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

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

We have examined the effect of steady-state hyperoxia on the ventilation of sea level (SL) cats and cats acclimatized to simulated high altitude (HA) at 5500 m for three weeks. Three groups of cats were studied. In group I, the ventilatory responses to 10%, 21% and 100% O2 were studied at SL, and after acclimatization to HA, the ventilatory responses to 10% and 100% O2 were measured. In group II the ventilatory responses and femoral artery and superior sagittal sinus blood gases were measured in two sets of cats, one at SL and one at HA, during exposure to the gases outlined in group I. In group III, we examined the effect of chronic vagotomy on the ventilatory responses to the gas mixtures outlined in group I. Breathing 100% O2 at SL had no significant effect on ventilation, tidal volume, respiratory frequency, or cerebral blood flow (inferred from the cerebral veno-arterial CO2 difference). Ventilation was constant in the HA acclimatized cats while breathing 10% and 100% O2, but the ventilatory pattern changed dramatically during hyperoxia: respiratory frequency increased and tidal volume fell. Breathing 100% O2 was associated with changes in CBF, and venous PCO2 that might be expected to stimulate ventilation, but the change in ventilatory pattern suggests to us that hyperoxic disinhibition of central respiratory processes (which were modified by HA acclimatization) is the mechanism whereby ventilation is sustained during hyperoxia at HA. After vagotomy at HA, ventilation remained constant while breathing 100% O2, but the changes in respiratory pattern were no longer apparent. Therefore, vagal afferents seems to have a role in determining the pattern, but not necessarily the absolute level, of ventilation during hyperoxia. Cats vagotomized at SL prior to HA exposure did not show any evidence of HA ventilatory acclimatization; thus, the vagi may also play a heretofore unrecognized role in the process of acclimatization.
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PMID:Hyperoxic ventilatory responses of high altitude acclimatized cats. 309 74

In pertaining to PO2 dependency of the pulmonary CO diffusing capacity during rebreathing, the O2 uptake (VO2) and cardiac output (Q) were measured at three different PO2 levels between 100 and 500 Torr. Since the VO2 measured by an O2 injection method is strongly influenced in hyperoxia by a gas exchange ratio (R), a simulation method using a R-PCO2 relation during rebreathing was developed. Gas volume in the lung-bag-system needed in the computation was measured from the difference in O2 concentration between before and after injecting a known amount of O2 into the rebreathing circuit. The accuracy of the volume was checked by comparing it with the volume measured successively with a body box. The VO2 was determined by comparing the simulated O2 and CO2 concentrations in rebreathing gas with the measured ones. The VO2 significantly increased by rebreathing in hyperoxia. To analyze the VO2 increase, the Q was computed by dividing the VO2 by the arteriovenous O2 content difference, which in turn was obtained by dividing the slope of the CO2 dissociation curve by that of the R-PCO2 line. The Q was almost linearly related to the VO2. Since there was no difference in VO2 in steady state breathing between normoxia and hyperoxia, the increase in VO2 and Q seemed to occur transiently. This finding is very important in evaluating the PO2 dependency of the pulmonary diffusing capacity for CO.
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PMID:Change in O2 uptake during rebreathing in hyperoxia in man. 310 39

Growth of the chick embryo is accelerated by brief (72-hr) exposure to 60% O2 beginning on day 16 of incubation, and acute (2-3 hr) hyperoxia stimulates oxygen consumption (VO2). However, the increment in VO2 that accompanies acute exposure to 60% O2 is only about half that required to account for the degree of growth acceleration observed during 72 hr of hyperoxia. We tested the hypothesis that the magnitude of the oxygen-induced change in embryonic metabolism depends on the length of exposure by making daily measurements of embryonic VO2 during brief (72-hr) exposure to 60% or 15% O2. White leghorn eggs were incubated in 21% O2 for 15 days. On day 16 the experimental eggs were switched to 60% or 15% O2; control eggs were maintained in 21% O2. Oxygen consumption and CO2 production (VCO2) were measured daily. Embryo and organ weights were compared on day 18. Wet and dry weights of briefly hyperoxic embryos were significantly greater than those of normoxic controls. The relative increase in wet weight was significant for the heart and liver but not the brain. Oxygen consumption increased 7% relative to control after 24 hr of hyperoxia and 17% after 72 hr; VO2/gm embryo was 9% greater than control on day 18. Normal growth deceleration was exaggerated by hypoxia; mean wet and dry weights of the briefly hypoxic embryos were significantly less than those of controls. Organ wet weights also showed growth retardation, although the relative decrease in brain weight was not significant. Body water concentration increased in briefly hypoxic embryos. Oxygen consumption was 13% less than control after 24 hr and 17% less after 72 hr.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of growth and metabolism of the chick embryo by a brief (72-hr) change in oxygen availability. 311 Mar 63

To study the interrelationship between blood O2, CO2, and acid-base status during rapid changes of alveolar gas composition unanesthetized dogs were made to inhale high CO2 gas mixtures following air breathing or to rebreathe high CO2 and O2 mixtures following hypoxia. Before and immediately after each change in alveolar gases, sequential blood samples were taken from the carotid artery for measurement of pH, PCO2 and PO2. In the experiments at normoxia the calculated base excess (BE) decreased by about 0.7 mmol/L after 10 sec and then returned to baseline level. A smaller decrease (averaging 0.4 mmol/L) was found with hyperoxia following hypoxia. The changes in BE can be attributed to bicarbonate (or H+) exchange between blood and tissue. Lung tissue is probably responsible for the rapid initial change in BE.
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PMID:Acid-base status immediately following rapid changes of alveolar gas composition in awake dogs. 311 Aug 92

The mechanisms whereby arterial carbon dioxide tension (PaCO2) remains constant despite varying rates of CO2 production are poorly understood. During the gynaecological operation of laparoscopy, the abdominal cavity is filled with CO2. An increase in the rate of CO2 delivery to the lung (less than 50%) occurs as a result of venous CO2 absorption. Respiratory control in 39 anaesthetized but spontaneously breathing women was studied during such exogenous CO2 loading. End-tidal CO2 tension (PACO2 - rapid infrared analyser) and minute-ventilation (Wright respirometer) were measured before and at 5 min intervals after peritoneal insufflation. Ventilation increased and mean PACO2 remained constant in these patients. Inhalational anaesthetics depress respiration and this was confirmed by raised control PACO2 values in this study. However, it appears that mechanisms underlying PACO2 homeostasis in the presence of a CO2 load are not depressed by inhalational anaesthetic in this study. These patients were probably hyperoxic. Peripheral arterial chemoreflexes are thought to be eliminated by hyperoxia. Therefore, it is likely that neural stimuli, from exploration of the abdomen, drove breathing. Furthermore, the fact that there was not a large fall in PACO2 may have been due to feedback via the central (brainstem) chemoreceptor.
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PMID:Ventilation during carbon dioxide loading in anaesthetized women. 311 69

1. The ventilatory sensitivity to CO2 obtained from a non-steady-state step-ramp CO2 challenge (analogous to the Read rebreathing method) was compared with the one of the steady-state method. 2. Experiments were performed during normoxia on twenty cats anaesthetized with chloralose-urethane. In eight of these cats additional measurements were carried out during metabolic acidosis and alkalosis. 3. The slope of the non-steady-state ventilatory response curve to CO2 was not significantly different from the steady-state one only if the ratio of the step-wise increase in end-tidal PCO2 (PET,CO2) (A) above its resting value and the subsequent rate of rise of the PET,CO2 (R) was equal to the time constant of the central chemoreflex pathway (tau c). This also held true during metabolic acidosis and alkalosis. 4. It is predicted that in human beings during hyperoxia the ventilatory response line obtained with Read's rebreathing method is to a fair approximation shifted to the right by a value of A with respect to the steady-state response line, provided A/R = tau c. 5. We argue that Read's prescription that a PET,CO2 equilibrium should be established between mixed venous blood, arterial blood and end-tidal gas has to be regarded as an experimental condition leading to stable-experiments rather than dictated by physiological mechanisms.
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PMID:A pseudo-rebreathing technique for assessing the ventilatory response to carbon dioxide in cats. 311 73

The effects of transitions from air-breathing to hyperoxia (100% O2), and the reverse, on respiration (phrenic activity) and on medullary extracellular fluid (ECF) pH, or hydrogen ion concentration [H+], were studied in 8 anesthetized, paralyzed, vagotomized and glomectomized cats whose end-tidal PCO2 was kept constant. The transition from air to hyperoxia (7 cats) led to a small (1.23 nmol/L [H+], 0.010 pH unit) acidic shift of medullary ECF and a 24% increase of neural tidal and minute respiratory activity with no significant change of frequency. Opposite changes of approximately equal magnitude followed the transition from hyperoxia to air (8 cats). We show that the slopes of the respiratory responses to changing ECF [H+] in the present study are not different than the slopes with CO2-induced changes of ECF [H+] in 25 other cats. Our findings indicate that most, if not all, of the respiratory increase after hyperoxia is due to accumulation of CO2 and H+ in medullary ECF that act on the central chemoreceptors. We suggest that decreased medullary blood flow and the Haldane effect are the main mechanisms causing the rise of medullary PCO2 and stimulation of breathing.
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PMID:Effects of hyperoxia on medullary ECF pH and respiration in chemodenervated cats. 311 30

Ventilatory effects of propofol, used as a sole agent for the induction and maintenance of general anaesthesia, were studied in 14 healthy unpremedicated patients. Subarachnoid anaesthesia was established before induction of general anaesthesia. Induction was with propofol 2.5 mg kg-1 given while the patients breathed 100% oxygen. We intended to start an infusion of propofol 100 micrograms kg-1 min-1; maintain it for at least 25 min; make a first set of quasi-steady-state observations; double the infusion; and repeat observations after 25 min. The single induction bolus plus single rate infusion was not totally satisfactory: further boluses were usually needed. At induction there was apnoea in all but three patients, sometimes lasting more than 3 min; hyperventilation before induction, combined with hyperoxia, probably exaggerated this. Established ventilatory rates were generally 30% higher than awake. One patient became bradypnoeic. Tidal volume and minute ventilation, and the Tl:Ttot ratio, were reduced. Doubling the infusion rate had no clear effect on frequency or tidal volume, but it further reduced the Tl:Ttot ratio and caused an increase in PE'CO2 of 1 kPa. The ventilatory response to carbon dioxide was 58% of baseline awake control (95% confidence limits +/- 26%) at the lower infusion rate, with further slight depression when the infusion rate was doubled. Doubling the rate of infusion of propofol did not give twice the effect on ventilation, and probably is not giving twice the "depth" of anaesthesia. We cannot say if this is for pharmacokinetic or pharmacodynamic reasons.
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PMID:Some ventilatory effects of propofol as sole anaesthetic agent. 312 6

We tested the hypothesis that postnatal resetting of the carotid chemoreceptors is initiated by, and is dependent on, the rise in arterial PO2 (PaO2) which normally occurs after birth as air breathing is established. Previous studies had indicated that this resetting takes at least 24 h. We applied a technique for ventilation of the lungs of fetal sheep in utero to 3 groups of fetuses of 140-142 days gestational age: group 1 were exposed to normocapnic hyperoxia (mean PaO2 179.9 +/- 22.2 mmHg) for 27.4 +/- 0.9 h; group 2 were exposed to normocapnic hyperoxia (mean PaO2 229.4 +/- 77.5 mmHg) for 7.0 +/- 0.3 h; group 3 were ventilated for 21.6 +/- 3.3 h with a nitrogen/CO2 mixture to maintain PaO2 and PaCO2 within the normal fetal range. At the end of the ventilation period the fetuses were delivered by caesarean section, anaesthetized, paralysed and ventilation was continued. The responses of single or few fibre carotid chemoreceptor preparations to isocapnic hypoxia were then determined. To compare their response curves quantitatively, hyperbolic curves were fitted to the data. No significant differences between any of the groups were found in the vertical or the horizontal asymptotes. There was no difference in the slope of the hyperbolic line between group 2 and group 3. However, this slope was significantly greater for Group 1 than for either group 2 or group 3. Our results show that a period of hyperoxia of 24-31 h in utero, although not a similar period of normoxic ventilation, initiates the process of carotid chemoreceptor resetting.
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PMID:Effects on carotid chemoreceptor resetting of pulmonary ventilation in the fetal lamb in utero. 313 5


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