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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review atherogenic factors are discussed in relation to the possibility of regression. Evidence for regression of human lesions comes mainly from postwar studies and observations on persons with chronic wasting diseases. The entry, exit and effects of lipids in the arterial wass are considered as important factors which might determine regression. A variety of experiments in different animals which have been done in order to study regression are described. Some involve cholesterol feeding and withdrawal, others are concerned with the effects of hyperoxia and drugs. It is concluded that certain forms of atheroma can be induced to regress.
Atherosclerosis
PMID:Is atheroma a reversible lesion? 17 24

Methemoglobin (MtHb) formation was studied during reconstructive operations on the abdominal aorta and its branches. It was established that the appearance of pain at rest and trophic tissue disorders in the lower extremities causes intensification of MtHb formation. The intensity of MtHb formation increases sharply during the operation and is determined by the injurious character of the intervention, level of arterial blood oxygenation, and the efficacy of nociceptive pulsation block. Arterial blood hyperoxia proved to be among the most important factors of increased MtHb formation and decreased blood oxygen capacity. Nociceptive pulsation block is less effective in general anesthesia than in epidural anesthesia and also increases the content of MtHb in the blood and the severity of the stress and reperfusion damages of the tissues and organs. On the basis of the results of the study it is concluded that normoxia of arterial blood and denervation of the operative zone reduce the risk of ischemic and hypoxic complications in patients with generalized atherosclerosis.
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PMID:[The effect of the methods of anesthesiological assistance and blood oxygenation on the oxygen-transport properties of the blood in reconstructive interventions on the abdominal aorta and vessels of the lower extremities]. 176 6

Werner syndrome (WS) is a recessive genetic condition associated with markedly reduced replicative lifespans of cells in culture, high chromosomal instability in vivo and in vitro, and premature appearance of many characteristics of normal aging, including an increased incidence of cancer. We have monitored plasmid homologous recombination frequencies in diploid fibroblasts from 6 Werner or Werner-like syndrome patients, following transfection with a plasmid substrate containing 2 overlapping fragments of the TN5 Neor gene. Plasmid DNA recovered from these cells was then assayed for homologous recombination by (a) transformation of recA- bacteria to Ampr (indicating total viable plasmid) or Neor (indicating viable recombinant plasmid), and (b) by limited-cycle polymerase chain reaction (PCR) to co-amplify a recombinant fragment containing the overlap region, and a control region of the same plasmid, without bacterial transformation. Bacterial assay data indicated that recombination rates in 3 of the 6 WS strains were significantly elevated above normal controls; 4 of 6 appeared elevated by PCR assay. The highest-recombination WS strain showed evidence of reduced degradation of transfected plasmid DNA. For this small sample of WS strains, clinical severity of WS was not well correlated with recombination rate as determined by either assay (Pearson r = 0.78, not significant, for PCR assay); elevated recombination may, however, define a subset of WS at greatest risk for cancer and/or atherosclerosis. PCR assay of a hyperoxia-resistant HeLa cell line, displaying substantially increased chromosome breakage, indicated increased recombination between direct-repeat fragments. Nevertheless, elevated recombination in WS strains is unlikely to be secondary to impaired replicative capacity characteristic of WS cells, or to defective repair of chromosome damage which is increased in WS, since recombination in non-WS strains was unaffected by passage level or repeated UV irradiation.
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PMID:Homologous recombination is elevated in some Werner-like syndromes but not during normal in vitro or in vivo senescence of mammalian cells. 207 65

The effect of hyperoxic or hypoxic inhalation on blood lipid levels and on the development of atherosclerosis was studied in young male WHHL rabbits. They were exposed to ordinary room air containing different concentrations of oxygen: 6 animals were exposed to 40% oxygen (hyperoxia group) or 5-10% oxygen (hypoxia group) for 5 h a day, 5 days a week for 8 weeks. Four control rabbits inhaled ordinary room air. The following results were obtained. (1) The severity of aortic lesions significantly decreased in the hyperoxia group and increased in the hypoxia group, when these two groups were compared. However, both hypoxic and hyperoxic groups did not statistically differ from the control. (2) Plasma cholesterol levels were not changed either by hyperoxic or hypoxic inhalation. (3) Plasma triglyceride levels were elevated only in the hypoxia group, with significant differences from the values in both control and hyperoxia groups. (4) There was no significant correlation between mean plasma lipid level and severity of aortic lesions. From these results, we conclude that hyperoxic or hypoxic inhalation respectively regresses or aggravates the development of atherosclerotic lesions, not by an indirect action on blood lipid concentrations but by a direct action on the vascular wall.
Atherosclerosis 1983 Apr
PMID:The effect of oxygen on the development of atherosclerosis in WHHL rabbits. 687 Sep 89

Lipid peroxidation and some parameters of hemostasis were studied during exposure to various hyperoxia schemes combined with heparin therapy before and after treatment in 124 patients aged 16 to 69 with CNS involvement which developed as a result of atherosclerosis and essential hypertension, 60 of whom presented with initial manifestations of cerebral circulation insufficiency (IMCCI), 33 with posthypoxic encephalopathies (PE), and 31 with ischemic stroke (IS). Hyperoxia mechanisms were differently directed in the studied groups of patients, this necessitating a differentiated approach to the choice of schemes of hyperbaric oxygenation. Use of a short course of hyperbaric oxygenation (up to 3 sessions at 1.2 to 1.25 atA) is recommended for patients with IMCCI and PE. For patients with IS in the acute period hyperbaric oxygenation at 1.4 atA is advisable combined with heparin therapy in doses of 150 to 300 U/kg b.w. a day.
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PMID:[Effects of hyperoxia regimes on the state of lipid peroxidation and hemostasis in patients with lesions of the central nervous system]. 789 81

Reactive oxygen species (ROS) have been implicated in the pathogenesis of many clinical disorders such as adult respiratory distress syndrome, ischemia-reperfusion injury, atherosclerosis, neurodegenerative diseases, and cancer. Genetically engineered animal models have been used as a tool for understanding the function of various antioxidant enzymes in cellular defense mechanisms against various types of oxidant tissue injury. Transgenic mice overexpressing three isoforms of superoxide dismutase, catalase, and the cellular glutathione peroxidase (GSHPx-1) in various tissues show an increased tolerance to ischemia-reperfusion heart and brain injury, hyperoxia, cold-induced brain edema, adriamycin, and paraquat toxicity. These results have provided for the first time direct evidence demonstrating the importance of each of these antioxidant enzymes in protecting the animals against the injury resulting from these insults, as well as the effect of an enhanced level of antioxidant in ameliorating the oxidant tissue injury. To evaluate further the nature of these enzymes in antioxidant defense, gene knockout mice deficient in copper-zinc superoxide dismutase (CuZnSOD) and GSHPx-1 have also been generated in our laboratory. These mice developed normally and showed no marked pathologic changes under normal physiologic conditions. In addition, a deficiency in these genes had no effects on animal survival under hyperoxida. However, these knockout mice exhibited a pronounced susceptibility to paraquat toxicity and myocardial ischemia-reperfusion injury. Furthermore, female mice lacking CuZnSOD also displayed a marked increase in postimplantation embryonic lethality. These animals should provide a useful model for uncovering the identity of ROS that participate in the pathogenesis of various clinical disorders and for defining the role of each antioxidant enzyme in cellular defense against oxidant-mediated tissue injury.
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PMID:The nature of antioxidant defense mechanisms: a lesson from transgenic studies. 978 1

Extensive research efforts during the last three decades resulted in a large body of experimental evidence that suggests an important role of the disbalance between generation and elimination of the oxygen and xenobiotic derived free radicals in physiological and pathological processes. Reactive oxygen species (ROS) are generated in many metabolic pathways, and are entering the organisms from exogenous sources, dominantly via airways and gut. ROS induced injuries, e.g. thermal, chemical, radiation, ischaemia/reperfusion, inflammation, hyperoxia, etc., result in diseases like atherosclerosis, ulcerative colitis, autoimmune diseases, asthma, etc. The current paper is designed to provide an overview of the effects ROS may exert in various tissues. Because of the effective defense systems, the tolerance of viable human cells to ROS is relatively high. The oxidant stress induced dysfunction of various systems, such as the gut, airways, nervous, cardiovascular system, etc., involve both direct and indirect mechanisms. Understanding of these molecular mechanisms is essential for a rational antioxidant therapy.
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PMID:Reactive oxygen species as mediators of tissue protection and injury. 1070 13

Heme oxygenases catalyze the rate-limiting step in heme degradation, resulting in the formation of carbon monoxide, iron and biliverdin that is subsequently reduced to bilirubin by biliverdin reductase. The products of this enzymatic reaction have important biological effects, including antioxidant, anti-inflammatory and cytoprotective functions. Three isoforms of heme oxygenase (HO) have been described: two constitutively expressed isoforms, HO-2 and HO-3, and an inducible isoform, HO-1 that is increased as an adaptive response to several injurious stimuli including heme, hyperoxia, hypoxia, endotoxin and heavy metals. Induction of HO-1 has been implicated in numerous clinically relevant disease states including transplant rejection, hypertension, atherosclerosis, lung injury, endotoxic shock and others. This review will focus on the protective functions of HO-1.
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PMID:Heme oxygenase-1 as a protective gene. 1549 91

Hypoxia increases and hyperoxia decreases experimental atherosclerosis, but it is unclear if repetitive hypoxic and hyperoxic insults affect intimal thickening after arterial injury. Rabbits on 2% cholesterol diet for 6 weeks underwent balloon injury to the abdominal aorta (AA) after week 3, and were then exposed to normoxia (n = 6), or 12 h daily of intermittent repetitive hypoxia (n = 6) or hyperoxia (n = 6). After week 6, damaged AA and undamaged thoracic aorta (TA) were assessed for intimal thickening and lipid content. Compared with normoxia, hypoxia and hyperoxia did not alter the rise in serum cholesterol related to cholesterol feeding. However, compared to normoxia, hypoxia markedly increased the intima-to-media ratio in AA (1.18 +/- 0.09 versus 1.96 +/- 0.14, P < 0.01) and TA (0.15 +/- 0.02 versus 0.41 +/- 0.01, P < 0.01) whereas hyperoxia had no effect on AA disease and increased intimal thickening in TA (0.26 +/- 0.03, P < 0.01). Hyperoxia promoted positive arterial remodeling in both TA and AA, resulting in larger luminal size. The cholesterol content in AA was increased by hypoxia and decreased by hyperoxia, but decreased by both treatments in TA. Lipophilic antioxidants and the proportion of arterial lipids that was oxidized were not altered by hypoxia or hyperoxia. These results suggest that intermittent repetitive hyperoxia is not protective and intermittent repetitive hypoxia promotes arterial disease in normal and injured arteries independent of lipid peroxidation.
Atherosclerosis 2006 Apr
PMID:Intimal thickening after arterial balloon injury is increased by intermittent repetitive hypoxia, but intermittent repetitive hyperoxia is not protective. 1606 Dec 36

The cores of rabbit plaques in vivo are hypoxic, suggesting that ATP depletion due to an insufficient supply of oxygen and nutrients could contribute to macrophage death in atherosclerotic plaques. During hypoxia, however, macrophages maintain ATP levels by anaerobic glycolysis. To directly assess ATP and glucose metabolites in plaques in vivo, we used bioluminescence imaging to map the concentrations of ATP, glucose, glycogen, and lactate in normal and atherosclerotic rabbit aortas in vivo. Hypoxia was assessed with NITP (7-(4'-(2-nitroimidazol-1-yl)-butyl)-theophylline). Normal aortas and plaques <500 microm thick were not hypoxic and had homogenous concentrations of energy metabolites. In plaques >500 microm thick, however, the cores were characterized by ATP depletion, low concentrations of glucose and glycogen, and a high concentration of lactate. A majority of ATP-depleted macrophages within the core were viable but severely hypoxic and glucose depleted. Hyperoxia in vitro reversed the ATP depletion in macrophages in viable areas of the core. Our findings suggest that ATP depletion contributes to the death of macrophages in atherosclerotic lesions and to the formation of a necrotic core.
Atherosclerosis 2006 Oct
PMID:ATP depletion in macrophages in the core of advanced rabbit atherosclerotic plaques in vivo. 1640 94


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