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Thèses sur le sujet « Ischemia »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 25 juillet 2025

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1

Du, Ying. "Ischemic and pharmacological preconditioning of rat myocardium : effects on ischemia-reperfusion injury /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20DU.

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2

Christensen, Thomas. "Experimental focal cerebral ischemia : pathophysiology, metabolism and pharmacology of the ischemic penumbra /." Copenhagen, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143698&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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3

Dowden, Jennifer. "Characterizing the neuroprotective efficacy of ischemic preconditioning (ischemic tolerance) : is age an important factor? /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/NQ54834.pdf.

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4

Harhous, Zeina. "Deciphering the Interlink between STAT3 and MAPKs in Ischemia/Reperfusion and Ischemic Conditioning." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1145.

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Les maladies cardiovasculaires sont une des principales causes de morbidité et de mortalité au monde. La plus courante est l’infarctus du myocarde définit pathologiquement par la mortalité cellulaire dû à une ischémie prolongée d’une partie du ventricule gauche. L'ischémie est caractérisée par un apport sanguin insuffisant causé par une obstruction d’une artère coronaire. La restauration, en clinique, du flux sanguin, appelée reperfusion, est considérée comme la méthode la plus efficace contre les dommages ischémiques. Paradoxalement, cette restauration du flux sanguin est associée à une exace

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5

Zhang, Jitian. "Nebulized phosphodiesterase 3 inhibitor during warm ischemia attenuates pulmonary ischemia-reperfusion injury." Kyoto University, 2009. http://hdl.handle.net/2433/126442.

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6

Li, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia." Connect to resource online, 2009. http://hdl.handle.net/1805/2021.

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Thesis (Ph.D.)--Indiana University, 2009.<br>Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).

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7

Keasey, Matthew P. "MicroRNAs in Cerebral Ischemia." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526014.

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8

Lipšic, Erik. "Erythropoietin in cardiac ischemia." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/293076030.

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9

Aoyama, Akihiro. "Post-ischemic Infusion of Atrial Natriuretic Peptide Attenuates Warm Ischemia-Reperfusion Injury in Rat Lung." Kyoto University, 2011. http://hdl.handle.net/2433/142544.

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10

Hultgren, Rebecka. "Lower limb ischemia in women /." Stockholm, 2004. http://diss.kib.ki.se/2003/91-7349-798-3.

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11

Molnar, Maria. "Hyperglycemia in Experimental Cerebral Ischemia." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247763.

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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

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12

Alrabadi, Nasr Nofal Salieba. "Novel Pharmacological Approaches for Understanding and Modulating the Pathology of Ischemic Heart Disease." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15926.

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Over the last century, ischemic heart diseases (IHD) have been the worldwide leading cause of death. Major improvement in the prevalence and prognosis of IHD is dominantly related to the modulation of disease (atherosclerosis) risk factors rather than developing pharmacological approaches to treatment. Excessive inflammatory response, especially after ischemia-reperfusion injury (IR), represents a key feature in the progressive pathology of IHD. The kinetics of this inflammatory infiltration is well organized in a timely manner. Both the classical pathological phases of post ischemic heart inj

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13

MACRI', MARIA LOREDANA. "Ruolo dello scambiatore Na+/Ca2+ nel precondizionamento ischemico in modelli sperimentali di ischemia-riperfusione cardiaca." Doctoral thesis, Università Politecnica delle Marche, 2015. http://hdl.handle.net/11566/242929.

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L’ischemia cardiaca è una delle principali cause di morbidità e mortalità nei Paesi occidentali. Alterazioni dei sistemi di trasporto del calcio cardiaco che causano aumento di calcio citosolico sono i principali responsabili del danno da I/R. Il precondizionamento ischemico (IPC) conferisce cardioprotezione attenuando tale aumento. Uno dei principali responsabili del controllo dell’omeostasi del calcio cellulare nel cuore è NCX1. Durante l’I/R, NCX1 induce l’influsso di Ca2+, pertanto per poterlo contrastare si potrebbe utilizzare l’inibitore SN6. Lo scopo del presente studio è stato di stud

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14

Tupling, Allan Russell. "Effects of ischemia and ischemia-reperfusion on sarcoplasmic reticulum structure and function in rat skeletal muscle." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ53520.pdf.

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15

Yamasaki, Kenzou. "Preconditioning with 15-min ischemia extends myocardial infarct size after subsequent 30-min ischemia in rabbits." Kyoto University, 1997. http://hdl.handle.net/2433/202231.

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16

Fröjse, Rolf. "Exploring Intestinal Ischemia : An experimental study." Doctoral thesis, Umeå universitet, Kirurgisk och perioperativ vetenskap, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-461.

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Background and aims: Unrecognized intestinal mucosal ischemia in severely ill patients may trigger development of multiple organ failure. Such ischemia can be evaluated by intraluminal tonometry reflecting mucosal PCO2 and intramucosal pH (pHi). The aims were to develop an apparatus for continuous saline tonometry (CST), to analyse circulatory control mechanisms during intestinal hypoperfusion and to evaluate the effect of dopexamine on intestinal circulation. Methods: A modified standard tonometry catheter was integrated in a closed system with circulating saline. By measuring saline PCO2 in

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17

Abunasra, Haitham Juma. "Gene therapy in myocardial ischemia-reperfusion." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404964.

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18

Bonneville, Marika. "Endocannabinoid Modulation of Post-Ischemia Depression." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35056.

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Post-ischemia depression (PID) is a condition that affects approximately 30% of survivors from stroke or cardiac arrest and has an important impact on patients’ quality of life. Previous studies support important roles of the endocannabinoid (eCB) system in depression and brain ischemia. This study attempts to link all three variables together by investigating the role and mechanism of eCB signaling in the development of PID. A global ischemia + hypotension model was used to induce a PID phenotype in CD1 mice. Three ischemic time frames were tested, and even though all three could induce signi

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19

Thorén, Anna. "Astrocyte metabolism following focal cerebral ischemia /." Göteborg : Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/744.

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20

Soundarapandian, Mangala Meenakshi. "Glutamate Excitotoxicity in Epilepsy and Ischemia." Doctoral diss., University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/3169.

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'Excitotoxicity' represents the excitatory amino acid mediated degeneration of neurons. Glutamate is the major excitatory neurotransmitter in the brain. Glutamate excitotoxicity has been implicated in a number of neurodegenerative disorders like Stroke, Epilepsy, Alzheimer's disease and traumatic brain injury. This neurotoxicity is summed up by the 'glutamate hypothesis' which describes the cause of neuronal cell death as an excessive release of glutamate causing over excitation of the glutamate receptors and subsequent increase in influx of calcium leading to cell death. An effort to countera

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21

Aluri, Hema. "INTRA-MITOCHONDRIAL INJURY DURING ISCHEMIA-REPERFUSION." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/474.

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Cardiac injury is increased following ischemia-reperfusion. Mitochondria are the “effector organelles” that are damaged during ischemia (ISC) when there is no blood flow. Resumption of metabolism by damaged mitochondria during reperfusion (REP) results in increased cell injury. Current therapeutic interventions to pre-condition and post-condition the heart during ISC are ineffective during certain conditions like aging and diabetes due to defects in the signaling cascades. In contrast, mitochondrial-based strategies are effective in protecting the heart during ISC-REP. Hence direct therapeutic

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22

Todd, Michael. "The effects of multiple ischemia and survival times on hippocampal CA1 neuronal cell loss in a rat model of global ischemia: A long-term ischemia maturation study." Thesis, University of Ottawa (Canada), 1998. http://hdl.handle.net/10393/4230.

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We investigated the effects of varying ischemia and survival times on CA1 neuronal loss. Histological analysis of the hippocampus was performed at 2, 7, 14, 28 and 90 days following 3, 5, 7, 10 and 13 minutes of global forebrain ischemia. Our results indicate that the ischemic maturation process extends beyond 7 days. Ten and thirteen minutes of ischemia produced a significant degree of cell loss by 7 days (70.53% and 83.25% respectively), while average cell death at 90 days survival was approximately 12% higher. Most strikingly, seven minutes of ischemia produced approximately 30% CA1 cell lo

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23

Todd, Mike. "The effects of multiple ischemia and survival times on hippocampal CA1 neuronal cell loss in a rat model of global ischemia, a long-term ischemia maturation study." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ36746.pdf.

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24

Thomas, Sunu Samuel. "Murine models of cerebral ischemia, development of a mouse model of global cerebral ischemia; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/MQ50439.pdf.

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25

Adhami, Faisal. "Differential Adult and Neonatal Response to Cerebral Ischemia-Hypoxia." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1196054266.

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26

Zouita, Abdel Hakim. "Ischemia modified-albumin as a biomarker of myocardial ischemia : early diagnosis of acute coronary syndrome and cost effectiveness analysis." Thesis, University of Portsmouth, 2016. https://researchportal.port.ac.uk/portal/en/theses/ischemia-modifiedalbumin-as-a-biomarker-of-myocardial-ischemia(326d84fe-6bb8-463d-b7fc-00ad3dfbc6c8).html.

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Ischemia modified-albumin (IMA®) is a useful early cardiac biomarker for the diagnosis of acute coronary syndrome. In this study the diagnostic efficiency and the cost effectiveness of the oxidative stress biomarker (ischemia modified-albumin), myocardial necrosis (high sensitivity cardiac troponin, heart fatty-acid binding protein), vascular stress (copeptin) and myocardial dysfunction and hemodynamic stress (B-type natriuretic peptide) were evaluated for the diagnosis of acute myocardial infarction and cost benefit in low risk patients presenting to the emergency department with chest pain.

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27

Venardos, Kylie M. "Myocardial Antioxidant Enzyme Systems, Ischemia-Reperfusion Injury, and Selenium." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365301.

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Coronary heart disease remains the greatest killer of Australian's, and given our ageing population, along with increasing risk factors, it is predicted to become an even more significant problem worldwide over the next 20 years. Reperfusion, without doubt is the most effective treatment for ischemic myocardium. However, this produces deleterious effects upon cells, and depending on the severity, may ultimately lead to cell death. While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating reactive oxygen species (ROS) as an initial c

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28

McDonough, Jason L. "Myofilament protein modifications in myocardial ischemia/reperfusion." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ65682.pdf.

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29

Snoeckx, Luc Henricus Elisabeth Hyacinthus. "Ischemia tolerance of the hypertrophied rat heart." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5399.

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30

Nelissen-Vrancken, Henrica Johanna Maria Gerardine. "Local renin angiotensin systems and peripheral ischemia." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1992. http://arno.unimaas.nl/show.cgi?fid=5719.

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31

Roekaerts, Paul M. H. J. "Alpha2-adrenergic receptor agonists in myocardial ischemia." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5784.

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32

Lips, Jeroen. "Experimental spinal cord ischemia detection and protection /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/62717.

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33

Winbladh, Anders. "Microdialysis in Liver Ischemia and Reperfusion injury." Doctoral thesis, Linköpings universitet, Kirurgi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-68651.

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Introduction: New chemotherapy regimens and improvements in surgical technique have increased the number of patients with liver tumours eligible for curative liver resection. There is a significant risk of bleeding during liver surgery, but this risk can be reduced if the portal inflow is temporarily closed; i.e. the Pringles maneuver (PM). If the PM is used, the liver will suffer from ischemia and reperfusion injury (IRI). If the liver remnant is too small or if the patient has chronic liver disease, the IRI may inhibit the regeneration of the liver remnant. The patient may then die from post

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34

Björnsson, Bergþór. "Methods to Reduce Liver Ischemia/Reperfusion Injury." Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110318.

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Introduction: During the last two decades, liver surgery has expanded enormously, partly due to improved surgical equipment and techniques as well as new and more powerful chemotherapy agents. As the liver is a very well-vascularized organ, there is an inherent risk of bleeding during liver resection. One of the most popular methods employed to reduce this risk is to close the vascular inflow to the liver using the Pringle’s maneuver (PM). However, this procedure has been recognized to cause ischemia/reperfusion injury (IRI) to the future liver remnant (FLR). In cases of extensive resection wh

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35

Karelina, Ekaterina. "MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479.

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36

Iwase, Tomoyuki. "Ischemic Preconditioning Is Associated With a Delay in Ischemia-Induced Reduction of β-Adrenergic Signal Transduction in Rabbit Hearts". Kyoto University, 1994. http://hdl.handle.net/2433/168855.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(医学)<br>甲第5551号<br>医博第1521号<br>新制||医||576(附属図書館)<br>UT51-94-C9<br>京都大学大学院医学研究科内科系専攻<br>(主査)教授北徹, 教授眞崎知生, 教授篠山重威<br>学位規則第4条第1項該当

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37

Li, Ping-An. "Mechanisms of acidosis-mediated ischemic brain damage histopathology and pathophysiology /." Lund : Lund University, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38158955.html.

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38

Ebert, Natalie Rut. "Cortical spreading ischaemia als Folge von freiem Hämoglobin und erhöhter Kaliumkonzentration im Subarachnoidalraum induziert cortikale Infakte bei der Ratte." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/14645.

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Die Pathogenese der verzögerten ischämischen Defizite (VIND) nach Subarachnoidalblutung wird mit Produkten der Hämolyse in Zusammenhang gebracht. Topische Hirnsuperfusion mit einer artifiziellen cerebrospinalen Flüssigkeit (ACSF), die L-NA, einen NOS-Inhibitor, in Kombination mit einer erhöhten Kaliumkonzentration erhielt, hat bei der Ratte zu Ischämien geführt. Dieses Phänomen wurde als Cortical spreading ischemia (CSI) bezeichnet. Dabei scheint es während der neuronalen Depolarisation zu einer gestörten Kopplung zwischen cerebralem Metabolismus und Blutfluß zu kommen, die zu einer Vasokonstr

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39

Hooshdaran, Bahman. "DUAL INHIBITION OF CATHEPSIN G AND CHYMASE AFTER ISCHEMIA REPERFUSION: THE ROLE OF INFLAMMATORY SERINE PROTEASES IN ISCHEMIA REPERFUSION INJURY." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/475423.

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Bioengineering<br>Ph.D.<br>Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality in the world (4). Restoration of coronary flow to the ischemic myocardium by interventions such as angioplasty, thrombolytic treatment or coronary bypass surgery is the current standard therapy for AMI (5). However, reperfusion of the ischemic myocardium may result in paradoxical cardiomyocyte dysfunction and worsen tissue damage, in a process known as “reperfusion injury” (6). Ischemic reperfusion (IR) injury may intensify pathological processes that contribute to the generation of oxyra

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40

Yusof, Mozow. "Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4779.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.<br>The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

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41

SAKAMOTO, NOBUO, TATSUAKI MATSUBARA, YOSHIHIRO KAKINUMA, and TATSUO HASHIMOTO. "MYOCARDIAL METABOLIC MARKERS OF TOTAL ISCHEMIA IN VITRO." Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/15927.

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42

Edrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.

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Cerebral small vessel pathology is now known to be associated with the development of cognitive impairment and mild motor impairments such as gait disturbance in a variety of neurodegenerative diseases. This dissertation explores the hypothesis that blood brain barrier dysfunction is an early event in cerebral ischemia and contributes to the development of cerebral small vessel disease (CSVD). A common rodent model of CSVD is permanent bilateral common carotid artery occlusion in the rat. This model was used to study several aspects of the progression of CSVD including the timecourse of blood

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43

Labruto, Fausto. "Modifications of cardiovascular response to ischemia and trauma /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-379-5/.

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44

Ng, Kit-ying. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634371.

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45

Bogart, Robert William. "The effect of stress on global cerebral ischemia." Connect to resource, 2008. http://hdl.handle.net/1811/32235.

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46

Ng, Kit-ying, and 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.

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47

Wang, Haihui. "Ribonomic control during global brain ischemia and reperfusion." Thesis, Wayne State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3641445.

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<p> The study presented here used "omic" technology to look at the mechanism behind the selective delayed death of hippocampus CA1 neurons after transient global brain ischemia. The main findings are summarized: 1. The main form of ELAV protein family member detected in CA1/CA3 in Hu protein immunoprecipitation and polysomes was HuB (Rel-N1). HuB is present in control CA3, 8 hr reperfused CA3, and 8 hr reperfused CA1, but absent from control CA1. AUF-1, hnRNP K, hnRNP M were also absent from control CA1 following Hu protein immunoprecipitation and Western blot, suggesting that HuB bound AUF-1,

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48

Duarte, Sérgio Miguel Coelho. "Matrix-leukocyte interactions in liver ischemia-reperfusion injury." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63694.

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Raghavan, Aparna. "Neuroprotective Potential of Withania Somnifera in Cerebral Ischemia." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1416570371.

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50

Moore, Rustin MacArthur. "Large colon ischemia-reperfusion injury in the horse /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487853913101881.

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