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

1. The pattern of breathing during the approach to the steady state following step changes of end-tidal P(CO2) and P(O2) has been determined in normal conscious human subjects. Three types of step were studied: (a) steps of P(A, CO2) against a constant background of hyperoxia (P(A, O2) approximately 200), an almost pure intracranial chemoreceptor stimulus, (b) steps of P(A, O2) between approximately 50 and 80 torr against a background of constant mild hypercapnia, an arterial chemoreceptor stimulus, and (c) steps of P(A, CO2) against a background of constant hypoxia (P(A, O2) approximately 50), a mixed stimulus. Steps were small and the responses barely detectable by the subjects.2. Steps of CO(2) in hyperoxia produced the slowest approach to the steady state. A single exponential fitted the ventilation response up to about 4 min (mean half time 83 sec for the ;up' and 69 sec for the ;down' transients). During the transient the pattern of change of tidal volume (V(T)) and expiratory time (T(E)) was the same as in the steady state. Inspiratory time (T(I)), however, in the early part of the transient, changed in the opposite direction to T(E), returning to its steady value only after 1(1/2)-3 min. This effect occurred in both ;up' and ;down' transients and resulted in a smaller change of respiratory frequency than would have been predicted from the steady-state response.3. Hypoxic steps produced the fastest approach to the steady state with mean half-times for ventilation of 10.9 sec for the ;up' transients and 6.6 sec for the ;down'. T(I) followed the same pattern during the transient as in the steady state, whereas T(E), following the step out of hypoxia, lengthened to far beyond its final steady value within five breaths of the step, only returning to its steady-state value 3-4 min after the step. This resulted in an exaggerated change of frequency during the early part of the transient.4. Steps of CO(2) in hypoxia, a mixed peripheral and central chemoreceptor stimulus, showed a ventilation response which was best fitted by two exponentials, the half-times of which were consistent with those obtained for the separate responses. The patterning was also consistent with a mixed response, more so for T(I) than for T(E).5. The steady-state pattern derived from the pre-switch means was consistent with the pattern previously described.6. Possible mechanisms are discussed. It is suggested that these results could explain the different patterns seen in the past by those using re-breathing and steady-state techniques.7. The validity of using one or two breath oxygen or nitrogen tests (or other similar tests) as a quantitative measure of the hypoxic response in man is questioned.
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PMID:The pattern of breathing following step changes of alveolar partial pressures of carbon dioxide and oxygen in man. 677 86

In the unanesthetized dogfish, Scyliorhinus canicula, oxygen and carbon dioxide partial pressures and concentrations in inspired and expired water and the acid-base balance of arterial blood, pHa and PcCO2, were determined. Each dogfish was exposed to waters differing in oxygenation and in CO2 levels, which was controlled with a pH-CO2-stat device, for successive 2- to 3-h periods. The four ambient conditions were: normoxia-normocapnia (inspired PO2, PIO2 ca 160 Torr; PICO2 ca 0.3 Torr), hyperoxia-normocapnia (PIO2 ca 730 Torr), hyperoxia-hypercapnia (PICO2 ca 1.0 Torr); normoxia-hypercapnia. At both low and high ambient CO2, the inspired-expired O2 and CO2 concentration differences increased in hyperoxia. Ventilation was depressed, and concomitantly, PACO2 increased and the arterial plasma pH decreased. The hypercapnic acidosis was rapidly but only partially compensated by an increase of the plasma bicarbonate concentration. Due to the buffer action of carbonate in sea water, low and high ambient CO2 levels corresponded respectively to high and low values of the CO2 capacitance coefficient, betaWCO2. At both ambient oxygenation levels, the expired-inspired PCO2 difference was greater at low than at high betaWCO2. At a given ambient CO2 level, expired PCO2, PECO2, wash higher in hyperoxia than in normoxia; an effect more marked at low than at high betaWCO2. Thus, the water capacitance coeffcient betaWCO2 is an important factor determining PECO2 values and probably arterial blood acid-base balance. As a general conclusion, the acid-base balance of the arterial blood in the dogfish is very much dependent on the conditions of the oxygenation and acid-base balance of the ambient water which consequently should be carefully controlled.
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PMID:Blood acid-base balance as a function of water oxygenation: a study at two different ambient CO2 levels in the dogfish, Scyliorhinus canicula. 677 56

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.
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PMID:Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats. 677 76

Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
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PMID:Effects of hypertension and hypercarbia on spinal cord tissue oxygen in acute experimental spinal cord injury. 677 23

The effect of hypoxia upon the fetus is dependent upon not only the degree of hypoxia induced but probably also upon gestational age and the initial level of fetal oxygenation. Mild hypoxia (12% or over) causes fetal tachycardia, while a more severe insult may cause bradycardia. The effect of hypoxia upon FBM in human pregnancy is uncertain, but depending upon the severity of the hypoxia, it is likely that FBM is reduced or abolished. Hyperoxia has little effect upon the fetal heart rate or FBM in normal circumstances, but an increase in FBM occurs in the presence of fetal hypoxia. No significant change in fetal heart rate in human pregnancy occurs during hypercapnia which is, however, a potent stimulus to fetal breathing. On the other hand, hypocapnia caused by hyperventilation is associated with a decrease in FBM with no obvious change in fetal heart rate. Smoking is associated with a fetal tachycardia and a decrease in FBM. The decrease in FBM is small, the effect being maximal at 30 min after smoking with recovery by 90 min.
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PMID:The fetal response to changes in the composition of maternal inspired air in human pregnancy. 677 32

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.
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PMID:Inhibitory and excitatory effects of dopamine on carotid chemoreceptors. 677 16

Arterial (PaCO2), alveolar (PACO2), mixed expired (PECO2) CO2 pressures, CO2 production (VCO2) as well as arterial O2 saturation (SaO2) were measured on 20 severely hypoxic and hypercapnic patients breathing air (A) and 100% O2 (HO). On HO, mean PaCO2 increased to 56.6 torr from 50.8 torr on A, whereas there was no significant change in PACO2 (38.3 on A, 38.6 on HO), so that the arterial-alveolar gradient (aADCO2) increased from 12.5 to 18.0 torr. PECO2 remained essentially the same. There was a statistically significant correlation between the increase in PaCO2 on HO and the arterial unsaturation (100 - SaO2) on A and also between PaCO2 on A and its increment on HO. When the rise in PaCO2 and aADCO2 were estimated which resulted from the shift in the Co2 dissociation curve due to complete oxygenation of hemoglobin on HO (Haldane effect), 78% of the observed change in PaCO2 could be accounted for. The deadspace/tidal volume ratio (VD/VT) increased from 0.59 on A to 0.64 and 87% of this difference could be attributed to the Haldane effect. The results emphasize the importance of considering this effect when interpreting alterations in PaCO2, aADCO2 and VD/VT on transition from air to hyperoxia, particularly in patients with severe hypoxemia and hypercapnia.
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PMID:Contribution of the Haldane effect to the rise of arterial Pco2 in hypoxic patients breathing oxygen. 678 Feb 65

In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated. Following total inactivation, the relationship between ventilation (V) and arterial PCO2 (PaCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further. Differential vagal cold blockade to a temperature (5-11 degrees C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration, TE) had no effect on V either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0 degrees C did the ventilatory depression during hypercapnia emerge, largely because TE failed to shorten in response to the hypercapnic stimulus. It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of V and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.
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PMID:The involvement of expiratory termination in the vagally mediated facilitation of ventilatory CO2 responsiveness during hyperoxia. 678 64

The effects of intravenous infusion of dopamine (20 microgram.min) on the steady-state ventilatory and carotid chemoreceptor responses to successive levels of isocapnic hypoxia and hyperoxic hypercapnia were investigated in cats anesthetized with alpha-chloralose. Dopamine infusion was followed by a maximal decrease in ventilation in about 20 s. Thereafter, the effect diminished and stabilized. Termination of dopamine infusion was promptly followed by an increase in ventilation. These ventilatory responses were smaller than the corresponding carotid chemoreceptor responses. The steady-state effect of dopamine infusion was to diminish ventilation at all levels of arterial O2 tension, the decrease being greater during hypoxia than that during hyperoxia. Bilateral section of the carotid sinus nerves significantly diminished but did not abolish the inhibitory effect of dopamine on ventilation during hyperoxia. Thus the ventilatory depression due to dopamine infusion is not entirely due to its effect on the carotid chemoreceptors. Dopamine decreased ventilatory responses to successive levels of hypercapnia by the same magnitude without changing the slope of the response curves. The steady-state relationship between chemoreceptor activity and ventilation shows that the ventilatory equivalent for carotid chemoreceptor activity is increased during dopamine infusion because of its greater inhibitory effect on carotid chemoreceptor activity than on ventilation with the decrease of arterial O2 tension.
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PMID:Effects of dopamine on chemoreflexes in breathing. 679 Apr 90

Arterial pressure of chick embryos was measured electromanometrically to investigate the effect of altered gaseous environments on blood pressure (BP) and heart rate (HR). The experiments were made in eggs incubated for 14-16 days at 38 degrees C without impeding the diffusive respiratory gas exchange through the shell and chorioallantois. In air, the HR was counted 260-270 beats/min and the BP increased from 14/7 Torr at day 14 to 21/12 Torr at day 16. Both the BP and HR decreased with hypoxia, whereas hyperoxia affected a slight increase in BP and little change in HR. Hypercapnia decreased the HR and tended to enhance a systolic maximum pressure. The effect of hypoxia was augmented markedly in the presence of hypercapnia and vice versa. When N2 was replaced with helium (He), the effect of hypoxia was mitigated significantly. On the contrary, replacement of N2 with sulfur hexafluoride (SF6) augmented the effect of hypoxia. Because the respiratory gas exchange of the egg takes place by diffusion through the shell and chorioallantoic capillaries, the effect of He and SF6 atmospheres on BP and HR is attributed to an altered diffusivity of O2 and CO2 in these inert gases.
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PMID:Effect of O2 and CO2 in N2, He, and SF6 on chick embryo blood pressure and heart rate. 679 62


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