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Thematische Bibliographien / Nitric oxide Pathophysiology

Auswahl der wissenschaftlichen Literatur zum Thema „Nitric oxide Pathophysiology“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 8. Februar 2022

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Bücher
Buchteile

Zeitschriftenartikel zum Thema "Nitric oxide Pathophysiology":

1

Conner, Elaine M., und Matthew B. Grisham. „Nitric Oxide: Biochemistry, Physiology, and Pathophysiology“. Methods 7, Nr. 1 (Februar 1995): 3–13. http://dx.doi.org/10.1006/meth.1995.1002.

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2

Ghosh, Sudakshina, und Serpil C. Erzurum. „Nitric oxide metabolism in asthma pathophysiology“. Biochimica et Biophysica Acta (BBA) - General Subjects 1810, Nr. 11 (November 2011): 1008–16. http://dx.doi.org/10.1016/j.bbagen.2011.06.009.

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3

Kiechle, Frederick L., und Tadeusz Malinski. „Nitric oxide: Biochemistry, Pathophysiology, and detection“. Journal of Pharmacological and Toxicological Methods 32, Nr. 2 (Oktober 1994): 123. http://dx.doi.org/10.1016/1056-8719(94)90064-7.

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4

Haynes, Virginia, Sarah Elfering, Rachel Squires, Nathaniel Traaseth, Joseph Solien, Adam Ettl und Cecilia Giulivi. „Mitochondrial Nitric-oxide Synthase: Role in Pathophysiology“. IUBMB Life 55, Nr. 10 (01.01.2004): 599–603. http://dx.doi.org/10.1080/15216540310001628681.

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5

Cipolla, Marilyn. „Pathophysiology and clinical applications of nitric oxide“. Journal of Vascular Surgery 31, Nr. 6 (Juni 2000): 1314–15. http://dx.doi.org/10.1067/mva.2000.105886.

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6

Moncada, S. „A2. Nitric oxide and bioenergetics: Physiology and pathophysiology“. Nitric Oxide 17 (2007): 9. http://dx.doi.org/10.1016/j.niox.2007.09.007.

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7

MONCADA, S. „Nitric Oxide in the Vasculature: Physiology and Pathophysiology“. Annals of the New York Academy of Sciences 811, Nr. 1 Atheroscleros (April 1997): 60–69. http://dx.doi.org/10.1111/j.1749-6632.1997.tb51989.x.

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8

Bredt, David S. „Endogenous nitric oxide synthesis: Biological functions and pathophysiology“. Free Radical Research 31, Nr. 6 (Januar 1999): 577–96. http://dx.doi.org/10.1080/10715769900301161.

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9

Baylis, C., und J. Bloch. „Nitric oxide (NO) in renal physiology and pathophysiology“. Nephrology Dialysis Transplantation 11, Nr. 10 (01.10.1996): 1955–57. http://dx.doi.org/10.1093/oxfordjournals.ndt.a027078.

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10

Lowe, Duane T. „Nitric Oxide Dysfunction in the Pathophysiology of Preeclampsia“. Nitric Oxide 4, Nr. 4 (August 2000): 441–58. http://dx.doi.org/10.1006/niox.2000.0296.

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Dissertationen zum Thema "Nitric oxide Pathophysiology":

1

Groves, Peter H. „The influence of exogenous nitric oxide on the pathophysiology of angioplasty injury“. Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308763.

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2

Evans, Kevin Andrew. „Hypoxia and vascular nitric oxide bioavailability : implications for the pathophysiology of high-altitude illness“. Thesis, University of South Wales, 2009. https://pure.southwales.ac.uk/en/studentthesis/hypoxia-and-vascular-nitric-oxide-bioavailability(3cd64bcd-5fb9-4209-a6f3-ab219e906a17).html.

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Introduction: Nitric oxide (NO) is an integral molecule implicated in the control of vascular function. It has been suggested that vascular dysfunction may lead to the development of acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE), though data to date remains scarce. Therefore, there is a clear need for further work to address the role of NO in the pathogenesis of high-altitude illness. Aims: There were two primary aims of the current work: (1) To examine whether hypoxia mediated changes in systemic NO metabolism are related to the development of AMS and sub-clinical pulmonary oedema and (2) to examine whether hypoxia mediated changes in the trans-cerebral exchange kinetics of NO metabolites are related to the development of AMS and headache. Hypothesis: We hypothesise that hypoxia will be associated with an increase in reactive oxygen species (ROS) formation, resulting in a decrease in vascular NO bioavailability (O2•- + NO → ONOO•-, k = 109 M.s-1). The reduction in NO will lead to vascular dysfunction and impaired oxygen (O2) delivery. Subsequent hypoxaemia will result in pulmonary vascular vasoconstriction and the development of sub-clinical pulmonary oedema within and mild brain swelling. Symptoms and reductions in NO bioavailability will be more pronounced in those who develop AMS since they are typically more hypoxaemic. Alternatively, a hypoxia mediated increase in NO, during vasodilatation, specifically across the cerebral circulation, may activate the trigminovascular system resulting in headache and by consequence, AMS. Methods: Study 1 – AMS symptoms, systemic venous NO concentration and nasal potential difference (NPD), used as a surrogate biomarker of extravascular lung oedema, were quantified in normoxia, after a 6hr passive exposure to 12% oxygen (O2) and immediately following a hypoxic maximal exercise challenge (≈6.5 hrs). Final measurements were 2 obtained two hours into (hypoxic) recovery. Study 2 – AMS, radial arterial and internal jugular venous NO metabolite concentrations and global cerebral blood flow (CBF), using the Kety-Schmidt technique, were assessed in normoxia and after a 9hr passive exposure to 12.9% O2. AMS was diagnosed if subjects presented with a combined Lake Louise score of ≥5 points and an Environmental Symptoms Questionnaire – Cerebral score of ≥0.7 points. Results: Hypoxia was associated with a reduction in total plasma NO, primarily due to a reduction in nitrate (NO3•) and a compensatory increase in red blood cell (RBC)-bound NO(P < 0.05 vs. normoxia) in both studies. Study 1 – Exercise reduced plasma nitrite (NO2•) (P< 0.05 vs. normoxia) whereas RBC-bound NO did not change. NO was not different in those who developed AMS (AMS+) compared to those who remained comparatively more healthy (AMS-) (P < 0.05). NPD was not affected by hypoxia or exercise and was not different between AMS+ and AMS- (P > 0.05). Study 2 – Hypoxia decreased arterial concentration of total plasma NO due primarily to a reduction in NO2•- and nitrate (NO3•-). Hypoxia did not alter the cerebral metabolism of RSNO, whereas the formation of RBC-bound NO increased. Discussion: These findings suggest that alterations in systemic or trans-cerebral NO metabolism are not implicated in the pathophysiology of AMS or sub-clinical pulmonary oedema. However, hypoxia was associated with an overall reduction in the total NO pool (NOx), whereas, selected alterations in more vasoactive NO metabolites were observed. Reductions in the partial pressure of O2 (pO2) were thought to be a key regulator in these changes. Overall net increases in RBC NO and corresponding reductions in plasma NO2• in the face of no alterations in NOx indicates that rather than being simply consumed, NO is reapportioned to other NO metabolites and this may be implicated in the pathophysiology of AMS.

3

Hill, Anita. „The Role of Complement and Nitric Oxide in the Pathophysiology of Paroxysmal Nocturnal Haemoglobinuria“. Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503289.

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4

Kerckx, Yannick. „Modeling nitric oxide production and transport in the human lung“. Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210324.

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Le travail présenté ici porte sur l’étude de la production et du transport du monoxyde d’azote (NO) dans le poumon humain. Le NO est une molécule dont l’implication dans des processus physiologiques n’a été mis en évidence qu’en 1987. Depuis, il a été démontré que le NO joue de nombreux rôles dans le corps humain. Le NO est un gaz labile (instable) dans les conditions physiologiques, il diffuse très facilement au travers des parois et il a une grande affinité pour l’hémoglobine. La production du NO est liée à 3 isoformes différentes de la protéine appelées synthases du NO ou NO synthases.

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Doctorat en sciences, Spécialisation physique
info:eu-repo/semantics/nonPublished

5

Collop, Natalie Chantel. „An investigation of the importance of the ATM protein in the endothelium and its role in the signalling pathways of NO production“. Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97067.

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Thesis (MScMedSc)--Stellenbosch University, 2015.
ENGLISH ABSTRACT: Ataxia telangiectasia (AT) is a well-characterized neurodegenerative disease resulting from a genetic defect in the Atm gene causing an absence or very low expression of the ATM protein. As AT patients are prone to the development of insulin resistance and atherosclerosis, the aim or the current study was to investigate the importance of the ATM protein in the endothelium and its role in the signalling pathways of nitric oxide (NO) production. To accomplish this, the first objective was to establish an in-house endothelial cell isolation technique harvested from normal and insulin resistant animals. Unfortunately, these cultures, although staining positive with an endothelial cell specific stain, were not pure enough and did not express endothelial NO synthase (eNOS), the central enzyme in NO production. The remainder of the study utilized commercial aortic endothelial cells (AECs) and found that there was a significant increase in NO production when the ATM protein was inhibited by the specific inhibitor, Ku-60019. The beneficial impact of increased NO production includes maintaining vascular homeostasis, promoting angiogenesis, initiating DNA repair by activating p53 and inhibiting smooth muscle cell proliferation. On the other hand, reactive oxygen species (ROS) and reactive nitrogen species (RNS) also generated by high levels of NO, can exert both protective and harmful effects. Examples of these include cell death due to high concentrations of ROS. However, Ku-60019 did not result in increased cell death of AECs. We demonstrated for the first time, a relationship between endothelial ATM protein kinase and the generation of NO. The signalling pathways involved in NO production and glucose utilization form a network of interrelationships. Central to both pathways is the activity of two protein kinases, PKB/Akt and AMPK. Both these kinases are known to phosphorylate the eNOS enzyme to produce NO on the one hand and AS160 to induce GLUT 4 translocation and glucose uptake on the other hand. Activation of the ATM protein is postulated to be a prerequisite for PKB/Akt activation and it may also result in activation of AMPK. However, using insulin to stimulate ATM, we could not show that inhibition of ATM in endothelial cells affected expression or insulin-stimulated activation of PKB/Akt while the PI3-K inhibitor wortmannin, inhibited the latter. In addition, inhibition of ATM negatively regulated the phospho/total ratio of AMPK. We therefore postulate that the NO production elicited by inhibition of ATM, may not be as result of eNOS activity. A second important observation was that inhibition of ATM significantly enhanced phosphorylation of the p85 regulatory subunit of PI3-K. This would imply that ATM normally has an inhibitory effect on p85 phosphorylation and therefore PI3-K activation. We base this assumption on previous publications showing that Ku-60019 does not inhibit PI3K. This again indicates that ATM has a hitherto unexplored regulatory role in endothelial function.
AFRIKAANSE OPSOMMING: Ataxia telangiectasia (AT) is a goed-gekarakteriseerde neurodegeneratiewe siekte a.g.v. ‘n genetiese afwyking in the Atm geen wat lei tot ‘n afwesige of lae uitdrukking van die ATM proteïen. Aangesien AT pasiënte geneig is om insulienweerstandigheid en aterosklerose te ontwikkel, was die doel van hierdie studie om die belang van die ATM proteïen in die endoteel, en sy rol in die seintransduksiepaaie betrokke by stikstofoksied (NO) produksie, te ondersoek. Om dit te bereik, was die eerste mikpunt om ‘n eie endoteelsel isolasie-tegniek (ge-oes van normale en insulienweerstandige diere) te vestig. Ongelukkig was hierdie selkulture nie suiwer genoeg nie.Ten spyte daarvan dat hulle positief getoets het met ‘n endoteelsel-spesifieke kleurstof kon geen uitdrukking van eNOS, die sentrale ensiem verantwoordelik vir NO produksie, waargeneem word nie. Die res van die studie het van kommersiële aorta endoteelselle (AES) gebruik gemaak, en daar is gevind dat die inhibisie van die ATM proteïen met die spesifieke inhibitor, Ku-60019, tot ‘n beduidende toename in NO produksie gelei het. Die voordelige impak van verhoogde NO produksie sluit die handhawing van vaskulêre homeostase, bevordering van angiogenese, inisiëring van DNA herstel deur p53 aktivering en inhibisie van gladdespiersel proliferasie in. Reaktiewe suurstofspesies (ROS) en reaktiewe stikstofspesies (RNS) wat ook a.g.v.verhoogde NO gegenereer word, kan egter beide beskermende sowel as skadelike effekte uitoefen. Voorbeelde sluit seldood a.g.v. hoë ROS konsentrasies in. Ku-60019 het egter nie tot ‘n toename in seldood van die AES gelei nie. Hierdie studie het vir die eerste keer aangetoon dat daar ‘n verwantskap tussen die endoteel ATM proteïen kinase en die produksie van NO bestaan. Die seintransduksie paaie betrokke by NO produksie en glukose verbruik vorm ‘n interafhanklike netwerk. Die aktiwiteit van twee proteïen kinases, PKB/Akt en AMPK, is sentrale rolspelers in beide paaie. Albei hierdie kinases is daarvoor bekend dat hulle die eNOS ensiem fosforileer om NO te produseer, maar terselfdertyd ook lei tot AS160 fosforilering, wat tot GLUT 4 translokering en glukose opname lei. Dis is voorgestel dat aktivering van die ATM proteïen ‘n voorvereiste vir PKB/Akt aktivering mag wees en verder kan dit ook tot aktivering van AMPK lei. Ons kon nie aantoon dat inhibisie van ATM in endoteelselle die uitdrukking of insulien-geïnduseerde aktivering van PKB/Akt onderdruk nie, terwyl die PI3-K inhibitor, wortmannin, wel laasgenoemde geïnhibeer het. Verder het die inhibisie van ATM die fosfo/totale AMPK verhouding negatief gereguleer. Ons postuleer dus dat die NO produksie waargeneem tydens ATM inhibisie, moontlik nie die gevolg van eNOS aktiwiteit was nie. ‘n Tweede belangrike waarneming was dat die inhibisie van ATM die fosforilering van die p85 regulatoriese subeenheid van PI3-K beduidend laat toeneem het. Dit impliseer dat ATM normaalweg ‘n inhibitoriese effek op p85 fosforilering, en dus PI3-K aktivering, het. Hierdie aanname word gemaak n.a.v. vorige publikasies wat getoon het dat Ku-60019 nie PI3-K inhibeer nie. Dit dui weer eens daarop dat ATM ‘n tot nog toe onbekende regulatoriese rol in endoteelfunksie het.

6

Warner, Anke Sigrid. „The expression, regulation and effects of inducible nitric oxide synthase in hibernating myocardium“. Title page, contents and summary only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phw279.pdf.

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Amendments inserted at back. "May 2002" Includes bibliographical references (leaves 237-290) Experiments described in this thesis address the potential role of inducible nitric oxide synthase (iNOS) in hibernating myocardium. Specifically it was sought to establish a cellular model of hibernating myocardium and investigate the expression, regulation and effects of iNOS in this model. Experiments were performed using primary cultures of neonatal rat ventricular myocytes.

7

Shukla, Nilima. „Pathophysiology and treatment of intimal hyperplasia and vein graft failure : a focus on risk factors, nitric oxide and oxidant stress“. Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397800.

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8

Ahlers, Belinda A. „Regulated L-Arginine transport in heart failure“. Monash University, Faculty of Medicine, 2003. http://arrow.monash.edu.au/hdl/1959.1/9521.

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9

Tolias, Christos. „Extracellular superoxide and nitric oxide : a real-time investigation in the role of free radicals in brain cell physiology and pathophysiology in vitro“. Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484267.

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Beamer, Edward. „A kainic acid-induced status epilepticus model of epileptogenesis in the C57BL/6J mouse : interventions targeting nitric oxide and NMDA receptor-mediated pathophysiology“. Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/11993/.

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In this thesis, the behavioral, electrographic and neurobiological effects of a period of kainic acid-induced status epilepticus (SE) on the C57BL/6J inbred mouse strain are characterised. The severity of epileptic behaviour was scored, used immunohistochemistry to investigate the anatomical distribution of c-Fos expression in the hippocampal formation following SE and recorded EEG during and after SE using an implantable, wireless telemetry device. Further to assessing the severity of SE, changes subsequent to seizures related to the emergence of chronic epilepsy were investigated, including reactive gliosis and synaptogenesis and epileptiform discharges in the EEG trace. I investigated the potential of a range of pharmacological agents for modulating the severity of induced seizures and disease progression. These included drugs targetting the NR2B subunit of the NMDA receptor (RO 25-6981), neuronal nitric oxide synthase (L-NPA), The post synaptic density protein 95 (Tat-NR2B9a) and inducible nitric oxide synthase (1400W). L-NPA, when administered prior to the induction of SE was found to profoundly suppress the emergence of epileptiform activity, including behavioural, electrographic and neurobiological indicators. Further, L-NPA’s modulation of the precipitating event lead to a decrease in neurobiological changes associated with epileptogenesis, such as reactive gliosis in the CA3 region of the hippocampus and 5 elevated synaptogenesis in th molecular layer of the hippocampus. This correlated with a marked decrease in epileptiform discharges in the EEG trace. A novel method of kainic acid administration was trialed, involving multiple small doses of the drug, titrated by the severity of behaviour. This method led to a decrease in mortality and an increase in the severity and inter-individual uniformity of SE, assessed by the analysis of behaviour, EEG and c-Fos expression in the hippocampus. Furthermore, this method induced neurobiological changes associated with epileptogenesis 3 days following SE and was associated with an increased frequency of epileptiform discharges for 7 days post SE.

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Bücher zum Thema "Nitric oxide Pathophysiology":

1

Biosciences, Berlex, Richmond und California USA. Pathophysiology and Clinical Applications of Nitric Oxide. Herausgegeben von Gabor M. Rubanyi. Abingdon, UK: Taylor & Francis, 1999. http://dx.doi.org/10.4324/9780203303726.

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2

Butler, Anthony. Life, death, and nitric oxide. Cambridge, UK: RSC, 2003.

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3

Koprowski, Hilary, und Hiroshi Maeda, Hrsg. The Role of Nitric Oxide in Physiology and Pathophysiology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79130-7.

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4

Lincoln, J. Nitric oxide in health and disease. Cambridge: Cambridge University Press, 1997.

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5

Giménez, Maria Sofia. Advances in chemistry and biology of nitric oxide. Kerala, India: Research Signpost, 2007.

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6

Laskin, Jeffrey D. Cellular and molecular biology of nitric oxide. New York: Marcel Dekker, 1999.

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7

Belvisi, Maria G., und Jane A. Mitchell, Hrsg. Nitric Oxide in Pulmonary Processes: Role in Physiology and Pathophysiology of Lung Disease. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8474-7.

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Wiggers Bernard Conference (4th 1994 Krumbach, Austria). Shock, sepsis, and organ failure--nitric oxide: Fourth Wiggers Bernard Conference 1994. Berlin: Springer-Verlag, 1995.

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Wiggers Bernard Conference (6th 1997 Vienna, Austria). Shock, sepsis, and organ failure: Scavenging of nitric oxide and inhibition of its production : sixth Wiggers Bernard Conference, 1997. Berlin: Springer, 1999.

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10

Murad, Ferid. Shen qi de yi yang hua tan: Nuobeier sheng li yi xue jiang de zhu Mulade jiao ni duo huo 30 nian = Magical nitric oxide. 8. Aufl. Nanjing Shi: Feng huang chu ban chuan mei ji tuan, 2012.

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Buchteile zum Thema "Nitric oxide Pathophysiology":

1

Förstermann, Ulrich, und Huige Li. „Nitric Oxide: Biological Synthesis and Functions“. In Gasotransmitters: Physiology and Pathophysiology, 1–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30338-8_1.

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Rossi-George, Alba, und Andrew Gow. „Nitric Oxide Biochemistry: Pathophysiology of Nitric Oxide-Mediated Protein Modifications“. In Oxidative Neural Injury, 29–44. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-342-8_2.

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Vallance, P., und S. Moncada. „Nitric Oxide and Hypertension: Physiology and Pathophysiology“. In Endothelial Function in Hypertension, 1–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60811-7_1.

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4

Sarti, Paolo, Marzia Arese, Elena Forte, Alessandro Giuffrè und Daniela Mastronicola. „Mitochondria and Nitric Oxide: Chemistry and Pathophysiology“. In Advances in Experimental Medicine and Biology, 75–92. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2869-1_4.

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Bishop-Bailey, David, und Jane A. Mitchell. „Nitric Oxide Synthesis and Actions“. In Nitric Oxide in Pulmonary Processes: Role in Physiology and Pathophysiology of Lung Disease, 3–20. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8474-7_1.

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Nijkamp, Frans P., und Gert Folkerts. „Nitric Oxide and Bronchial Hyperresponsiveness“. In Nitric Oxide in Pulmonary Processes: Role in Physiology and Pathophysiology of Lung Disease, 111–26. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8474-7_6.

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Li, Huige, Ning Xia und Ulrich Förstermann. „Nitric Oxide Synthesis in Vascular Physiology and Pathophysiology“. In Endothelial Signaling in Development and Disease, 381–97. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2907-8_16.

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Henry, Yann A. „Overproduction of Nitric Oxide in Physiology and Pathophysiology: EPR Detection“. In Nitric Oxide Research from Chemistry to Biology, 235–70. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4613-1185-0_12.

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Gustafsson, Åsa B., und Laurence L. Brunton. „Interactions of the Cyclic AMP and Nitric Oxide Pathways in Cardiac Fibroblasts“. In Pathophysiology of Cardiovascular Disease, 109–23. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4615-0453-5_9.

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Thiemermann, Christoph. „Combined Use of Nitric Oxide and Nitric Oxide Synthase Inhibitors as a Possible Therapeutic Approach“. In Nitric Oxide in Pulmonary Processes: Role in Physiology and Pathophysiology of Lung Disease, 209–25. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8474-7_12.

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