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acetylcysteine/hypoxia
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N-Acetylcysteine reduces hyperacute intermittent hypoxia-induced sympathoexcitation in human subjects.
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UNASSIGNED
What is the central question of this study? This study evaluated the following central question: does N-acetylcysteine (N-AC), an antioxidant that readily penetrates the blood-brain barrier, have the capability to reduce the increase in sympathetic nerve activity observed during
Protective effect of N-acetylcysteine on liver damage during chronic intrauterine hypoxia in fetal guinea pig.
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Chronic exposure to hypoxia during pregnancy generates a stressed intrauterine environment that may lead to fetal organ damage. The objectives of the study are (1) to quantify the effect of chronic hypoxia in the generation of oxidative stress in fetal guinea pig liver and (2) to test the protective
[EVALUATION OF NEUROPROTECTIVE ACTIVITY OF COMPLEX IMPACT OF MAGNESIUM OF SULFATE, LAMOTRYGINE AND N-ACETYLCYSTEINE UNDER CONDITIONS OF COMBINED NORMOBARIC HYPOXIA WITH LIGATION OF RIGHT CAROTID ARTERY IN RATS].
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Cerebrovascular diseases of ischemic origin still remain the leading cause of death and disability of the population. In acute cerebral discirculation conditions, anaerobic glycolysis is activated, ATP formation rate decreases, the ion pumps work is disrupted and superoxide radicals are formed.
N-acetylcysteine protects hepatocytes from hypoxia-related cell injury.
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Effects of N-acetylcysteine on tissue oxygenation in patients with multiple organ failure and evidence of tissue hypoxia.
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Covert tissue hypoxia, particularly of the splanchnic region, appears important in the pathogenesis of multiple organ failure (MOF). This investigation evaluates the effects of N-acetylcysteine (NAC) upon several measures of tissue oxygenation in 10 patients with severe MOF and evidence of
Chronic Intermittent Hypoxia-Induced Vascular Dysfunction in Rats is Reverted by N-Acetylcysteine Supplementation and Arginase Inhibition.
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Chronic intermittent hypoxia (CIH), the main attribute of obstructive sleep apnea (OSA), produces oxidative stress, endothelial dysfunction, and hypertension. Nitric oxide (NO) plays a critical role in controlling the vasomotor tone. The NO level depends on the L-arginine level, which can be reduced
The antioxidant N-acetylcysteine prevents HIF-1 stabilization under hypoxia in vitro but does not affect tumorigenesis in multiple breast cancer models in vivo.
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Intratumoral hypoxia is a poor prognostic factor associated with reduced disease-free survival in many cancer types, including breast cancer. Hypoxia encourages tumor cell proliferation, stimulates angiogenesis and lymphangiogenesis, and promotes epithelial-mesenchymal transition and metastasis.
[A study of the related pathways of oxidative stress in chronic intermittent hypoxia rats and the effect of N-acetylcysteine].
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OBJECTIVE
To study the relation of oxidative stress with systolic blood pressure (SBP) and renin-agiotensin system (RAS) in a rat model of chronic intermittent hypoxia (CIH), and to investigate the preventive effect and mechanism of N-acetylcysteine (NAC) in CIH-induced
N-acetylcysteine inhibits hypoxic pulmonary hypertension most effectively in the initial phase of chronic hypoxia.
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Exposure to chronic hypoxia results in hypoxic pulmonary hypertension (HPH). In rats HPH develops during the first two weeks of exposure to hypoxia, then it stabilizes and does not increase in severity. We hypothesize that free radical injury to pulmonary vascular wall is an important mechanism in
[The anti-apoptotic effects of N-acetylcysteine in neonatal rat cardiomyocytes underwent hypoxia-reoxygenation injury].
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OBJECTIVE
To evaluate the effects of N-acetylcysteine (NAC) on hypoxia-reoxygenation (H/R) injury induced apoptosis in neonatal rat cardiomyocytes.
METHODS
Neonatal rat cardiomyocytes were cultured for 48 h and then randomized into control group, H/R group and H/R + NAC group. Cardiomyocytes
Histological analysis of the intestinal wall of newborn rats submitted to hypoxia and reoxygenation to evaluate the protective effect of N-Acetylcysteine
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Purpose: To evaluate the effect of N-Acetylcysteine (NAC) in newborn rats submitted to hypoxia and reoxygenation (H/R) conditions in an experimental model of necrotizing enterocolitis.
Methods:
Pathogenesis of Abnormal Hepatic Lipid Metabolism Induced by Chronic Intermittent Hypoxia in Rats and the Therapeutic Effect of N-Acetylcysteine.
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BACKGROUND The pathogenesis of chronic intermittent hypoxia (CIH)-induced abnormal hepatic lipid metabolism in rats remains unclear. Here, we investigated the therapeutic effect of N-acetylcysteine (NAC) on abnormal hepatic lipid metabolism. MATERIAL AND METHODS Rats were subjected to hypoxia and
Cerebral amino acid profiles after hypoxia-reoxygenation and N-acetylcysteine treatment in the newborn piglet.
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BACKGROUND
Neonatal hypoxia-ischemia (HI) is a common clinical occurrence. Recently, much evidence has been gathered to suggest that oxygen free radicals are implicated in the pathogenesis of hypoxia-reoxygenation injury through the initiation and propagation of toxic cascades including glutamate
[Effect of chronic intermittent hypoxia on the expression of CXC chemokine ligand-10 in rat liver and the interventional effect of N-acetylcysteine].
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OBJECTIVE
To explore the effect of chronic intermittent hypoxia (CIH) on liver injury and to examine the expression of liver CXC chemokine ligand-10 (CXCL10) in the rats, and to explore the effect of N-acetylcysteine (NAC).
METHODS
A total of 21 male SD rats were randomly divided into a control
Co-loading antioxidant N-acetylcysteine attenuates cytotoxicity of iron oxide nanoparticles in hypoxia/reoxygenation cardiomyocytes.
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