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Factors regulating arteriolar tone during microvascular growthBalch Samora, Julie. January 2007 (has links)
Thesis (Ph. D.)--West Virginia University, 2007. / Title from document title page. Document formatted into pages; contains xxiii, 251 p. : ill. Vita. Includes abstract. Includes bibliographical references.
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On endothelial function in type 2 diabetic patients with coronary artery disease /Nyström, Thomas, January 2005 (has links)
Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 5 uppsatser.
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Protective role of coronary endothelium during the development of cardiac hypertrophy insights from pharmacological intervention studies /Sun, Xiaowei. January 2008 (has links) (PDF)
Thesis (Ph.D.)--University of Alabama at Birmingham, 2008. / Title from PDF title page (viewed on July 16, 2010). Includes bibliographical references.
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Identification de nouveaux mécanismes régulateurs des pulsars calciques endothéliaux d’artères mésentériques de sourisToussaint, Fanny 06 1900 (has links)
No description available.
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Avaliação temporal da função vascular em aorta de camundongos com deleção dos receptores <font face=\"symbol\">a2A e <font face=\"symbol\">a2BC adrenérgicos. / Time-dependent characterization of vascular reactivity in aorta of <font face=\"symbol\">a2A and <font face=\"symbol\">a2C-adrenoceptors knockout mice.Gisele Kruger Couto 10 September 2007 (has links)
Este estudo avaliou a função vascular em anéis de aorta e no leito vascular mesentérico (LVM) de camundongos com deleção dos receptores <font face=\"symbol\">a2A e <font face=\"symbol\">a2Cadrenérgicos (KO) com 3, 5 e 7 meses, os quais apresentam uma hiperatividade simpática acompanhada de cardiomiopatia. Os KO apresentaram um aumento da freqüência cardíaca em todos os grupos avaliados, e hipertrofia ventricular esquerda aos 5 e 7 meses. Na aorta, o relaxamento dependente (acetilcolina) e independente (nitroprussiato de sódio) do endotélio e da via font face=\"symbol\">a-adrenérgica (isoproterenol), assim como a contração (fenilefrina e serotonina) e a mobilização de Ca2+ não foram alterados nos KO aos 3, 5 e 7 meses. Nos KO aos 3 meses, o relaxamento mediado pelos receptores ?2-adrenérgicos (clonidina) foi reduzido. Tanto a contração (noradrenalina) como o relaxamento (acetilcolina) no LVM dos KO aos 7 meses não foi alterado. Assim, sugere-se que os vasos arteriais parecem ser menos sensíveis do que o coração aos efeitos crônicos da hiperatividade simpática nos camundongos com deleção dos receptores <font face=\"symbol\">a2A e <font face=\"symbol\">a2C adrenérgicos. / This study assed the vascular function in aortic rings and in mesenteric vascular bed (MVB) from mice with disruption of <font face=\"symbol\">a2A and <font face=\"symbol\">a2Cadrenoceptors (KO) with 3, 5 and 7 months of age, that present sympathetic hyperactivity associated with cardiomyopathy. Heart rate was increased in all KO groups, and left ventricular hypertrophy was observed only in 5 and 7 month-old KO. There are no changes in the relaxation induced by acetylcholine (ACh), sodium nitroprusside and isoproterenol in aortic rings from all groups. In addition, the contraction induced by phenylephrine and serotonin, and Ca2+ handling did not change. However, in aorta from 3 month-old KO the relaxation induced by clonidine (<font face=\"symbol\">a2-adrenergic agonist) was reduced. In MVB from 7 month-old KO, neither the contraction (noradrenaline) nor relaxation (ACh) was modified. The results suggest that arterial vessel has been more resistant than heart to chronic effects induced by sympathetic hyperactivity observed in mice with disruption o<font face=\"symbol\">a2A and <font face=\"symbol\">a2C-adrenoceptors.
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Efeito vasorelaxante da estrona sobre aorta torácica de ratos: contribuição ao estudo do mecanismo de ação / Vasorelaxant effect of estrone on rat thoracic aorta: contribution to the mechanism of action studyOliveira, Thiago Sardinha de 19 September 2014 (has links)
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Previous issue date: 2014-09-19 / Endogenous estrogens have been associated with greater vascular protection
in premenopausal women, and the increased risk of cardiovascular diseases in
postmenopausal women can be associated to the decrease in plasma estrogen
levels. Furthermore recently studies showed that the use of estrogens, like estrone,
exhibits remarkable vascular effect when used on isolated arteries, however any
investigation was made to elucidate the mechanism of action of this compound. So,
the present study was designed to investigate the ability of estrone to induce
vascular relaxation and modulate NO-dependent signaling pathway and analyzed the
role of estrogens receptor on estrone-mediated vascular relaxation, compared with
the effects promoted by 17β-estradiol. 12 week-old male Wistar rats were used to the
vascular reactivity, which was performed in an organ bath study for an isometric
tension recording. To the experimental protocols, concentration-response curves (0.1
- 100μM) to estrone or 17β - estradiol were performed. The mechanism contributing
to estrone-induced effects were determined comparing with the vascular effects
induced by 17β - estradiol that have its effect vascular well characterized. It was
observed that the vascular relaxation promoted by estrone is dependent on the
endothelium and the estrogen receptor. The vasorelaxant effect promoted by estrone
was significantly altered in the presence of the inhibitor of PI3K signaling pathway
(wortmannin) and the Ca2+-CaM complex inhibitor (calmidazolium), showing the
involvement of PI3K/Ca2+-CaM signaling pathways. This study demonstrate that
estrone promoted vasorelaxant effect on rat thoracic aortic on endotheliumdependent
manner and its effect depends on the estrogen receptors that activate the
PI3K pathway and the Ca2+-calmodulin complex which subsequently activates the
NO/cGMP pathway. These results contribute to the better understanding of the role
of estrone in the conjugated equine estrogen (CEE) which could be associated to the
benefits effects of estrogens in the CEE therapy. / Os estrogênios endógenos têm sido associados com uma maior proteção do
sistema vascular em mulheres na pré-menopausa, uma vez que os riscos de
doenças cardiovasculares em mulheres na pós-menopausa são maiores, alterações
estas que se devem à diminuição nos níveis plasmáticos de estrogênios. Além disso,
estudos recentes mostraram que o uso de estrogênios, como a estrona, apresenta
notável efeito vasorelaxante quando avaliado seu efeito em artérias isoladas, no
entanto, nenhuma investigação foi realizada para elucidar o mecanismo de acção
deste composto. Assim, o presente estudo procurou investigar o efeito da estrona
em aorta de ratos, verificando seu efeito em induzir o relaxamento vascular e
modular a via de sinalização dependente do óxido nítrico (NO), e ainda o papel dos
receptores de estrogênios, comparando com os efeitos promovidos pelo 17β-
estradiol. Os animais utilizados neste estudo foram ratos Wistar com 12 semanas de
idade, os quais foram utilizados para realização da reatividade vascular em banho
de órgãos isolados. Para os protocolos experimentais, curvas de concentraçãoresposta
(0,1-100μM) foram feitas para a estrona ou para o 17β-estradiol e as
tensões isométricas gravadas. Os mecanismos envolvidos no efeito induzido pela
estrona foram determinados através da incubação de inibidores farmacológicos e
comparado ao efeito do 17β-estradiol, que tem seu efeito vascular bem
caracterizado. Observou-se que a estrona promove efeito vasorelaxante em aorta
torácica de ratos, e que o relaxamento vascular promovido por ela é dependente do
endotélio e do receptor de estrogênios. Após ativação do receptor de estrogênios,
este ativa as vias de sinalização PI3K e Ca2+-CaM que posteriormente ativam a via
NO/GMPc. Estes resultados contribuem para o melhor entendimento do papel da
estrona em preparações de estrogênios conjugados equinos (CEE), que pode estar
associado aos efeitos de benefícios dos estrogênios na terapia CEE.
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Potential of omega-3 EPA/DHA 6/1 to ameliorate ageing-related endothelial dysfunction / Potentiel de la formulation omega-3 EPA/DHA 6/1 à améliorer la dysfonction endothéliale liée à l’âgeFarooq, Muhammad Akmal 17 October 2018 (has links)
La présente étude évalue la capacité de la formulation d’oméga-3 EPA:DHA 6:1, une formulation capable d’induire la formation continue de monoxyde d’azote par la NO synthase endothéliale, à améliorer la dysfonction endothéliale liée à l’âge établie chez le rat. La dysfonction endothéliale liée à l’âge est caractérisée par une altération des composantes de la relaxation et une augmentation des réponses contractiles dépendantes de l’endothélium. L’âge augmente le stress oxydant vasculaire, l’expression de la NADPH oxydase, COX-2, eNOS, ACE, AT1R, et des marqueurs de senescence, alors que la COX-1 est sous-exprimé. La formulation EPA:DHA 6:1 améliore la composante NO, diminue l’EDCF et le stress oxydant vasculaire, et normalise l’expression des protéines cibles. En conclusion, la consommation chronique de EPA:DHA 6:1 améliore la dysfonction endothéliale liée à l’âge chez le rat, probablement en prévenant l’activation du système angiotensine locale et le stress oxydant en résultant. / EPA:DHA 6:1 omega-3 formulation has been shown to induce a sustained endothelial NO synthase-derived formation of nitric oxide. This study examined if the intake of EPA:DHA 6:1 improves an established ageing-related endothelial dysfunction. Ageing-related endothelial dysfunction was characterized by a blunted NO-mediated component of relaxation, abolished EDH-mediated component and increased COX-derived endothelium-dependent contractile responses. Ageing increased vascular oxidative stress, expression of NADPH oxidase subunits, COX-2, eNOS, ACE, AT1R, and senescence markers, whereas COX-1 was down-regulated. Chronic intake of EPA:DHA 6:1 improved the NO-mediated relaxations, reduced EDCFs, vascular oxidative stress and normalized the expression of protein markers. In conclusion, chronic intake of EPA:DHA 6:1 prevented the ageing-related endothelial dysfunction in old rats, most likely by preventing activation of the local angiotensin system and the subsequent vascular oxidative stress.
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Conception, synthèse et évaluation de nouveaux édifices supramoléculaires : dosages et diagnostics pour l'angiogenèse tumorale / Design, synthesis and evaluation of new supramolecular assemblies : quantification and diagnosis for tumoral angiogenesisSoum, Claire 15 December 2014 (has links)
Actuellement, il n’existe pas de techniques fiables pour la détection de marqueurs du cancer ou le suivi de l’administration de médicaments tels que les anticorps monoclonaux. Cette détection est essentielle pour réaliser un diagnostic précoce et ainsi améliorer le pronostic de survie des patients, et d’autre part adapter la posologie et un traitement personnalisé à chaque patient. L’objectif majeur de ce travail a été de concevoir et de développer des systèmes dits biocapteurs répondant à ces problématiques : d’une part, la détection et la quantification de l’activité des métalloprotéinases matricielles (MMP) en tant que nouvel outil de diagnostic de la progression et du développement tumoral; et d’autre part, le dosage d’un anticorps anti-VEGF, le bevacizumab, impliqué dans les biothérapies antiangiogéniques. La quantification de l’activité métalloprotéasique a été rendue possible grâce à la conception d’un biocapteur basé sur un édifice supramoléculaire. Celui-ci est constitué de substrats peptidiques fluorogéniques des MMP et d’une surface fonctionnalisée par des cyclodextrines. Une détection par fluorescence a alors permis d’évaluer l’efficacité et la spécificité de ce système à quantifier l’activité des MMP in vitro et ex vivo en conditions de biopsie tumorale. D’autre part, nous avons conçu des biocapteurs basés sur un mime peptidique du VEGF, permettant le dosage du bevacizumab. L’utilisation de ce mime en remplacement du VEGF humain a été démontrée, et plusieurs systèmes supramoléculaires fonctionnalisés par ce peptide ont été synthétisés, en vue de la conception d’une plateforme de détection régénérable des interactions peptide/protéine par transduction acoustique. / Nowadays, there are no reliable techniques for detecting biomarkers of cancer or for monitoring therapeutic drugs such as monoclonal antibodies in blood samples. This detection is essential in order to highlight the early onset of a disease prior to the appearance of clinical symptoms and therefore ensure a greater therapeutic effect, but also to provide a personalized treatment for each patient. The major goal of this thesis work was to design and develop plateforms of detection called biosensors answering these problematics: on one hand, detection and monitoring of matrix metalloproteinases (MMP) activities as a new tool for the diagnosis of tumoral progression, and on the other hand, quantification of an anti-VEGF antibody named bevacizumab, involved in antiangiogenic therapies. Monitoring of MMP activities was made possible by the design of a biosensor based on a supramolecular assembly between fluorogenic susbtrates of MMP and cyclodextrins functionalized surface. Fluorescence detection has enabled to evaluate the efficacity and specificity of this system to quantify MMP activities in vitro and ex vivo in tumoral biopsy conditions. On the other hand, we have designed biosensors based on a cyclopeptide mimicking human VEGF for the monitoring of bevacizumab. The ability of this peptide to substitute the human protein has been demonstrated and several supramolecular assemblies functionalized by this peptide have been synthesized in order to create a regenerable biosensor screening peptide/protein interactions by acoustic transduction.
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Vascular endothelial and smooth muscle function in children at risk of cardiovascular disease and the effect of folic acid supplementation.Peña Vargas, Alexia Sophie January 2008 (has links)
Cardiovascular disease secondary to atherosclerosis is the most common cause of human morbidity and mortality. An early and fundamental event in the development of atherosclerosis is abnormal vascular endothelial and smooth muscle function. This can be measured by flow mediated dilatation and glyceryl trinitrate mediated dilatation in children at risk of atherosclerosis. Folic acid improves endothelial function (flow mediated dilatation) in adults with coronary artery disease. No studies have previously investigated the effects of folic acid on vascular function in at risk children with diabetes or obesity. In a cross sectional study an evaluation of vascular endothelial and smooth muscle function and their determinants was performed in 159 children with type 1 diabetes, 58 children with obesity, and 53 healthy children. Children with type 1 diabetes and children with mild to moderate obesity had comparable and severe vascular dysfunction but different determinants. Vascular function in healthy and obese children related to both body mass index and weight (adjusted for age and sex), and blood glucose. Children with obesity had lower folate levels and higher homocysteine levels than children with type 1 diabetes, an abnormal lipid profile and raised inflammatory markers. A randomised double blind placebo controlled cross over trial of 8 weeks of folic acid supplementation was performed in 38 children with type 1 diabetes. In these children, folic acid improved endothelial function with a sustained increase in folate levels but independent of homocysteine levels. Folic acid did not improve smooth muscle function. A randomised double blind placebo controlled parallel trial of 8 weeks folic acid supplementation was performed including 53 obese children. Folic acid did not improve vascular function in obese children in spite of sustained increase in folate levels, and a decrease in homocysteine levels. It was concluded that children with type 1 diabetes and obesity have comparable and severe endothelial and smooth muscle function. Determinants of vascular function in children, including weight and glucose, represent a continuum effect. Folic acid supplementation improved endothelial function in children with type 1 diabetes but not in children with obesity, whose metabolic changes causing endothelial dysfunction differ from children with diabetes. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1317003 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2008
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Vascular endothelial and smooth muscle function in children at risk of cardiovascular disease and the effect of folic acid supplementation.Peña Vargas, Alexia Sophie January 2008 (has links)
Cardiovascular disease secondary to atherosclerosis is the most common cause of human morbidity and mortality. An early and fundamental event in the development of atherosclerosis is abnormal vascular endothelial and smooth muscle function. This can be measured by flow mediated dilatation and glyceryl trinitrate mediated dilatation in children at risk of atherosclerosis. Folic acid improves endothelial function (flow mediated dilatation) in adults with coronary artery disease. No studies have previously investigated the effects of folic acid on vascular function in at risk children with diabetes or obesity. In a cross sectional study an evaluation of vascular endothelial and smooth muscle function and their determinants was performed in 159 children with type 1 diabetes, 58 children with obesity, and 53 healthy children. Children with type 1 diabetes and children with mild to moderate obesity had comparable and severe vascular dysfunction but different determinants. Vascular function in healthy and obese children related to both body mass index and weight (adjusted for age and sex), and blood glucose. Children with obesity had lower folate levels and higher homocysteine levels than children with type 1 diabetes, an abnormal lipid profile and raised inflammatory markers. A randomised double blind placebo controlled cross over trial of 8 weeks of folic acid supplementation was performed in 38 children with type 1 diabetes. In these children, folic acid improved endothelial function with a sustained increase in folate levels but independent of homocysteine levels. Folic acid did not improve smooth muscle function. A randomised double blind placebo controlled parallel trial of 8 weeks folic acid supplementation was performed including 53 obese children. Folic acid did not improve vascular function in obese children in spite of sustained increase in folate levels, and a decrease in homocysteine levels. It was concluded that children with type 1 diabetes and obesity have comparable and severe endothelial and smooth muscle function. Determinants of vascular function in children, including weight and glucose, represent a continuum effect. Folic acid supplementation improved endothelial function in children with type 1 diabetes but not in children with obesity, whose metabolic changes causing endothelial dysfunction differ from children with diabetes. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1317003 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2008
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