-inducible RNA-binding protein (CIRP) is an intracellular RNA-chaperone and extracellular promoter of inflammation, which is increasingly expressed and released under conditions of hypoxia and cold stress. The functional relevance of CIRP for angiogenesis and regeneration of ischemic muscle tissue has never been investigated and is the topic of the present study. We investigated the role of CIRP employing CIRP deficient mice along with a hindlimb model of ischemia-induced angiogenesis. Read More

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Single cell sequencing reveals endothelial plasticity with transient mesenchymal activation after myocardial infarction.

Nat Commun 2021 01 29;12(1):681. Epub 2021 Jan 29.

Institute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.

Endothelial cells play a critical role in the adaptation of tissues to injury. Tissue ischemia induced by infarction leads to profound changes in endothelial cell functions and can induce transition to a mesenchymal state. Here we explore the kinetics and individual cellular responses of endothelial cells after myocardial infarction by using single cell RNA sequencing. Read More

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January 2021

Potential Therapeutic Application of Zinc Oxide Nanoflowers in the Cerebral Ischemia Rat Model through Neuritogenic and Neuroprotective Properties.

Bioconjug Chem 2020 03 25;31(3):895-906. Epub 2020 Feb 25.

Department of Applied Biology, CSIR-Indian Institute of Chemical Technology, Uppal Road, Tarnaka, Hyderabad 500007, India.

Neuritogenesis, a complex process of the sprouting of neurites, plays a vital role in the structural and functional restoration of cerebral ischemia-injured neuronal tissue. Practically, there is no effective long-term treatment strategy for cerebral ischemia in clinical practice to date due to several limitations of conventional therapies, facilitating the urgency to develop new alternative therapeutic approaches. Herein, for the first time we report that pro-angiogenic nanomaterials, zinc oxide nanoflowers (ZONF), exhibit neuritogenic activity by elevating mRNA expression of different neurotrophins, following PI3K/Akt-MAPK/ERK signaling pathways. Read More

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Green Tea Extract Ameliorates Ischemia-Induced Retinal Ganglion Cell Degeneration in Rats.

Oxid Med Cell Longev 2019 9;2019:8407206. Epub 2019 Jul 9.

Joint Shantou International Eye Center of Shantou University and the Chinese University of Hong Kong, Shantou, Guangdong, China.

Purpose: Oxidative stress induced by reduced blood circulation is a critical pathological damage to retinal ganglion cells (RGCs) in glaucoma. We previously showed that green tea extract (GTE) and its catechin constituents alleviate sodium iodate-induced retinal degeneration in rats. Here, we investigated the therapeutic effect of GTE on ischemia-induced RGC degeneration in rats. Read More

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January 2020

Effect of cardiac arrest on cognitive impairment and hippocampal plasticity in middle-aged rats.

PLoS One 2015 1;10(5):e0124918. Epub 2015 May 1.

Cerebral Vascular Disease Research Laboratories, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America; Evelyn F. McKnight Brain Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America; Department of Neurology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America; Neuroscience Program, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, United States of America.

Cardiopulmonary arrest is a leading cause of death and disability in the United States that usually occurs in the aged population. Cardiac arrest (CA) induces global ischemia, disrupting global cerebral circulation that results in ischemic brain injury and leads to cognitive impairments in survivors. Ischemia-induced neuronal damage in the hippocampus following CA can result in the impairment of cognitive function including spatial memory. Read More

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January 2016

Coxsackie and adenovirus receptor is a modifier of cardiac conduction and arrhythmia vulnerability in the setting of myocardial ischemia.

J Am Coll Cardiol 2014 Feb 27;63(6):549-59. Epub 2013 Nov 27.

Heart Failure Research Center, Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam, the Netherlands. Electronic address:

Objectives: The aim of this study was to investigate the modulatory effect of the coxsackie and adenovirus receptor (CAR) on ventricular conduction and arrhythmia vulnerability in the setting of myocardial ischemia.

Background: A heritable component in the risk of ventricular fibrillation during myocardial infarction has been well established. A recent genome-wide association study of ventricular fibrillation during acute myocardial infarction led to the identification of a locus on chromosome 21q21 (rs2824292) in the vicinity of the CXADR gene. Read More

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February 2014

Anthranilate fluorescence marks a calcium-propagated necrotic wave that promotes organismal death in C. elegans.

PLoS Biol 2013 Jul 23;11(7):e1001613. Epub 2013 Jul 23.

Institute of Healthy Ageing, and Research Department of Genetics, Evolution and Environment, University College London, London, United Kingdom.

For cells the passage from life to death can involve a regulated, programmed transition. In contrast to cell death, the mechanisms of systemic collapse underlying organismal death remain poorly understood. Here we present evidence of a cascade of cell death involving the calpain-cathepsin necrosis pathway that can drive organismal death in Caenorhabditis elegans. Read More

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Blockade of electron transport before ischemia protects mitochondria and decreases myocardial injury during reperfusion in aged rat hearts.

Transl Res 2012 Sep 17;160(3):207-16. Epub 2012 Feb 17.

Department of Medicine, Division of Cardiology, Case Western Reserve University, Cleveland, Ohio, USA.

Myocardial injury is increased in the aged heart following ischemia and reperfusion (I-R) in both humans and experimental models. Hearts from aged 24-month-old Fischer 344 rats sustain greater cell death and decreased contractile recovery after I-R compared with 6-month-old adult controls. Cardiac mitochondria incur damage during I-R contributing to cell death. Read More

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September 2012

Up-regulation of P2X7 receptor-immunoreactivity by in vitro ischemia on the plasma membrane of cultured rat cortical neurons.

Neurosci Lett 2008 Nov 17;446(1):45-50. Epub 2008 Sep 17.

Rudolf-Boehm-Institute of Pharmacology and Toxicology, University of Leipzig, D-04107 Leipzig, Germany.

Mixed neuronal/astrocytic cortical cell cultures of the rat were incubated for 2 or 12h under normoxic or ischemic conditions. Subsequent flow cytometric analysis with an anti-P2X7 receptor antibody directed against an extracellular epitope indicated the up-regulation of these receptors at the plasma membrane by 12h of ischemia. Labelling of MAP-2 immunopositive neurons by an anti-P2X7 antibody directed against a C-terminal epitope, documented the selectivity of the ischemia-induced increase in receptor-density for the neuronal population. Read More

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November 2008

Simulated ischemia-induced preconditioning of isolated ventricular myocytes from young adult and aged Fischer-344 rat hearts.

Am J Physiol Heart Circ Physiol 2008 Aug 20;295(2):H768-77. Epub 2008 Jun 20.

Dept. of Pharmacology, Dalhousie Univ., 5850 College St., Sir Charles Tupper Medical Bldg., Halifax, NS, Canada B3H 1X5.

The impact of ischemic preconditioning (IPC) on contraction, Ca(2+) homeostasis, and cell survival was compared in isolated ventricular myocytes from young adult ( approximately 3 mo) and aged ( approximately 24 mo) male Fischer-344 rats. Myocytes were field stimulated at 4 Hz (37 degrees C). Contraction (edge detector) and intracellular Ca(2+) (fura-2) were measured simultaneously. Read More

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Increased sensitivity to transient global ischemia in aging rat brain.

Adv Exp Med Biol 2007 ;599:199-206

Case Western Reserve University, Cleveland, Ohio 44106, USA.

Transient global brain ischemia induced by cardiac arrest and resuscitation (CAR) results in reperfusion injury associated with oxidative stress. Oxidative stress is known to produce delayed selective neuronal cell loss and impairment of brainstem function, leading to post-resuscitation mortality. Levels of 4-hydroxy-2-nonenal (HNE) modified protein adducts, a marker of oxidative stress, was found to be elevated after CAR in rat brain. Read More

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December 2007

Inhibition of phosphatase activity enhances preconditioning and limits cell death in the ischemic/reperfused aged rat heart.

Life Sci 2005 Nov 15;77(26):3375-88. Epub 2005 Aug 15.

Department of Physiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.

Brief, nonlethal episodes of ischemia in the mammalian heart provide cardioprotection against the detrimental effects of a longer duration ischemia. The manifestation of this preconditioning (PC) phenomenon is initiated by the enhanced phosphorylation state of signal transduction proteins. We reported previously that PC is decreased in the aged rat myocardium. Read More

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November 2005

Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport.

Neurobiol Dis 2005 Mar;18(2):336-45

Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid (UCM), 28040 Madrid, Spain.

Background And Purpose: Cytidine-5'-diphosphocholine (citicoline or CDP-choline), an intermediate in the biosynthesis of phosphatidylcholine, has shown beneficial effects in a number of CNS injury models including cerebral ischemia. Citicoline is the only neuroprotectant that has proved efficacy in patients with moderate to severe stroke. However, the precise mechanism by which citicoline is neuroprotective is not fully known. Read More

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VEGF-A splice variants and related receptor expression in human skeletal muscle following submaximal exercise.

J Appl Physiol (1985) 2005 Jun 20;98(6):2137-46. Epub 2005 Jan 20.

Karolinska Institute, Berzelius Väg 35, Stockholm 171 77, Sweden.

VEGF-A contributes to muscle tissue angiogenesis following aerobic exercise training. The temporal response of the VEGF-A isoforms and their target receptors has not been comprehensively profiled in human skeletal muscle. We combined submaximal exercise with and without reduced leg blood flow to establish whether ischemia-induced metabolic stress was an important physiological stimuli responsible for regulating the VEGF-A system in humans. Read More

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Inhibition of glutamate release by delaying ATP fall accounts for neuroprotective effects of antioxidants in experimental stroke.

FASEB J 2003 Nov 18;17(14):2082-4. Epub 2003 Sep 18.

Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, 28040 Madrid. Spain.

Excitotoxic neuronal injury related to excessive glutamate release is believed to play a key role in the pathogenesis of focal cerebral ischemia. Reversal of neuronal glutamate transporters caused by ATP fall and subsequent imbalance of membrane ionic gradients accounts for most glutamate release after cerebral ischemia. ATP synthesis from oxidative phosphorylation derives from the coupled functioning of the mitochondrial respiratory chain (MRC) and the ATP synthase; interestingly, the MRC is one of the main sites of cellular reactive oxygen species (ROS) generation even in physiological circumstances. Read More

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November 2003

L-arginine levels in blood as a marker of nitric oxide-mediated brain damage in acute stroke: a clinical and experimental study.

J Cereb Blood Flow Metab 2003 Aug;23(8):978-84

Department of Neurology, Hospital Doctor Josep Trueta, Girona, Spain.

There are no useful markers in blood of nitric oxide (NO)-mediated brain damage. Because l-arginine (l-arg) is the only known substrate for NO generation, the authors investigated the plasma profile of l-arg after cerebral ischemia, and the relationship of L-arg concentrations in blood with stroke outcome and infarct volume in a clinical and experimental study. l-Arg levels were determined with high-performance liquid chromatography in blood and CSF samples obtained on admission, and in blood 48 hours after inclusion, in 268 patients admitted with a hemispheric ischemic stroke lasting 8. Read More

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Exercise training attenuates age-associated diastolic dysfunction in rats.

Circulation 2001 Jul;104(2):221-6

Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, MA 02118, USA.

Background: In contrast to systolic function, which is relatively well preserved with advancing age, diastolic function declines steadily after age 30. Our goal was to determine whether changes in diastolic function that occur with aging could be reversed with exercise training. Methods and Results-- Adult (6-month-old) and old (24-month-old) Fischer 344/BNF1 rats were studied after either 12 weeks of treadmill training or normal sedentary cage life. Read More

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In vivo diffusion-weighted magnetic resonance microscopy of rat spinal cord: effect of ischemia and intrathecal hyperbaric 5% lidocaine.

Reg Anesth Pain Med 1999 Jul-Aug;24(4):311-8

Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710, USA.

Background And Objectives: Pathophysiologic mechanisms underlying persistent neurologic deficits after continuous spinal anesthesia using hyperbaric 5% lidocaine are still not well understood. It has been suggested that high-dose intrathecal lidocaine induces irreversible conduction block and even ischemia in white matter tracts by breakdown of the blood-nerve barrier. In this study, we use diffusion-weighted magnetic resonance microscopy to characterize the effect of intrathecal hyperbaric 5% lidocaine in rat spinal cord. Read More

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September 1999

Hypothyroidism-evoked shifts in hippocampal adrenergic receptors: implications to ischemia-induced hippocampal damage.

Mol Cell Biochem 1998 Aug;185(1-2):161-9

Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.

Hypothyroidism was induced in a group of male Fischer 344 rats by administration of 0.05% propylthiouracil (PTU) in the drinking water for 12 weeks. Control rats were not treated. Read More

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Infarct volume varies with rat strain and vendor in focal cerebral ischemia induced by transcranial middle cerebral artery occlusion.

Brain Res 1995 Nov;699(2):329-31

Department of Pharmacology, College of Medicine, University of California, Irvine 92717, USA.

We recently reported that the outcome of focal cerebral ischemia induced by intraluminal middle cerebral artery occlusion may differ depending upon a rat's strain and/or vendor. Sprague-Dawley rats originating from Taconic Laboratories and Charles River Laboratories had infarct volumes several fold larger than Sprague-Dawley rats originating from Simonsen Laboratories. The present study sought to determine whether these differences were restricted to an intraluminal technique or whether strain and vendor dependent differences will also exist in rats subjected to a transcranial method of focal cerebral ischemia. Read More

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November 1995

Cerebroprotective effect of lamotrigine after focal ischemia in rats.

Stroke 1995 Jan;26(1):117-21; discussion 121-2

Department of Neurology, Institute of Psychiatry, De Crespigny Park, Denmark Hill, UK.

Background And Purpose: Glutamate receptor antagonists are protective in animal models of focal cerebral ischemia. Lamotrigine (3,5-diamino-6-[2,3-dichlorophenyl]-1,2,4-triazine) is an anticonvulsant drug that blocks voltage-gated sodium channels and inhibits the ischemia-induced release of glutamate. We describe the cerebroprotective effect of lamotrigine (as the isethionate salt) after middle cerebral artery occlusion in rats. Read More

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January 1995

Perioperative assessment of cardiac energy metabolism by means of arterio-coronary venous difference in lactate concentration (acDL). A parameter for optimizing ventricular function of the postcardioplegic myocardium.

Eur J Cardiothorac Surg 1990 ;4(5):278-83

Clinic of Surgery, Martin-Luther-University, Halle-Wittenberg, GDR.

Fourty-three patients undergoing open heart surgery were subjected to extended hemodynamic and metabolic monitoring (arterial and coronary sinus (CS) lactate concentration). In 95% of patients investigated, a significant increase in CS lactate concentration above the arterial lactate concentration was established at the beginning of reperfusion (RPT). In these cases, a decrease in the CS lactate below the arterial concentration occurs within the RPT creating a cross-over point (COP) from negative to positive lactate extraction values. Read More

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Forebrain ischemia induced by temporary bilateral common carotid occlusion in normotensive rats.

J Neurol Sci 1989 Apr;90(2):155-65

Department of Neurological Sciences, Tohoku University School of Medicine, Sendai, Japan.

Ischemic brain lesions were induced in adult Wistar and Fischer rats by temporary occlusion of the bilateral common carotid artery. The severity of ischemic lesions depended on the duration of carotid occlusion. While 2 h occlusion resulted in 15 deaths among 40 rats and the development of ischemic lesions in 16 of 25 asymptomatic survivors, none died after 0. Read More

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Nifedipine: a myocardial protective agent.

Am J Cardiol 1979 Oct;44(5):825-31

The effectiveness of the calcium antagonist nifedipine in preserving postischemic myocardial function and structural integrity was experimentally demonstrated in isolated rabbit hearts, in conscious dogs subjected to myocardial infarction, in open chest anesthetized dogs with normothermic regional ischemia induced for 1 to 2 hours and in dogs undergoing hypothermic global ischemia for 2 hours followed by 2 hours of reperfusion. Nifedipine had a beneficial effect on postischemic myocardial stiffness and mitochondrial calcium accumulation, which were correlated. Administration of nifedipine at the onset of myocardial infarction increased blood flow to ischemic zones of myocardial infarction and resulted in less loss of creatine kinase. Read More

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October 1979
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