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

Bidirectional laser Doppler velocimetry and monochromatic fundus photography were used to investigate retinal hemodynamics before and after panretinal photocoagulation (PRP) in 25 eyes of 23 diabetic patients with proliferative retinopathy. After PRP, there was a significant decrease in retinal volumetric blood flow rate and an increase in the retinal vascular regulatory response to hyperoxia (R). A significant association was found between the presence or absence of regression of neovascularization and the increase or decrease in R after PRP. Eyes that showed regression of neovascularization had significantly larger average R after PRP than eyes that did not show regression. Lack of improvement in R after PRP may be related to the presence of remaining ischemia or hypoxia in eyes that continue to show proliferation after PRP.
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PMID:Retinal blood flow regulation and the clinical response to panretinal photocoagulation in proliferative diabetic retinopathy. 258 47

The lung is especially sensitive to a variety of vastly different agents and conditions including hyperoxia, certain drugs and xenobiotics, particulate debris, and ischemia/reperfusion. There is a growing body of experimental data to suggest that most, if not all, of these agents or conditions mediate pulmonary injury by forming reactive O2 metabolites such as O2-., H2O2.OH, HOCl, and RNHCl. The presence mechanisms by which these different agents converge to produce free radical-mediated pulmonary injury is not entirely clear. The lung does contain several metabolic pathways that will produce large amounts of reactive O2 metabolites. For example, hyperoxia-induced pulmonary injury may be mediated by oxidants produced by both mitochondrial and microsomal electron transport. Certain drugs and xenobiotics may be metabolized by nonspecific flavoproteins found in the mitochondrial electron transport chain and associated with microsomal mixed function oxidase system to yield a variety of free radicals and oxidants. Inhalation of particulate debris will activate resident phagocytic leukocytes to produce large quantities of cytotoxic oxidants. Ischemia and reperfusion appear to produce substantial amounts of xanthine oxidase-derived oxy-radicals that recruit and activate inflammatory phagocytes to produce cytotoxic HOCl and N-chlorinated oxidants. Finally, inappropriate metabolism of arachidonate by prostaglandin synthetase in the presence of NADH (NADPH) produces a burst of O2-. The fact that the lung contains so many different metabolic avenues for oxidant and free radical production suggests that this particular organ may be the most sensitive to oxidative insult.
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PMID:Metabolic sources of reactive oxygen metabolites during oxidant stress and ischemia with reperfusion. 265 Sep 65

Measurement of TcPO2 in arterial diseased patient is a reliable and reproductible method for evaluation in stages III and IV of the degree of tissue ischemia which can serve to establish the viable prognosis of the limb. One of the disadvantages of this technique is the relatively long time taken. By contrast the Doppler-laser, a more recently introduced technique, can be used to measure superficial cutaneous flow. One of its advantages is the rapidity of its instantaneous measurements. Before testing this technique in arterial disease sufferers it was felt to be of interest to determine the possible existence in the healthy subject of a correlation between TcPO2 and laser-Doppler flow. The study involved 15 healty subjects, 8 men and 7 women, with a mean age of 24.2 years. TcPO2 and laser-Doppler measurements were carried out in the fore-foot at 38 degrees and 44 degrees, under basal conditions and then after ischemia each time for 5 minutes, finally followed by a 10-minute 100% hyperoxia test. There was only a slight correlation at 38 degrees between the two methods and no correlation was found at 44 degrees. With oxygen therapy TcPO2 increased considerably and there was a nonsignificant decrease in laser-Doppler flow. In total, the two methods did not truly explore the same microcirculatory data and clinical studies would appear necessary to determine whether laser-Doppler flow measurements in the arterial disease patient may prove to be as useful as those of TcPO2.
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PMID:[Comparative study of transcutaneous oxygen pressure and laser- Doppler flow in the feet of 15 healthy subjects]. 297 61

The presence of hyperoxia during reperfusion following brain ischemia has been shown in experimental animals to result in increased mortality and increased lipid peroxidation. Although no human studies have been reported, prolonged hyperoxia after resuscitation from cardiac arrest probably would result in increased cerebral injury. We report the case of an 88-year-old man who had a 5- to 6-minute cardiac arrest and then had decerebrate posturing during the post-resuscitation period, indicating that he had suffered a significant ischemic/anoxic insult. Early attention was paid to normalizing the arterial Po2 following resuscitation, which, according to experimental evidence, contributed to his eventual complete recovery of neurologic function, including mental state.
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PMID:Successful resuscitation of an elderly patient following cardiac arrest: possible role of reduction of reactive oxygen. 312 Jul 40

During experiments (128 rabbits) it was shown that under ischemia and hyperoxia the pharmacodynamics of lidocaine, anaprilin and ethacizine changed in centrogenic and peripheral arrhythmias induced by aconitine. Hyperoxia significantly potentiated the antiarrhythmic effect of the drugs except lidocaine action in centrogenic arrhythmias.
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PMID:[Action of anti-arrhythmia agents in ischemia and hyperoxia]. 336 Jan 6

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

Knowledge of the interrelation of the central nervous system-respiratory axis is crucial to the management of patients with head injuries with or without concomitant pulmonary-thoracic problems. Damage to the central nervous system (CNS) can result in unexplained hypoxemia, noncardiac pulmonary edema, altered patterns of respiration, and an increased risk of aspiration. The damaged thorax and lung can contribute to brain ischemia and rises in intracranial pressure. The treatment of one end of the CNS-respiratory axis is not without effect on the other end of the continuum. Corticosteroids, diuretics, mannitol, iatrogenic hyperventilation, barbiturates, and vasopressors are used in the management of patients with head trauma, but may have an impact on oxygenation and ventilation. When positive end expiratory pressure is used in the management of a pulmonary process, it should be optimized and used with caution while monitoring for its effect on intracranial pressure. Pulmonary toilet, while remaining a necessity, must be performed in a manner so as to minimize potential negative effects on the brain. Hyperoxia and hypothermia should be avoided. Mechanical ventilation should be used as dictated by the desired PaCO2 and not as a mandatory adjunct to endotracheal intubation.
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PMID:Pulmonary effects of head trauma. 679 86

Tissue injury that occurs as a result of ischemia and subsequent reperfusion is characterized by endothelial cell injury, edema formation, and the influx of inflammatory leukocytes. Two macrophage-derived proinflammatory cytokines which may play a critical role in cellular injury and leukocyte recruitment/activation that occurs in the setting of ischemia-reperfusion injury are tumor necrosis factor alpha (TNF) and macrophage inflammatory protein-1 alpha (MIP-1 alpha). To determine if modulation of ambient oxygen tensions in vitro alters the expression of proinflammatory cytokines from activated macrophages, murine alveolar macrophages (AMO) were cultured in various combinations of ambient oxygen concentrations, then the supernatant fluid and cell pellet assayed for the presence of TNF and MIP-1 alpha messenger RNA (mRNA) and protein. We demonstrated that conditions of anoxia (95% nitrogen/5% CO2) or hyperoxia (95% oxygen/5% CO2) independently resulted in the increased expression of both TNF and MIP-1 alpha mRNA and protein from lipopolysaccharide (LPS)-stimulated AMO, as compared with cells cultured in room air. The specific culture condition of anoxia (x 6 h) followed by hyperoxia (x 18 h) produced the greatest increases in both TNF and MIP-1 alpha, suggesting that when following a period of anoxic priming, oxygen stress results in exaggerated cytokine production. A period of at least 4.5 to 6 h of anoxia prior to hyperoxic exposure was found to be the minimal time required for anoxic priming. Furthermore, the coincubation of LPS-treated AMO with dimethyl sulfoxide (DMSO) attenuated the anoxia-hyperoxia-induced increases in TNF and MIP-1 alpha mRNA by 23% and 34%, respectively. These findings suggested that alterations in ambient oxygen tension can regulate the expression of TNF and MIP-1 alpha from activated AMO, and that oxidant-related cytokine production may represent an important mechanism by which inflammation occurs in the clinical settings of ischemia-reperfusion injury and hyperoxia.
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PMID:Alterations of ambient oxygen tension modulate the expression of tumor necrosis factor and macrophage inflammatory protein-1 alpha from murine alveolar macrophages. 754 69

Leukemia inhibitory factor (LIF) and tumor necrosis factor (TNF) have been shown to protect animals from radiation, hyperoxia, and endotoxic shock. TNF is also known to induce the expression of manganese superoxide dismutase (MnSOD) in vitro and in vivo. We therefore examined the effects of these cytokines on reperfusion injury in the isolated rabbit heart model. Rabbits were injected intravenously with 10 micrograms of either human TNF-alpha or lymphotoxin (TNF-beta), or murine TNF-alpha or murine LIF dissolved in saline. Control animals were injected with an equal volume of saline. After 24 h, hearts were isolated and perfused. Following an equilibration period, the hearts were subjected to 1 h ischemia and 1 h of reperfusion. All treated groups showed significant increases in percent recovery of developed tension (% preischemic) when compared to saline-treated control hearts. In addition there were significant decreases in lactate dehydrogenase release (LDH), accumulation of thiobarbituric acid reactive substances (TBARS), and accumulation of carbonyl proteins. These results correlate with increases in myocardial MnSOD activity. Thus, the protection from myocardial reperfusion injury seen in the pretreated group may be due to a mechanism that involves the induction of MnSOD.
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PMID:Leukemia inhibitory factor and tumor necrosis factor induce manganese superoxide dismutase and protect rabbit hearts from reperfusion injury. 776 Mar 46

It has not been clear whether or not pulmonary ischemia-reperfusion injury would occur while ischemic lungs were maintained in a well-oxygenated state. Our aim was to develop an ischemic lung model whose oxygen tension was maintained and to determine whether or not ischemia without hypoxia would injure the lung. Rat lungs isolated, ventilated, and perfused with Krebs-Henseleit solution (0.04 ml/gm body weight) were obtained by a standard technique, and the left and right pulmonary arteries were isolated to enable selective perfusion to either lung. After the left lung was exposed to ischemia for 60 minutes with ventilation maintained by a normoxic (20% O2, 5% CO2, 75% N2; normoxia) or a hyperoxic (95% O2, 5% CO2; hyperoxia) gas mixture, it was reperfused for 30 minutes either in a forced way (occluding the right pulmonary artery for 10 minutes followed by perfusion of both lungs for another 20 minutes) or in the natural way (distribution of flow dependent on vascular resistance) to compose three experimental groups (forced reperfusion-normoxia, natural reperfusion-normoxia, and forced reperfusion-hyperoxia).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unilateral lung injury caused by ischemia without hypoxia in isolated rat lungs perfused with buffer solution. 820 Dec 60


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