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

Large-for-delivery date babies, considered characteristic of diabetic pregnancy, are believed to result from fetal hyperinsulinemia. Paradoxically, infant birth weights tend to be low-for-delivery date in mothers with more severe diabetes. We tested the hypothesis that hypoxemia in such fetuses leads to sympathoadrenal stimulation and inhibition of insulin secretion; and, thus, produces a net reduction in the growth-promoting effects. Fetal sheep were prepared with chronic peripheral and adrenal cannulas. Fetal blood gases, lactate, norepinephrine, and epinephrine secretion rates; and plasma norepinephrine, glucose, and immunoreactive insulin concentrations were determined at 30-min intervals during a 2-h baseline period and a 4-h period of hyperglycemia divided into 2-h segments of hypoxemia (with and without alpha-blockade) and hyperoxia. Hypoxemia-hyperoxia sequences were varied randomly. Well-oxygenated fetuses responded to a threefold increase in glucose with a sixfold increase in plasma immunoreactive insulin. With hypoxemia, norepinephrine and epinephrine secretion were elevated and the insulin response was blocked. With hypoxemia and phentolamine blockade, the insulin response was enhanced with a 10-fold increase above baseline. In severe maternal diabetes with vascular disease or with poor control and very high glucose levels, the fetus is likely to be relatively hypoxemic. Our experiments suggest that in this situation, the fetal insulin response to hyperglycemia will be attenuated; this effect is mediated, at least partly, through sympathoadrenal stimulation.
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PMID:Hypoxia-induced sympathetic inhibition of the fetal plasma insulin response to hyperglycemia. 840 4

We investigated the influence of hyperoxia (arterial pO2 446 +/- 43 mmHg) and hyperglycemia (blood glucose 19.4 mmol/l) on somatosensory stimulation (whisker deflection) employing laser Doppler flowmetry (LDF). Our aim was to test the hypothesis that a possible substrate-sensing mechanism for glucose and oxygen contributes to the coupling between cortical activity and regional cerebral blood flow (rCBF) in order to match increased demand with substrates. In addition, we looked at the influence of hyperglycemia (blood glucose 17.9 mmol/l) and hypercapnia (arterial pCO2 62 mmHg) on rCBF (LDF) and regional cerebral blood oxygenation changes (rCBO) in the even stronger metabolic stimulus of cortical spreading depression (CSD). For the latter we employed the new non-invasive technique of near infrared spectroscopy (NIRS). All experiments were done using chloralose/urethane-anesthetized rats. Somatosensory stimulation increased rCBF by about 20% of baseline, in the case of both norm- and hyperoxia as well as both normo- and hyperglycemia. The blood-flow response to CSD consisted of a temporary sharp increase in rCBF to more than 400%. At the same time, the concentration of oxyhemoglobin [HbO2] increased, while deoxyhemoglobin [Hb] decreased, indicating excessive oxygenation. Hyperglycemia altered neither the rCBF nor the rCBO response. Preexisting hypercapnia, however, produced reductions in both hyperperfusion (rCBF) and hyperoxygenation (rCBO) during CSD. We found that, for experimental hyperglycemia, i.v. may be superior to i.p. application of glucose because of the latter's side effects in connection with blood flow. Our findings cannot support the hypothesis of a substrate sensing mechanism in coupling.
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PMID:Excessive oxygen or glucose supply does not alter the blood flow response to somatosensory stimulation or spreading depression in rats. 925 28

It seems clear that the abundance of potential treatment options reflects the dearth of proved, effective options. Thus, although we appear to be on the brink of many potentially major breakthroughs in treatment, there currently remains a multitude of unanswered questions and the need for further study. At this point clinical recommendations must be limited to supportive care with moderation: oxygenation without hyperoxia; ventilation without hypocarbia; avoiding extremes of blood pressure, hematocrit, blood glucose, and body temperature. Unfortunately, data from human trials are extremely limited and often poorly controlled. Furthermore, even those few existing human studies have rarely--if ever--dealt with newborns infants (Table 2). In addition, many of the existing studies do not relate to generalized asphyxia but rather to single-organ reperfusion insults. Finally, there is the critical issue of timing. Unfortunately, much of the existing experimental data relate to prophylaxis rather than treatment, severely limiting their potential for clinical applicability. Interventions may have quite different effects when administered at different phases of this most intricate process. Hyperglycemia, for example, may be neuroprotective before an insult but detrimental if induced after an asphyxial episode. Conversely, the NMDA blocker MK-801 can adversely affect outcome when given before a global asphyxial insult but can reduce seizure-related damage when given during the hyperexcitability phase. Insulin-like growth factor is also neuroprotective only when given after an insult, but it is not helpful if given before. An intimate understanding of the pathophysiologic processes involved is essential before any attempts at applying the diverse data derived from numerous animal studies to the human situation in an intelligent manner. Future studies may focus on cocktails of different mixtures of the compounds discussed or on single multipotential drugs, which would make possible a multipronged approach. However, it is essential to investigate fully the potential for toxic drug interactions, as some combinations may be produce serious consequences. For example, Gluckman and Williams evaluated the potential of combining calcium channel blockers with NMDA receptor antagonists in hypoxic-ischemic rats and found that this combination led to rapid cardiovascular collapse. Other enticing approaches for future investigations will probably include some genetic-engineering-related studies in attempt to enhance endogenous antioxidant defenses with regulon stimulation or the administration of neurotrophic growth factors. Unavoidably, the trip from the laboratory to the bedside must of necessity be an arduous and rigorous one.
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PMID:Ischemia and reperfusion injury. The ultimate pathophysiologic paradox. 977 46

In this study we compare oxygen tension (PO2) histograms measured with O2 microelectrodes and a new optical PO2 measurement device, the OxyLite, in normal tissues (mouse spleen and thymus) and in tumors (R3230Ac in rats) (n = 5-6). The transient response to glucose infusion or 100% O2 breathing (hyperoxia) was also measured in tumors. PO2 histograms of spleen and thymus with the two devices were not different. The OxyLite tumor PO2 histogram, however, was left-shifted compared with the microelectrode (median PO2 1.0 vs. 4.0 mmHg, P = 0.016). Both probes responded to acute hyperglycemia with a mean increase of 3-6 mmHg, but the microelectrode change was not significant. The OxyLite consistently recorded large PO2 increases (approximately 28 mmHg) with hyperoxia, whereas the microelectrode response was variable. The OxyLite averages PO2 over an area that contains interstitial and vascular components, whereas the microelectrode measures a more local PO2. This study demonstrates the importance of considering the features of the measurement device when studying tissues with heterogeneous PO2 distributions (e.g., tumors).
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PMID:Comparison of tumor and normal tissue oxygen tension measurements using OxyLite or microelectrodes in rodents. 1135 8

Nerve regeneration in diabetes is essential for reversal of neuropathy as well as the recovery of nerves from injury due to acute nerve compression and entrapment. Endoneural hypoxia due to hyperglycemia-induced blood flow reductions is observed early in the course of diabetes, and the resultant ischemia plays a role in the diminished neural regeneration. Hyperbaric oxygen therapy is capable of producing tissue hyperoxia by raising oxygen tensions in ischemic tissues, and was shown to be beneficial in the reversal of experimental ischemic neuropathy. In this study, an experimental diabetes model was used to evaluate the functional and histomorphological effects of hyperbaric oxygen therapy on early diabetic nerve regeneration. Our results indicate that there is significant histomorphological impairment of nerve regeneration, even in very early stages of diabetes. However, no beneficial effects of hyperbaric oxygen therapy could be demonstrated at this stage.
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PMID:Effect of hyperbaric oxygen therapy on nerve regeneration in early diabetes. 1516 Mar 86

We have shown that neural tube defects (NTD) in a mouse model of diabetic embryopathy are associated with deficient expression of Pax3, a gene required for neural tube closure. Hyperglycemia-induced oxidative stress is responsible. Before organogenesis, the avascular embryo is physiologically hypoxic (2-5% O(2)). Here we hypothesized that, because O(2) delivery is limited at this stage of development, excess glucose metabolism could accelerate the rate of O(2) consumption, thereby exacerbating the hypoxic state. Because hypoxia can increase mitochondrial superoxide production, excessive hypoxia may contribute to oxidative stress. To test this, we assayed O(2) flux, an indicator of O(2) availability, in embryos of glucose-injected hyperglycemic or saline-injected mice. O(2) flux was reduced by 30% in embryos of hyperglycemic mice. To test whether hypoxia replicates, and hyperoxia suppresses, the effects of maternal hyperglycemia, pregnant mice were housed in controlled O(2) chambers on embryonic day 7.5. Housing pregnant mice in 12% O(2), or induction of maternal hyperglycemia (>250 mg/dl), decreased Pax3 expression fivefold, and increased NTD eightfold. Conversely, housing pregnant diabetic mice in 30% O(2) significantly suppressed the effect of maternal diabetes to increase NTD. These effects of hypoxia appear to be the result of increased production of mitochondrial superoxide, as indicated by assay of lipid peroxidation, reduced glutathione, and H(2)O(2). Further support of this interpretation was the effect of antioxidants, which blocked the effects of maternal hypoxia, as well as hyperglycemia, on Pax3 expression and NTD. These observations suggest that maternal hyperglycemia depletes O(2) in the embryo and that this contributes to oxidative stress and the adverse effects of maternal hyperglycemia on embryo development.
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PMID:Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress. 1592 21

Cardiopulmonary bypass (CPB) is associated with surgical stress, hypothermia, hyperoxia, enhancement of neuroendocrine outflow, and administration of glucogenic catecholamines that are associated with glucogonolysis and glucogenesis that result in hyperglycemia. The hyperglycemic state during CPB has been associated with adverse outcomes, such as infection, neurological impairment, cardiac dysfunction, prolonged hospitalization, and higher mortality rates. This report justifies vigilant monitoring of blood glucose levels and a rational protocol for the treatment of hyperglycemia of all open heart surgical patients that may improve post-CPB surgical outcomes.
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PMID:Hyperglycemia as an effect of cardiopulmonary bypass: intra-operative glucose management. 1692 93

The aim of this study was to investigate the effects of an increase in the saturation of blood oxygen (SaO2) and/or serum glucose on photoreceptor sensitivity in normal subjects and in patients with diabetes mellitus. We monitored cone and rod sensitivity by recording dark-adaptation curves to both green and red test stimuli while inhaling either air (20% O2 + 80% N2) or 100% oxygen in 12 normal subjects and 12 diabetic patients with no (10) or mild (2) retinopathy. We also repeated the experiment in 10 of the normal subjects under hyperglycemia (mean serum glucose: 161 mg/dl). Results show that in normal subjects the dark-adapted cone sensitivity is improved by an increase in SaO2 or by hyperglycemia. Final rod sensitivity is unchanged during hyperoxia and during hyperglycemia when measured with a green test spot. However the kinetics of dark adaptation are altered during hyperglycemia, and an increase in final sensitivity is observed when measured with the red test spot. Inhalation of oxygen during hyperglycemia in normal subjects reduces cone sensitivity compared to that found during hyperglycemia alone (Pasteur effect). In diabetic subjects the dark-adapted cone threshold is comparable to that found in normal subjects, and sensitivity also increases with an increase in SaO2. The final rod threshold, however, is impaired compared to that of the control group, and rod sensitivity is improved by increasing the SaO2. The results suggest that the metabolism of rods and cones may differ in normal subjects: in cones, the rate of metabolism can be augmented by increasing the available oxygen or glucose, whereas rods appear more insensitive to increased blood oxygen saturation and hyperglycemia. In diabetic subjects, both cone and rod metabolism can be increased by supplemental oxygen, indicative of an early rod deficit. The study lends weight to the hypothesis that dark-adapted rods in diabetics are hypoxic before the onset of retinopathy.
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PMID:Hyperoxia, hyperglycemia, and photoreceptor sensitivity in normal and diabetic subjects. 1696 9

Cardiopulmonary resuscitation does not end with restoration of spontaneous circulation; rather, it must be continued with the application of all the measures that allow organ function to be maintained. The initial goal of hemodynamic treatment is to achieve normal blood pressure for the patient's age by means of fluids and/or vasoactive drugs. The aim of respiratory treatment is to normalize ventilation and oxygenation without causing further lung injury, avoiding hyperoxia and hyperventilation as well as hypoxia and hypercapnia. Neurological stabilization aims to reduce secondary brain damage, by avoiding hypertension and hypotension, maintaining normal ventilation and oxygenation, and treating hyperglycemia, agitation and seizures. Although no specific studies in children are available, data from adults have shown that early moderate hypothermia attenuates brain damage secondary to cardiorespiratory arrest, without increasing complications. After the arrest, the need for analgesia and/or sedation must be considered. The process of transportation to the pediatric intensive care unit (PICU) requires the following steps: stabilizing the patient, checking for and stabilizing fractures and external wounds, ensuring a stable airway and intravenous lines, assessing the need for nasogastric and bladder tubes, taking blood samples for analyses, contacting the PICU and informing the staff about the child's condition, choosing the optimal vehicle for transportation according to the child's condition and the distance, checking pediatric equipment and medications, selecting experienced staff and, finally, maintaining close surveillance and monitoring during transportation.
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PMID:[Post-resuscitation stabilization and transportation]. 1734 Jul 87

Hyperglycemia and hypoxia synergistically retard diabetic wound healing. We investigated the direct effect of hyperbaric and normobaric hyperoxia on skin fibroblasts cultured in a high-glucose medium. Detroit 551 human dermal fibroblasts cultured in Dulbecco's modified Eagle's medium containing d-glucose had reduced cell survival compared with cells grown in normal glucose medium; survival was 27.5+/-3.8% lower in 25 mM glucose and 30.6+/-3.7% lower in 50 mM glucose. Cell survival decreased because of inhibition of cell proliferation and enhanced cell death. Daily hyperbaric oxygen therapy at 2.5 atmosphere absolute for 90 minutes on 3 consecutive days reduced cell proliferation and increased cell death in normal cultured fibroblasts. Hyperbaric oxygen therapy and high-glucose medium had a synergistic effect and reduced survival by 37.6+/-4.4% (25 mM glucose) and 39.6+/-5.1% (50 mM glucose). The effects of hyperbaric oxygen and high-glucose medium were associated with overproduction of reactive oxygen species. Our results suggest that direct exposure of skin fibroblasts to hyperbaric oxygen affects cell growth and superimposes the toxic effect of high glucose. This cytotoxicity may be related to the production of reactive oxygen species in the fibroblasts.
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PMID:Hyperbaric oxygen attenuates cell growth in skin fibroblasts cultured in a high-glucose medium. 1863 70


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