Academic literature on the topic 'Hypoxie chronique intermittente'
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Dissertations / Theses on the topic "Hypoxie chronique intermittente":
Mentek, Marielle. "Impact de l'hypoxie intermittente chronique sur la rétine et le nerf optique du rat : aspects vasculaire et inflammatoire." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAS032/document.
Obstructive sleep apnea (OSA) has recently been associated with the occurrence of optic neuropathies, especially acute non-arteritic anterior ischemic optic neuropathy (NAION). Among the mechanisms of NAION onset potentially associated with OSA, vascular dysregulation and inflammation may play a role. There is still no data on the effect of chronic intermittent hypoxia (IH) on vascular function of the eye. The purpose of this work was to develop techniques for assessing rat ocular vascular function and apply them to the study of the ocular vascular consequences of IH. Thus, two complementary models have been developed: 1) a laser Doppler flowmeter (LDF) prototype adapted for rodents, to evaluate in vivo retinal and optic nerve head (ONH) blood perfusion and 2) in vitro model of rat ophthalmic artery (OA) study by myography. Preliminary work on healthy rat enabled us to validate the relevance of retinal arteries LDF signal, but not that of the ONH. Retinal blood velocity (VelART) dropped by 17.0 ± 13.7% in response to pure oxygen inhalation. We did not observe any significant change in VelART signal after intracarotidian endothelin 1 (ET -1) injection, despite strong vasoconstriction of retinal vessels. OA reactivity study by myography in rats exposed to a 14-day IH showed increased contraction to ET-1, associated with an increased endothelin receptor A-mediated (ETRA) response and ETRA overexpression within the AO. NO-dependent relaxation is reduced in IH rats, and associated with a shift towards vasoconstrictive effects of cytochrome P450 products. These responses were associated with an increase in superoxide anions in the OA wall. Further studies are needed to explore the underlying mechanisms of these vascular changes, particularly the role of oxidative stress. Understanding of the LDF signal is partial and should be further explored to permit application to the study of IH rat
Béguin, Pauline. "Caractère biphasique de l'hypoxie intermittente : mécanismes cardioprotecteurs induits par une exposition aiguë et conséquences inflammatoires d'une exposition chronique." Phd thesis, Université Claude Bernard - Lyon I, 2006. http://tel.archives-ouvertes.fr/tel-00149355.
Le but de ce travail est de caractériser d'une part, les effets sur la fonction cardiaque d'une exposition aiguë chez le rat, et d'autre part, les conséquences inflammatoires, marqueurs précoces de l'athérogenèse, d'une exposition chronique chez la souris.
24 h après une exposition aiguë à l'HI (4 h à 10% d'O2) une récupération fonctionnelle post-ischémique et une réduction de la nécrose cellulaire sont observées suite à une séquence d'ischémie-reperfusion dans un modèle de cœur isolé. Ces évènements reflètent un phénomène de protection myocardique retardée, encore appelé préconditionnement (PC) myocardique. Ce PC induit par l'HI, semble impliquer divers acteurs, la p38 MAP kinase et Erk1/2 comme initiateurs, la PKC, la iNOS et les canaux KATP mitochondriaux comme médiateurs. La compréhension du rôle de chacun de ces acteurs permettrait d'utiliser ces cibles potentielles afin de prévenir les maladies cardiovasculaires.
L'exposition chronique à l'HI (5, 14 et 35 jours à 5% d'O2), induit une augmentation de la prolifération cellulaire, des taux de chimiokines inflammatoires ainsi que du phénomène de «rolling» leucocytaire. L'analyse approfondie de ce phénotype inflammatoire chez l'animal, permettrait de comprendre dans une perspective thérapeutique, l'athérogenèse développée par les patients porteurs de SAOS.
Lefebvre, Blandine. "Syndrome d'apnées du sommeil et morbidité cardiovasculaire : étude des conséquences vasculaires d'une exposition chronique à l'hypoxie intermittente chez le rat et étude de la production de leucotriènes chez les patients apnéiques." Grenoble 1, 2008. http://www.theses.fr/2008GRE10055.
'Obstructive sleep apnea (OSA) is associated with cardiovascular morbidity and mortality. Reccurent decrease of 02 partiel pressure seems to play a role in vascular alterations and inflammatory state observed in OSA. The development of animal models of OSA, as chronic intermittent hypoxia (CIH) exposure, allowed to isolate one feature of OSA and to study its consequences. Ln addition, leukotrienes (LTs) which are metabolites of 5-lipoxygenase pathway display vascular properties and are involved in atherosclerosis. Theses studies were performed to characterise cardiovascular effects of CIH in rat and to determine if L Ts production was increased in OSA. We observed an early vascular remodelling in rat after 14 or 35 days of CIH exposure that was compatible with adaptative mechanisms in response to the increase of parietal stress. These results could explain the absence ofhemodynamic and vascular reactivity changes. However, response to endothelin-l was increased in hypoxic rats. These result suggested that endothelin-l system was activated in CIH. Last, our results suggested a sensitisation effect of intermittent hpoxia on hypertension development in rat genetically predisposed to arterial hypertension. Further studies on longer exposure are required. LTs production was increased in OSA and was correlated with hypoxic severity. Moreover, L Ts production was correlated with subclinical atherosclerosis markers. These results suggested that L Ts may act in early vascular remodelling process in OSA. Experimental studies should be performed in order to determine whether 5-LO actors are surexpressed in CIH mode\
Morand, Jessica. "Dysfonction cardiovasculaire et arythmies ventriculaires de l’ischémie-reperfusion : effets délétères de l’hypoxie intermittente et protecteurs de la supplémentation en zinc." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV015/document.
Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality. Intermittent hypoxia (IH), one of the major consequences of apneas, leads to oxidative stress, activation of HIF-1 (hypoxia inducible factor 1) and endothelin (ET-1) expression, all known to play an important role in the cardiovascular consequences of OSA.First, we have demonstrated that IH increases the incidence of ischemia-related lethal ventricular arrhythmias. Among the potential mechanisms involved, spectral analysis of heart rate and blood pressure variability and catecholamine assay, showed a sympathetic activation in animals exposed to IH. IH was also responsible for alterations in ventricular repolarisation (increased QTc and Tpeak-Tend intervals) and dispersion of the transmural gradient (increased endocardial action potential duration). These alterations were associated with increased expression of endocardial LTCC and TRPC calcium channels.The second part of the thesis aimed at investigating zinc homeostasis in response to the oxidative stress induced by ischemia-reperfusion (IR) or IH as well as the beneficial effects of zinc supplementation in this context. We observed that IR and IH induced a decrease in myocardial and plasma zinc concentrations, respectively. We also highlighted the protective effects of zinc supplementation during reperfusion against the ventricular arrhythmias and myocardial dysfunction induced by IR. Zinc administration during reperfusion also abolished the increase in infarct size induced by chronic IH exposure.Finally, we investigated the effects of zinc depletion in endothelial cells exposed to TPEN, a specific zinc chelator. We observed that TPEN induced a nuclear translocation of HIF-1α and an increase in ET-1 secretion with a resulting increase in endothelial cell migration. Thus, zinc depletion appears to promote activation of the HIF-1-ET-1 axis, known for its deleterious effects upon IH.In summary, chronic IH exposure enhances ventricular arrhythmias and increases infarct size upon myocardial I/R. Sympathetic activation, oxidative stress and alterations of zinc homeostasis appear to be contributing factors. Pharmacological targeting of these alterations should be performed in order to confirm their role as well as to potentially prevent the deleterious cardiovascular consequences of IH and OSA
El, Dirani Zeinab. "Effet de l’hypoxie intermittente et de l’entraînement physique intensif sur la structure et la fonction du tissu musculaire chez le rat." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAV067/document.
Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by repeated interruptions of breathing during sleep due to the temporary closure of the upper airway. Its prevalence increases with the increasing in prevalence of obesity, especially in developed countries.Chronic intermittent hypoxia (IH) resulting from this transient closure of the upper airway is one of the major consequences of OSAS and is responsible of most of the complications related to this pathology, including hypertension, myocardial infarction, atherosclerosis and more generally cardiovascular remodeling.On the other hand, intensive physical training(IT) is well known to have benefits on cardiovascular system, thus we hypothesize that physical training can reverse the deleterious effects of IH on reactivity and vascular remodeling as well as intracellular calcium signaling in muscle cells.To answer this question, we chose the rat as an animal model to study the potential effect of IT in the prevention and reversal of deleterious (IH) effects in terms of reactivity and calcium signaling in muscle tissue.Rats were exposed for 21 days to intermittent hypoxia and housed in cages specially equipped to maintain an airflow alternating between 21% and 5% PO2 in cages containing hypoxic rats and 21% PO2 in cages containing the control rats. During the last two weeks of exposure to IH, a group of hypoxic rats and one of the normoxic rats underwent IT sessions on a treadmill at a speed of 16m / min to 30m / min.Physiological parameters were measured (blood pressure, heart rate, hematocrit), the aorta was removed to study the vascular reactivity, then vascular smooth muscle cells were removed and cultured to study calcium signaling by EPIfluorescence microscopy. Finally, the genes coding for the key mediators of the calcium signaling: RyR1, RyR2 RyR3, (ryanodine receptors), TRPV4 (transient receptor potential channel), SERCA1, SERCA2 (Sarco / Endoplasmic Reticulum Ca2 + -ATPase) and IP3R1 , 5-Trisphosphate Receptor) in various vascular and skeletal tissues were studied at the molecular level as mRNA by Q-PCR or as protein by Western Blot.Our results show that IH induces a significant increase in blood pressure and hematocrit and a decrease in acetylcholine-induced aortic relaxation pre-contracted with phenylnephrine. This was consistent with our observation that HI increases the level of intracellular calcium in cultured aortic smooth muscle. On the other hand, IT induced a significant decrease in hematocrit and aortic vasoconstriction induced by phenylnephrine and endothelial-1, consistant with the observation that IT reduces the IH-N difference in the calcium response. On the molecular scale, IH induces a significant increase in the expression of RyR1, RyR2, RyR3, SERCA1, SERCA2, TRPV4 and IP3R1 at the mRNA level in the tissues of all groups with a greater amount of RyR1,RyR2,& RyR3 higher in IH tissue of smooth muscles (mainly in the thoracic and abdominal aorta) and SERCA1 (9-fold higher in IH tissues) and SERCA2 (10-fold higher in IH tissues) in the skeletal muscles (Gastrocnemius, plantaris and soléus). In addition, IH induces a significant increase in RYR1, RYR2 and TRPV4 at the protein level in the thoracic and abdominal aorta; And IT reduces the difference in expression between animals N and IH.Our results suggest that IT is a promising, non-pharmacological or complementary treatment for limiting cardiovascular complications induced by IH and muscle remodeling in patients with OSAS
Yang, Tianxiang. "Influence of chronic intermittent hypoxia (CIH) in retinal neovascularization and vascular remodeling." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS059.pdf.
Neovascular retinopathies and edema are sight threatening complications of ischemic retinopathies, such as retinopathy of prematurity (ROP) and diabetic retinopathy (DR). Sleep apnea that leads to chronic intermittent hypoxia (CIH) is an independent risk factor for severe disease, but the underlying mechanisms are unknown. Here we show that experimental CIH during the ischemic phase of oxygen induced retinopathy in mice severely reduces beneficial revascularization of the ischemic retina, and increases neuronal loss and pathological neovascularization. Mechanistically we demonstrate that CIH reduces both colony stimulating factor 1 (CSF-1) expression and the ischemia-induced increase of retinal microglial cells that promotes the revascularization of the ischemic retina in the absence of CIH. Local CSF1R inhibition during ischemic retinopathy reduced the number of microglial cells, inhibited revascularization, and exacerbated pathological neovascularization, recapitulating several effects of CIH. Our findings provide a novel mechanism by which sleep apnea and CIH aggravate ischemic retinopathies, underscoring the importance of treating apnea in ROP and DR to help prevent sight threatening severe disease
Minovés-Kotski, Mélanie. "Effets délétères de l’hypoxie intermittente associée au syndrome d’apnées obstructives du sommeil sur la croissance et la dissémination métastatique du cancer du sein : implication de la voie HIF1/VEGF/Endothéline." Thesis, Université Grenoble Alpes, 2021. https://thares.univ-grenoble-alpes.fr/2021GRALV001.pdf.
Obstructive Sleep Apnea Syndrome (OSA) is a prevalent disease characterised by the occurrence of repeated nocturnal episodes of apnea leading to recurrent cycles of hypoxia-reoxygenation called intermittent hypoxia (IH). Intermittent hypoxia is a chronic and systemic stimulus which is considered as the main factor responsible for the deleterious cardiovascular and metabolic effects induced by OSA. Recent clinicalstudies have showed OSA is associated with excess mortality due to cancer and preclinical studies have confirmed that OSA promote tumour development. In animals, exposure to intermittent hypoxia has been shown to promote primary and metastatic tumour growth, particularly in murin models of melanoma. To date, no study has evaluated the impact of intermittent hypoxia on growth and metastatic power of breast cancer in apreclinical study.The main objective of this thesis was to explore the impact of intermittent hypoxia on the development of breast cancer and to understand how the imbalance induced by intermittent hypoxia at the macro-environmental scale contributes to tumour development. Involvement of the endothelin pathway was evaluated by an ET-1 receptor antagonist.The experimental protocol was carried out on preclinical models combining a mouse model of orthotopic mammary tumour and two additional cell culture models. This mixed approach has been carried out thanks to the development of an in vitro device for cellular exposure to intermittent hypoxia.This cross-sectional work has shown that intermittent hypoxia induced by OSA leads to accelerated tumour growth and favours tumour dissemination in exposed animals and that this phenomenon involved the endothelin 1 pathway.Keywords: OSA, intermittent hypoxia, breast cancer, endothelin 1, macitentan, macroenvironment, preclinical studies