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

Maximum oxygen uptake (VO2max) was measured in six college-aged males under normoxic (NVO2max) and hyperoxic (HVO2max; 70% oxygen) conditions. Subjects then randomly performed the following three 20-min submaximal exercise bouts: 75% normoxic VO2max under normoxia (NVO2N), 75% normoxic VO2max under hyperoxia (NVO2H), and 75% hyperoxic VO2max under hyperoxia (HVO2H). Metabolic parameters were obtained at 5-min intervals. Hyperoxia resulted in a 13% increase (P less than 0.01) in VO2max (NVO2max = 3.54 l X min-1 vs HVO2max = 4.00 l X min-1). Significant (P less than 0.05) decreases were observed in VE (ventilation) (13%), epinephrine (37%), norepinephrine (26%), and blood lactate (28%), with no change in oxygen uptake (VO2), carbon dioxide production (VCO2), or respiratory exchange ratio (R) during hyperoxia at the same absolute power output (NVO2N vs NVO2H). However, at the same relative power outputs (NVO2N vs HVO2H) no significant changes in VE, epinephrine, norepinephrine, or blood lactate were observed when hyperoxia and normoxia were compared.
Med Sci Sports Exerc 1984 Dec
PMID:Submaximal exercise quantified as percent of normoxic and hyperoxic maximum oxygen uptakes. 651 75

The radioactive microsphere technique was used in 13 newborn dogs to determine the effect of a metabolic (lactic)acidosis upon cardiac output (CO), cerebral blood flow (CBF), and autoregulation of cerebral blood flow. The animals were mechanically ventilated with supplemental oxygen to ensure normocarbia and hyperoxia throughout the experiments. Baseline cardiac output and cerebral blood flow measurements were made, followed by a lactic acid infusion to maintain pH less than 7.25. Metabolic acidosis produced a 27% fall in cardiac output and no change in cerebral blood flow (19 ml/100 g/min). Autoregulation was tested in 6 of the acidemic puppies by acute volume depletion to reduce blood pressure by 30% of baseline, followed by rapid volume re-expansion of the withdrawn blood. With volume depletion, CO decreased by 38%, and with volume re-expansion CO returned to baseline. The CBF remained at baseline levels with volume depletion but was slightly increased after rapid volume re-expansion. Five acidemic controls maintained CO and CBF constant with time. Thus cerebral autoregulation is preserved in the newborn dogs during metabolic acidosis, although cerebral blood flow was slightly increased following volume re-expansion.
Brain Res 1984 Dec 17
PMID:The effect of metabolic acidosis upon autoregulation of cerebral blood flow in newborn dogs. 651 78

The influence of variations in inspired PO2 on dynamic and static muscle performance of the left quadriceps muscle was studied. Eight subjects performed (1) 60 maximal consecutive dynamic contractions and (2) one sustained exhaustive static contraction at 27% of maximal voluntary contraction (MVC). Breathing mixtures containing 11%, 21% or 99% O2, were administered. Peak torque as an average of the 60 knee extensions was higher (p less than 0.01) during hyperoxia (mean +/- SE = 104 +/- 4 Nm) than during normoxia (98 +/- 4 Nm), but did not differ significantly between hypoxia (95 +/- 5 Nm) and normoxia. Peak torque of individual extensions declined more rapidly during hypoxia than during normoxia, differing in the final 12 extensions by 11% from normoxic values. Static endurance time was reduced (p less than 0.02) during hypoxia (152 +/- 12 s) as compared to normoxia (189 +/- 13 s) and hyperoxia (169 +/- 11 s). No significant difference in endurance time was demonstrated between hyperoxia and normoxia. Thus, hypoxia impaired muscle performance in both dynamic and sustained static exercise, whereas acute hyperoxia improved dynamic but not static muscle performance. The results are interpreted in terms of differences in rate of intramuscular H+ accumulation.
Acta Physiol Scand 1984 Dec
PMID:Effects of hyperoxia and hypoxia on dynamic and sustained static performance of the human quadriceps muscle. 652

Hyperoxia brought about substantial accumulation of primary and end products of lipid peroxidation (LPO) and a significant lowering of alpha-tocopherol content in rat brain tissues. Preinjection of animals with synthetic and natural antioxidants (4-methyl-2,6-ditretbutylphenol and alpha-tocopherol) prevented LPO activation and decreased the frequency of epileptiform seizures induced by hyperoxia. Administration of a mixture of unsaturated fatty acids led to an opposite effect. The changes in the properties of serotonin receptors were found to be dependent on the hyperoxia-induced LPO. These changes were marked by the reduced specific binding of serotonin with neuronal membranes of the rat brain cortex. The data obtained allowed the conclusion about the key role played by LPO activation in toxic action of hyperbaric activation on the brain.
Biull Eksp Biol Med 1983 Dec
PMID:[Role of lipid peroxidation in damage to serotonin receptors and development of epileptiform seizures during hyperoxia]. 666 40

Whole-body O2 uptake (VO2) in rats was reported not to increase when total O2 transport (TOT = cardiac output X arterial O2 concentration) was increased above normal ranges when body temperature was kept at 38 degrees C (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 660-664, 1982). Similar experiments were performed to see if hypothermic rats at 34 degrees C would increase VO2 with an increased TOT in an effort to generate heat. Anesthetized rats were ventilated with 9 or 12% O2 (hypoxia), room air (normoxia), and O2 (hyperoxia) to vary TOT from 52.6 to 6.6 ml X kg-1 X min-1. VO2 was measured in a closed-circuit, double servospirometer system. Although VO2 was significantly lower at 34 degrees C than the values previously found at 38 degrees C with normoxia and hyperoxia, there was no increase with increasing values of TOT. In spite of a lower plateau value of VO2 at 34 degrees C, the critical value of TOT below which VO2 could not be maintained was nearly the same as at 38 degrees C (22 ml X kg-1 X min-1). The reason for this was that O2 was less completely extracted as TOT was lowered below the critical value in the hypothermic animal. Some of the difficulty in extracting O2 at the tissues was probably due to the decrease in P50 (PO2 at 50% saturation) that occurs with decreased body temperature.
J Appl Physiol Respir Environ Exerc Physiol 1983 Dec
PMID:Critical O2 transport values at lowered body temperatures in rats. 666 61

The effect of intravenous dopamine on carotid body chemoreceptor activity was investigated in 6 anesthetized cats which were paralyzed and artificially ventilated. Studies were performed at 4 steady-state PaO2 levels at a constant PaCO2 and at 4 levels of PaCO2 during hyperoxia. Dopamine inhibited carotid chemoreceptors before and excited them after haloperidol. Moderate stimulation of the receptors by hypoxia and hypercapnia augmented dopamine's effects. These results indicate that both inhibitory and excitatory dopamine receptors are present in the carotid body.
Neurosci Lett 1980 Dec
PMID:Inhibitory and excitatory effects of dopamine on carotid chemoreceptors. 677 16

Hemolymph acid-base variables (pH, PCO2 and CCO2), hemolymph Ca2+ and Na+ concentrations, and osmolality were measured in unrestrained crabs, Cancer productus, before, during and following 4 hr emersion and 43 hr hyperoxia (460-510 Torr), both at 10 degrees C. Emersion and hyperoxia provoked an acidosis associated with elevation of hemolymph CCO2 and PCO2, yet attempts to calculate PCO2 from measured pH and CCO2 always resulted in values greater than those measured directly. This discrepancy between measured and calculated PCO2, was associated with base excess, and was eliminated upon in vitro equilibration of the hemolymph and more slowly in vivo, suggesting that metabolic compensation for the acidosis occurred more rapidly than could acid-base equilibration. During emersion, increases of CCO2 and [Ca2+] provide evidence that the internal CaCO3 stores, possibly from the exoskeleton, were mobilized during acid-base compensation. Hyperoxia provoked no such increase in Ca2+, and branchial uptake of HCO3- may make a major contribution to the elevation of CCO2 during hyperoxia. It is suggested that shell buffering by aquatic crustaceans provides a means of compensation for acidosis under conditions during which branchial function is impaired.
Respir Physiol 1980 Dec
PMID:Non-equilibrium acid-base status in C. productus: role of exoskeletal carbonate buffers. 678 8

Blood acid-base balance, blood gases, respiration, ventilation, and renal function were studied in the rainbow trout during and following sustained environmental hyperoxia (PIO2 = 3.50-650 Torr). Animals were chronically fitted with dorsal aortic cannulae for repetitive blood sampling, oral membranes for the measurement of ventilation, and bladder catheters for continuous urine collection. Hyperoxia caused a proportional increase in arterial O2 tension and a stable 60% reduction in ventilation volume (Vw), the latter mainly due to a decrease in ventilatory stroke volume. O2 consumption exhibited a short-term elevation. Arterial CO2 tension (PaCO2) rose within 1 h, causing an immediate drop in arterial pH (pHa), and continued to increase gradually thereafter, reaching a value 2-4x the normoxic control level after 96-192 h. Compensation of the associated acidosis by the accumulation of [HCO3-] in the blood plasma started within 5-6 h, and was complete by 48 h. Therefore, further compensation occurred simultaneously with the gradual rise in PaCO2. The kidney played an important active role in this compensation by preventing excretion of the accumulated [HCO3-]. Upon reinstitution of normoxia, PaCO2 dropped to control levels within 1 h, and restoration of blood acid-base status by reduction of [HCO3-] had commenced by this time. A complete return to control values occurred within 20 h. During hyperoxia, an experimental elevation of the depressed Vw above control normoxic levels caused only a minor and transient reduction in PaCO2 and no change in pHa, but injection of branchial vasodilator 1-isoprenaline (10 mumol/kg) produced a large drop in PaCO2 and rise in pHa. It is concluded that the rise in PaCO2 during hyperoxia is mainly due to internal diffusive and/or perfusive limitation associated with branchial vasoconstriction, rather than to external convective limitation associated with the decreased Vw.
Respir Physiol 1980 Dec
PMID:Blood acid-base regulation during environmental hyperoxia in the rainbow trout (Salmo gairdneri). 678 12

The effects of intravenous injection of naloxone (0.4 mg.kg-1), an opiate antagonist, on the responses of carotid body chemoreceptor discharge and ventilation to steady-state levels of hypoxia and hypercapnia were investigated in 12 anesthesized cats. After naloxone, carotid chemoreceptor response to hypoxia (PaO2 60--30 Torr) was enhanced, a finding that suggested that the endogenous enkephalin-like peptide present in the carotid body inhibits carotid chemoreceptors. This reasoning is supported by the observation that close intra-arterial injection of met-enkephalin inhibits carotid chemoreceptors and that the effect is blocked by naloxone. After naloxone, ventilation was stimulated even in the absence of a significant stimulation of carotid chemoreceptors during hyperoxia, indicating that ventilation is normally suppressed by endogenous opiates in the central nervous system, an effect disinhibited by naloxone. Also, the ventilatory effect of the peripheral chemoreceptor input was augmented after naloxone.
J Appl Physiol Respir Environ Exerc Physiol 1981 Dec
PMID:Effects of naloxone on carotid body chemoreception and ventilation in the cat. 679 1

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.
Neurosurgery 1981 Dec
PMID:Pulmonary effects of head trauma. 679 86


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