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

Inhalation of the equimolecular mixture N2O - O2 rapidly achieves good analgesia in cases of coronary occlusion. This mixture was used with 51 patients (37 to 85 years old) with beneficial results on pain in 4 cases out of 5. This effect can be improved by giving a small amount of pethidine with the inhalation. In this way the respiratory depression of the full dose of narcotic analgesics is avoided. In halation of the mixture does not produce undesirable cardio-circulatory or respiratory changes. The oxygen content of the mixture increases patients' PaO2 without the risk of hyperoxia.
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PMID:[Nitrous oxide analgesia in myocardial infarction (author's transl)]. 60 76

An in-vitro experiment demonstrated the concentration effect of N2O (3% versus 75%) during elimination and during uptake. Other pulmonary absorption-excretion phenomena also occur simultaneously, as paired events during uptake and then during elimination:diffusion hyperoxia and diffusion anoxia; alveolar concentration of CO2, and alveolar dilution of CO2. These clinical phenomena, as well as the second gas effect, are all related, and the pulmonary absorption-excretion volume is found to depend in part on the type of ventilation:volume controlled, pressure controlled, or spontaneous respiration.
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PMID:The pulmonary absorption-excretion volume effect. 94 30

The haemodynamic effects of nitrous oxide in normoxia (20% oxygen) and in hyperoxia (50% oxygen) were investigated in 13 dogs. Nitrous oxide in hyperoxia caused a significant rise in total peripheral resistance and a significant decrease in cardiac output, heart rate, myocardial contractility (dP/dt max) and cardiac work. On the other hand, nitrous oxide in normoxia seemed to reverse these findings and did not exert negative inotropic effects on the myocardium. The results indicate that the earlier reported sympathetic activation of the circulation may be related to hyperoxia and not to nitrous oxide as such.
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PMID:The haemodynamic effects of nitrous oxide anaesthesia on systemic and pulmonary circulation in dogs. 99 63

It is now becoming increasingly clear that free radicals contribute to brain damage in several conditions, such as hyperoxia and trauma. It has been more difficult to prove that free radical production mediates ischemic brain damage, but it has often been suggested that it may be a major contributor to reperfusion damage, observed following transient ischemia. Recent results demonstrate that cerebral ischemia of long duration, particularly when followed by reperfusion, leads to enhanced production of partially reduced oxygen species, notably hydrogen peroxide (H2O2). It has also been suggested that postischemic hyperoxia, e.g. an increased oxygen tension during the recirculation period, adversely affects recovery following transient ischemia. Other data support the notion that brain damage caused by permanent ischemia (stroke) is significantly influenced by production of free radicals. The present study, however, fails to show that recirculation following brief periods of ischemia (15 min) leads to an enhanced H2O2 production, and that hyperoxia aggravates the ischemic damage. This study was undertaken to reveal whether variations in oxygen supply in the postischemic period following forebrain ischemia in rats affect free radical production and the brain damage incurred. To that end, rats ventilated on N2O/O2 (70:30) were subjected to 15 min of transient ischemia. Normoxic animals were ventilated with the N2O/O2 mixture, hyperoxic animals with 100% O2, and hypoxic ones with about 10% O2 (balance either N2O/N2 or N2) during the recirculation. At the end of this period, the animals were decapitated for assessment of H2O2 production with the aminotriazole/catalase method. This method is based on the notion that aminotriazole interacts with H2O2 to inactivate catalase; thus, the rate of inactivation of catalase in aminotriazole treated animals reflects H2O2 production. In a parallel series, animals ventilated with one of the three gas mixtures in the early recirculation period, respectively, were allowed to recover for 7 days, with subsequent perfusion-fixation of brain tissues and light microscopical evaluation of the brain damage. Animals given aminotriazole, whether rendered ischemic or not, showed a reduced tissue catalase activity, reflecting H2O2 production in the brain. Hyperoxic animals failed to show increased tissue H2O2 production, while hypoxic ones showed a tendency towards decreased production. However, all three groups (hypo, normo- and hyperoxic) had similar density and distribution of neuronal damage. These results suggest that although postischemic oxygen tensions may determine the rates of H2O2 production, variations in oxygen tensions do not influence the final brain damage incurred.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Free radical production and ischemic brain damage: influence of postischemic oxygen tension. 205 15

Reported is a system of apparatures to control characteristic changes of cardiorespiratory function during different methods of endoscopic ventilation. The aim of the study is to measure and record simultaneously and continuously ECG, thoracic movement, tracheal pressure, pulmonary artery pressure and arterial oxygen pressure using transcutaneous technique. Measurements of arterial blood pressure and blood gas analysis (PaO2, PaCO2, BE, HCO3-, pH) are carried out in intervals. Four different methods of injector-ventilation are compared with the conventional laryngoscopic ventilation on the basis of a test program. Laryngoscopic ventilation as well as injectorventilation by CARDEN-Tubus make it possible to achieve a hyperoxaemic situation by normofrequent ventilation. Despite of hyperventilation it is not possible in every case to achieve an increased capillary oxygen pressure of 200 to 300 mm Hg by injector-ventilation with Venturi effect because of a smaller oxygen proportion. In jet-ventilation with N2O/O2-mixture (3:1) there is no appreciable hyperoxia, but a small reduction of systemic arterial blood pressure. With all techniques of mechanical respiration usual middle intratracheal pressure of respiration was not exceeded. Traumatic pressure of jets was only indirectly shown in steep rises of pressure by the applied technique of measurement.
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PMID:[Monitoring respiratory and circulatory parameters in comparing various jet ventilation procedures]. 211 91

Cerebrovascular dilation over PaO2 ranging from hyperoxia to moderate hypoxia is unexplained. We hypothesize that tissue acidosis is the cause. Local cortical cerebral blood flow (LCBF), tissue hydrogen ion concentration [H+]t, and tissue PO2 (PtO2) were measured with microelectrodes in the parietal cortex of 18 rats during a 30-min steady state on 60 to 10% inspired O2 (PaO2, 300 to 40 torr) during 40% N2O analgesia. Five rats kept on 60% O2/40% N2O served as controls. In 18 rats at a PaO2 of 275 +/- 7 torr (mean +/- SEM) and PaCO2 of 35 +/- 1 torr, cerebral values were: LCBF = 129 +/- 23 (mean +/- SEM) ml.100 g-1.min-1; [H+]t = 62 +/- 6 nM; and PtO2 = 25 +/- 3 torr. As PaO2 was reduced from about 300 to 40 torr, changes in these variables in percentage of control with respect to PaO2, were described by the following equations, all at P less than 0.0001: LCBF = 85.9 + 5,572/Pao2; [H+]t = 97.15 + 1,012/PaO2; and PtO2 = 108.8 - 3,492/PaO2. Simultaneous solution of the LCBF and [H+]t equations at various PaO2 revealed a slope of 8.82%/nM. Direct correlation between LCBF in ml.100 g-1.min-1 and [H+]t in nM revealed a linear relationship defined by the equation Y = -7.472 + 1.6705X (r = 0.6426) for [H+]t between 56 and 160 nM (pH = 7.25 and 6.80) but no correlation at [H+]t values between 56 and 32 nM (pH = 7.25 to 7.50). Cerebrovascular tone is directly correlated with [H+]t during progressive, 30-min steady-state reduction in PaO2 from 350 to 40 torr.
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PMID:Mechanisms of cerebrovascular O2 sensitivity from hyperoxia to moderate hypoxia in the rat. 292 Dec 94

The effects of inhalation of different gases were studied in neonatal rabbits with the following results: In neonates with normal heart rate (HR), hyperoxia induced by O2 inhalation did not appreciably affect HR, but it increased cerebral tissue PO2, while decreasing cerebral blood flow (CBF). In many of those which fell into a state of marked bradycardia, not only HR and CBF but also cerebral tissue PO2 levels were recovered as a result of O2 inhalation. CBF was increased even when HR was hardly changed (at least when the HR decrease was 10% or less) by hypercarbia due to inhalation of CO2 mixed air. Severe hyperoxia induced by N2O inhalation caused bradycardia and reduced CBF.
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PMID:Experimental study on the hemodynamics of the neonatal brain. 309 67

The value of continuous transcutaneous oxygen (PtcO2) monitoring in the presence of halothane and nitrous oxide (N2O) was studied in 10 infants. All infants were continuously monitored during the study with a Clark-type skin electrode with Mylar membrane. The polarization voltage of the membrane was changed to 600 mV to make it insensitive to N2O and halothane. The accuracy of PtcO2 electrode was compared with simultaneously measured PaO2 at different intervals. Correlation of PaO2 with PtcO2 was sought during hypoxic-normoxic state (PaO2 between 27--92 torr) and hyperoxic state (PaO2 between 105--439 torr). During hypoxic-normoxic state, the correlation between PaO2 and PtcO2 values was 0.94. During the hyperoxic state, poor correlation existed between PaO2 and PtcO2 (r = 0.51). Although PtcO2 did not correlate with PaO2 during hyperoxia, it consistently overestimated PaO2 and thereby, provided a predictive ability by over-diagnosing hyperoxia. When combined with continuous monitoring of inspired oxygen tension to maintain normoxia, continuous monitoring of PtcO2 will reduce the frequency of PaO2 analysis and improve patient care during anesthesia.
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PMID:Transcutaneous PO2 monitoring during pediatric surgery. 728 9

Patients treated with bleomycin (BLM) are at risk of developing acute respiratory distress syndrome (ARDS) post-operatively, and this has been associated with high intraoperative concentrations of oxygen. We report progressive arterial desaturation noticeable 2 h after the start of a 4-h radical neck dissection for which the anaesthesia included 50% O2 in N2O. The patient had received two courses of bleomycin within the previous 2 months and had undergone an uneventful right hemiglossectomy under shorter but otherwise similar anaesthesia 4 weeks previously. His pulmonary function tests before the second procedure showed a slight depression of diffusing capacity (DLco) to 80% of predicted and minimal airway obstruction consistent with his history of smoking. The pulse oximetric reading during his second procedure reached 75%, but rose to 95% after treatment with methylprednisolone salbutamol and inspired O2 concentrations between 80% and 100%. By the end of the procedure, he satisfied the criteria for ARDS and was transferred to the ICU, where he developed bilateral pneumonia, deteriorated and died of multiple organ failure. This case suggests that the risk of hyperoxic pulmonary damage in patients exposed to bleomycin may increase not only with the degree and duration of hyperoxia in a given exposure, but also with the latent effects of recent previous exposure. Near normality of pulmonary function tests cannot be taken as reassurance, and small changes may have more adverse prognostic significance than in patients who have not been exposed to bleomycin.
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PMID:Intraoperative respiratory failure in a patient after treatment with bleomycin: previous and current intraoperative exposure to 50% oxygen. 1008 4