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hypercholesterolemia/hypoxia
L'enllaç es desa al porta-retalls
Pàgina 1 des de 72 resultats
Cerivastatin and hypercholesterolemia reduce apoptosis of cardiomyocytes in guinea pig papillary muscle subjected to hypoxia/reoxygenation.
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The aim of this study was to assess how cerivastatin influences contractility and degree of myocardial damage in papillary muscle subjected to hypoxia-reoxygenation in hypercholesterolemic guinea pigs. Study group consisted of guinea pigs, fed standard, hypercholesterolemic or hypercholesterolemic
Hypercholesterolemia blunts forearm vasorelaxation and enhances the pressor response during acute systemic hypoxia.
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OBJECTIVE
During hypoxia, active substances released by the endothelium play a key role in the cardiovascular and respiratory responses elicited to optimize oxygen delivery. As hypercholesterolemia is a major cause of endothelial dysfunction, it may interfere with these responses.
RESULTS
We studied
Statin restores cardiac autonomic response to acute hypoxia in hypercholesterolaemia.
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BACKGROUND
Hypercholesterolaemia may alter cardiovascular autonomic function. We investigated the autonomic cardiovascular regulation during normoxia and hypoxia in familial isolated HC patients with or without statin treatment.
METHODS
Low (LF-RR) and high (HF-RR) components of spectral analysis of
[The attenuation of myocardial susceptibility to ischemia/reperfusion injury by ischemic postconditioning in hypercholesteremia rats and the role of hypoxia inducible factor-1alpha].
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OBJECTIVE
To explore whether ischemic postconditioning can attenuate the myocardial injury induced by ischemia/reperfusion (I/R) in hypercholesteremic rats and whether hypoxia inducible factor-1alpha (HIF-1alpha) play a role in the protection.
METHODS
Adult male Wistar rats received a high fat diet
Hypercholesterolemia enhances tolerance to lethal systemic hypoxia in middle-aged mice: possible role of VEGF downregulation in brain.
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Hypercholesterolemia (HCL) is commonly associated with impaired vascular relaxation response and augmented vasoconstriction. Interestingly, it was shown that animals with HCL were less vulnerable to seizures and several clinical studies also revealed a better outcome after stroke in the patients
Hypercholesterolemia-induced increase in plasma oxidized LDL abrogated pro angiogenic response in kidney grafts.
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Inflammation contributes to the atherogenic role of intermittent hypoxia in apolipoprotein-E knock out mice.
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BACKGROUND
Obstructive sleep apnea results in nocturnal intermittent hypoxia (IH) as a main trigger for cardiovascular morbidity, including atherosclerosis. IH induces hemodynamic, hormono-metabolic and also immuno-inflammatory alterations that could differentially contribute to atherosclerosis. Our
Hypoxemia During Sleep and the Progression of Coronary Artery Calcium
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The aim of this study was to evaluate the associations between objective sleep parameters of obstructive sleep apnea (OSA) and progression of subclinical cardiovascular disease as measured by the coronary artery calcium (CAC) score. We reviewed the medical records of 196 patients who underwent both
Hypoxia and atherosclerosis: re-evaluation of an old hypothesis.
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It was hypothesized over 40 years ago that a decrease in the oxygenation of the vascular wall might somehow be involved in atherogenesis. Recent studies concerning the mechanism of oxygenation indicate that diffusion through plasma is of major importance, meaning that a moderate, prolonged hypoxia
[The nondrug treatment of hypertension patients by their adaptation to periodic hypoxia in a barochamber].
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Patients with essential hypertension were exposed to periodic hypoxia in a pressure chamber. It is shown that adaptation to periodic hypoxia results in improvement of general condition of patients who exhibited a decline in blood pressure, minute blood volume, serum sodium concentrations as well as
[Endothelium-dependent vascular response in rabbits during prolonged experimental hypercholesterolemia].
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It was shown in experiments on anesthetized rabbits that disturbances in endothelium-dependent relaxant (Ach-induced) and constrictor (hypoxia-induced) vascular responses depended on duration of high hypercholesterol diet and on the structural damage of the vascular wall as well as on changes in the
[Morphofunctional basis for disturbances of transport-trophic myocardial function in hypercholesterolemia].
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Adaptive and pathologic changes limiting the myocardial circulation and changing the microvessel circulation are described in rabbits with alimentary hypercholesterolemia. The most important changes were the sludge-syndrome, multifactorial endotheliocyte deformity and capillary compression in the
Nocturnal hypoxia is associated with silent cerebrovascular disease in a high-risk Japanese community-dwelling population.
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BACKGROUND
Sleep-disordered breathing (SDB) is recognized as a risk factor for cerebrovascular disease. The objective of this study was to investigate the relationship between nocturnal hypoxia and silent cerebral infarct (SCI) in the general population.
METHODS
In the 2001 annual health check in
Chronic intermittent hypoxia exposure induces atherosclerosis in ApoE knockout mice: role of NF-κB p50.
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Current animal models of chronic intermittent hypoxia (CIH)-induced atherosclerosis have limitations. Mechanisms of CIH-induced atherosclerosis are poorly understood. This study tested new mouse models of CIH-induced atherosclerosis and defined the role of NF-κB p50 in CIH-induced atherosclerosis.
Altered mechanisms of endothelium-dependent dilation in skeletal muscle arterioles with genetic hypercholesterolemia.
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With most cardiovascular disease risk factors, endothelium-dependent dilation of skeletal muscle resistance arterioles is compromised, although with hypercholesterolemia, impairments to reactivity are not consistently observed. Using apolipoprotein E (ApoE) and low-density lipoprotein receptor
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