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

When mixed venous blood is oxygenated in alveolar air with higher PCO2, the PCO2 within the red cell is though to exceed the alveolar PCO2 due to the Haldane effect and to block the inward CO2 diffusion. If the direction of the CO2 diffusion is not reversed during the contact time, the HCO2-gain in the plasma will not exceed the amount estimated from venoalveolar PCO2 difference by using a CO2 dissociation curve of separated plasma. In order to clarify the validity of the above thought, the venoarterial CO2 content difference was measured by using a van Slyke apparatus and a PCO2 electrode at various alveolar PCO2 levels in rebreathing dogs. The HCO3-rise in the whole blood was obviously reduced when acute hypercapnia was administered in both normoxia and hyperoxia. Quantitatively, the decrease of CO2 content under hypercapnia corresponded to the difference in CO2 content between the true and separated plasma. The reduction, however, was slightly stronger in normoxia than in hyperoxia with alveolar PO2 of 300 to 420 mmHg. These data seem to support the following explanation: When venous blood was oxygenated in normoxic air with PCO2 higher than true venous, the inward CO2 diffusion was inhibited by the Haldane effect and the reversed diffusion after the oxygenation could also be disregarded during the contact time. Because the oxygenation was accelerated in hyperoxia and the direction of the CO2 diffusion was reversed earlier than in normoxia, the plasma CO2 content became higher in hyperoxia than in normoxia.
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PMID:Relationship between venoarterial CO2 content difference and venoalveolar PCO2 difference in acute hypercapnia in dogs. 679 75

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.
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PMID:Effects of naloxone on carotid body chemoreception and ventilation in the cat. 679 1

Periodic breathing of the Biot or cluster type was induced in spontaneously breathing, pentobarbital anesthetized cats by placing bilateral lesions within the pneumotaxic system of the rostral pons. Control lesions positioned outside of the critical nuclei never resulted in Biot breathing. The periodic pattern was characterized by clusters of breaths which were separated by distinct periods of apnea and was clearly not of Cheyne-Stokes quality. Test gas challenges inducing hypoxia and hypercapnia tended to diminish the apneic breatholds, whereas hyperoxia potentiated the periodic breathing by increasing the duration of the non-ventilatory phase. Only hypercapnia significantly altered the tidal volume of Biot breaths by increasing the depth of breathing. No conclusions can be drawn as to whether the Biot pattern arises from an inherent central respiratory controller periodicity, or from oscillations in arterial blood gas tensions and peripheral chemoreceptor (and mechanoreceptor) inputs. It is suggested that the experimental model for Biot breathing may be of unique importance for studying the control of expiratory duration, particularly apnea. Also, it is of interest that similar breathing patterns and gas responses occur in the neonate and adult.
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PMID:Experimental Biot periodic breathing in cats: effects of changes in PiO2 and PiCO2. 679 61

Fifteen normal pregnant subjects inhaled a 7% CO2 mixture over a period of 5 min, resulting in a markedly increased rate of fetal breathing. In a further 15 normal pregnant subjects, an 80% O2 mixture was administered over a period of 10 min; during the second half of this stimulation period a significant increase in fetal breathing rate was noted. Finally, a 7% CO2 mixture was administered during a 5-min period to a total of 26 pregnant patients with fetal growth retardation. Seventeen of these 26 patients were subsequently administered an 80% O2 mixture during a 10-min period, immediately followed by a mixture of 80% O2 and 7% CO2 over a 5-min period. During both maternal hypercapnia and hyperoxia a marked increase in fetal breathing rate was noted, which was not essentially different from that seen in normal pregnancy. Administration of a mixture of O2 and CO2 did not result in any significant change in fetal breathing activity. At birth, all growth-retarded infants had an Apgar score of 6 or more at one minute. It can be concluded that respiration in both the normal and the clinically non-hypoxic growth-retarded fetus shows a similar reaction pattern towards alterations in maternal gaseous exchange.
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PMID:The effect of maternal hypercapnia and hyperoxia on breathing movements in the normal and growth-retarded fetus. 680 49

We studied the effects of hyperoxia and hypercapnia on obstructive apneic episodes (OAE) in a 39-year-old male with the sleep apnea and hypersomnolence syndrome (SAHS). While inspiring room air, our patient spent approximately 50% of his non-REM sleep time in OAE. When the inspired gas was changed to 100% oxygen, the frequency of the OAE decreased slightly, but a statistically significant increase in the duration of each episode was noted. Additionally, a CO2 rebreathe under hyperoxic conditions was carried out during non-REM sleep; no OAE were noted during this rebreathe. Therefore, this latter observation suggests that hypercapnia under hyperoxic conditions may reduce the frequency of OAE in patients with the SAHS.
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PMID:Effects of respiratory gases on the frequency and duration of obstructive apneic episodes in a patient with the sleep apnea-hypersomnolence syndrome. 680 21

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.
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PMID:Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat. 681 27

Changes in components of the electroretinogram during hyperoxia, hypoxia, and hypercapnia were studied to demonstrate retinal vascular autoregulation by electrophysiologic means. Autoregulation of the retinal arterial network is shown to stabilized the b-wave during hyperoxia (arterial PO2 of 395 mm Hg). During marked hypoxia, under ventilation with 10% and 5% O2, the b-wave decreased, indicating failure of autoregulation at the corresponding arterial PO2 levels of 30 and 26 mm Hg. During hypercapnia, possible autoregulatory effects were counteracted by a low arterial pH, which decreased the b-wave amplitude. The findings provide new electrophysiologic evidence for autoregulation of the retinal vessels. The c-wave during changes in arterial PO2 and PCO2 underwent changes that correlate inversely with fluctuations in blood pressure that occurred during ventilation with test gas mixtures. Considering the linear relationship between blood pressure and choroidal flow, we suggest that the latter influences the amplitude of the c-wave.
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PMID:Effects of changes in arterial Po2 and Pco2 on the electroretinogram in the cat. 681 84

The effect of metabolic acidosis on the activity of aortic chemoreceptor afferents and their responses to hypoxia and hypercapnia were investigated in nine cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. This effect was compared with that on simultaneously recorded activity of carotid chemoreceptor afferents in three separate cats. The activity of a single or paucifiber preparation of chemoreceptor afferents was recorded at five steady-state levels of arterial O2 tension (PaO2) at a constant arterial CO2 tension (PaCO2) and at three levels of PaCO2 during hyperoxia (PaO2 greater than 400 Torr) before and after slow injection of 1 M lactic acid in the average dose of 2.6 +/- 0.6 mmol X kg-1. On the average, arterial pH decreased from 7.445 +/- 0.046 to 7.222 +/- 0.041 at PaO2 of 98 +/- 5 Torr and PaCO2 of 34 +/- 1 Torr. This decrease in pHa during normoxia increased the aortic chemoreceptor activity from 0.8 +/- 0.2 to 1.4 +/- 0.3 imp X s-1. Metabolic acidosis increased the excitatory effect of hypoxia and hypercapnia. The stimulatory effect of CO2 for the same increase in arterial [H+] was greater than that of metabolic acidosis, indicating a dominant effect of molecular CO2 on aortic chemoreceptors. Simultaneous measurements of carotid and aortic chemoreceptor activities showed that their responses to metabolic acidosis were qualitatively similar. Quantitatively, the response of aortic chemoreceptor afferents was less than that of carotid chemoreceptors.
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PMID:Aortic and carotid chemoreceptor responses to metabolic acidosis in the cat. 684 73

Cochlear microcirculation was studied with oxygen-sensitive microelectrodes simultaneously in all three scalas during anoxia, hyperoxia, and hypercapnia. The anoxia caused a sharp decline of Po2 in the scala media (SM), scala vestibuli (SV), and scala tympani (ST). Hyperoxia and hypercapnia resulted in an elevation of Po2 in all three scalas. During anoxia, the SM showed the earliest and largest decline in Po2, with the shortest recovery and reoxygenation time. When Po2 slopes (during anoxia) were compared, the SM to ST and the SM to SV were substantially different and remained different even when the partial pressures of oxygen quantified as oxygen in nanomoles. Our experiments also showed that changes in Po2 within the SM closely correlate with changes of endocochlear potential and BP.
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PMID:Perilymphatic and endolymphatic PO2. Variations during anoxia, hyperoxia, and hypercapnia. 698 2

The response (imp . s-1) of single- or few-fiber preparations from the carotid body (10 experiments) and the aortic body (5 experiments) to various levels of hypercapnia on different backgrounds of hypoxia were analyzed by two statistical techniques--analysis of variance and the Duncan's new multiple-range test. These analyses showed an initial statistically significant increase in the slope of the response to increasing arterial pressure of CO2 (PaCO2) as PaO2 fell. But the slope of the response to carbon dioxide later showed a clear tendency to become less; i.e., no significant increase in imp . s-1 when a PaCO2 rose (substantially) with normoxic (carotid body) and hypoxic (carotid and aortic bodies) backgrounds. The response of the aortic body to hypercapnia showed no statistically significant increase if the background was hyperoxia or normoxia. The characteristic of the chemoreceptor to become saturated in its response to carbon dioxide while still retaining its ability to respond to hypoxia suggests the possibility that at least some of the mechanisms involved in the chemoreception of hypoxia differ from those involved in the chemoreception of hypercapnia.
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PMID:Neural responses of the cat carotid and aortic bodies to hypercapnia and hypoxia. 706 74


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