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

After voluntary hyperventilation, normal humans do not develop a significant ventilatory depression despite low arterial CO2 tension, a phenomenon attributed to activation of a brain stem mechanism referred to as the "afterdischarge." Afterdischarge is one of the factors that promote ventilatory stability. It is not known whether physiological stimuli, such as hypoxia, are able to activate the afterdischarge in humans. To test this, breath-by-breath ventilation (VI) was measured in nine young adults during and immediately after a brief period (35-51 s) of acute hypoxia (end-tidal O2 tension 55 Torr). Hypoxia was terminated by switching to 100% O2 (end-tidal O2 tension of first posthypoxic breath greater than 100 Torr). Brief hypoxia increased VI and decreased end-tidal CO2 tension. In all subjects, termination of hypoxia was followed by a gradual ventilatory decay; hyperoxic VI remained higher than the normoxic baseline for several breaths and, despite the negative chemical stimulus of hyperoxia and hypocapnia, reached a new steady state without an apparent undershoot. We conclude that brief hypoxia is able to activate the afterdischarge mechanism in conscious humans. This contrasts sharply with the ventilatory undershoot that follows relief of sustained hypoxia, thereby suggesting that sustained hypoxia inactivates the afterdischarge mechanism. The present findings are of relevance to the pathogenesis of periodic breathing in a hypoxic environment. Furthermore, brief exposure to hypoxia might be useful for evaluation of the role of afterdischarge in other disorders associated with unstable breathing.
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PMID:Hypoxic exposure and activation of the afterdischarge mechanism in conscious humans. 212 78

1. Synchronization of spontaneous sympathetic discharge during the respiratory cycle was studied in the cervical and renal nerves of vagotomized, normotensive Wistar-Kyoto rats (WKYs) and age-matched spontaneously hypertensive rats (SHRs). Phrenic nerve discharge was used as an index of central inspiratory activity. 2. In normotensive Wistar-Kyoto rats depression of sympathetic activity appeared at the onset of inspiration reaching a minimum at mid-inspiration. Peak maximal sympathetic discharge corresponded to postinspiratory phase; a second increase sometimes appeared in late expiration. Variations of respiratory frequency over wide range of experimental conditions by hypoxia, hyperoxia, hyper- or hypocapnia and transection of carotid sinus nerves did not affect this pattern. 3. In SHRs the respiratory-phase-related timing of sympathetic discharge was variable. In normoxia, the maximal sympathetic activity occurred in late inspiration, preceded by short depression at early inspiration and followed by postinspiratory depression. A second increase in sympathetic activity was observed in mid-expiration. 4. The pattern of respiratory phase modulated sympathetic activity in SHRs was altered by hypoxic stimulation of the peripheral chemoreceptors. The early inspiratory depression of sympathetic activity was substantially prolonged and the maximal sympathetic discharge was shifted from inspiration to early expiration. This effect was abolished after carotid sinus nerves had been cut. 5. Hypercapnic stimulation of central chemoreceptors in SHRs with carotid sinus nerves cut did not influence the timing of the sympathetic activity in relation to the respiratory phase, though the magnitude of rhythmical sympathetic discharges was increased. 6. We discuss the possibility that altered synchronization between central respiratory drive and sympathetic neuronal system may contribute to the neurogenic mechanisms of arterial hypertension in SHRs.
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PMID:Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat. 223 3

The relative contributions of O2- and CO2-sensitive chemoreceptor information to centrally generated respiratory patterns have changed dramatically during vertebrate evolution. Chemoafferent input from branchial O2 chemoreceptors modulates centrally generated respiratory patterns but is not critical for respiratory rhythmogenesis in fishes. In air-breathing fishes, branchial O2 chemoreceptors monitoring internal and external stimuli control the relative contributions of the gills and air-breathing organ to net ventilation, and chemoafferent input is necessary for initiating air breathing. In the transition from water to air breathing by amphibious vertebrates, rhythmic patterns of branchial ventilation are completely replaced by arrhythmic and intermittent patterns of air breathing, and there is progressive dependence on CO2 as a source of respiratory drive. Periodic initiation of air breathing in resting animals appears to depend on attaining a threshold level of afferent activity from O2- and CO2/pH-sensitive chemoreceptors, since hyperoxia and/or hypocapnia can abolish air breathing in all air-breathing vertebrates. Conversely, chemoreceptor stimulation in amphibians and reptiles converts intermittent to more continuous air breathing patterns, suggesting that adequate biasing input from chemoreceptors activates a central rhythm generator. Chemoafferent input in homeotherms serves as one of several sources of drive for rhythmic breathing and supplies feedback for blood gas homeostasis in the face of metabolic or environmental change.
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PMID:Chemoreceptor modulation of endogenous respiratory rhythms in vertebrates. 224 Feb 73

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.
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PMID:Ventilatory response of spinal cord-lesioned subjects to electrically induced exercise. 238 11

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.
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PMID:EEG and spectral analysis in acute hyperventilation. 241 22

Contribution of autonomic nervous system activity to the heart rate and blood pressure responses during chemoreceptor excitations by systemic hypoxia and hypercapnia and to hyperoxia and hypocapnia was analyzed in the urethane-anesthetized, artificially ventilated rats. Systemic hypoxia induced a co-activation of two antagonistic nerves: an increase in cardiac sympathetic and in cardiac vagal efferent nerve discharges. Increased heart rate was due to predominance of the cardiac sympathetic over the cardiac vagal activation. In spite of a marked reflex increase in the renal and cardiac sympathetic nerve activities, the local vasodilator effect of hypoxia prevented consistent changes in arterial blood pressure. Bilateral section of the carotid sinus nerves (CSN) mostly abolished autonomic nerve responses and produced a profound decreases in the blood pressure during hypoxia. Hyperoxia elicited a pressor response due to peripheral vasoconstriction with no significant change in the autonomic nerve activities except for a decrease in the cardiac sympathetic nerve discharges. Hypercapnia significantly increased blood pressure and renal nerve sympathetic activity. In contrast to hypoxia, hypercapnia excited cardiac sympathetic and inhibited cardiac vagal activity. This reciprocal effect did not elicit neurogenic cardioacceleration, because it was masked by the local inhibitory action of CO2 on the heart rate. The increase in sympathetic activities and in blood pressure during hypercapnia persisted after bilateral CSN section indicating that the responses were mediated by central rather than by peripheral chemoreceptors. Hypocapnia produced a significant increase in cardiac vagal discharges yet a cardioacceleratory response occurred due to the local effect upon heart rate. The present results indicate that in the rat, autonomic nervous responses differ depending on the type, i.e. hypoxic or hypercapnic, chemoreceptor stimuli. Reflex heart rate and blood pressure responses do not follow the autonomic nerve activities exactly. Circulatory responses are greatly modified by local peripheral effects of hypoxic, hyperoxic, hypocapnic or CO2 stimuli on the cardiovascular system. Species differences characterizing the autonomic nerve responsiveness to chemical stimuli in the rat are described.
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PMID:Autonomic nerve and cardiovascular responses to changing blood oxygen and carbon dioxide levels in the rat. 251 Dec 37

The effects of the level of oxygenation on the respiratory response to heat exposure have been studied in conscious cats during normoxia, severe or mild hypocapnic hypoxia [inspired O2 fraction (FIO2) = 0.11 or 0.13], or hyperoxia. Several cats were also studied during severe normocapnic hypoxia. Experiments were repeated while the same animals were chronically carotid body denervated (CBD). The increase in respiratory frequency (f) leading to thermal tachypnea occurred at a lower body temperature (Tb) in severe hypocapnic hypoxia than in ambient air, but this effect was less pronounced when hypocapnia was corrected. No significant changes were observed during mild hypoxia or hyperoxia compared with normoxia in intact animals. After CBD, thermal tachypnea occurred at lower Tb in air than it did with intact animals in three of five cats, and it also occurred at lower Tb in mild hypocapnic hypoxia compared with air. It appears, therefore, that in conscious cats exposed to heat load 1) severe hypoxia enhances thermal tachypnea, 2) this effect persists after CBD, which suggests that it originates from a central action of hypoxia, and 3) the chemoreceptor afferents, to some degree, inhibit the onset of thermal tachypnea, as was previously observed for hypoxic tachypnea, which appears only in CBD cats (J. Appl. Physiol. 49: 769-777, 1980). Therefore, triggering of thermal and hypoxic tachypnea may involve common central mechanisms, probably located in the diencephalic structures under the control of afferents from arterial chemoreceptors.
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PMID:Effects of hypoxia on thermal polypnea in intact and carotid body-denervated conscious cats. 279 59

1. The effect of varying artificial respiratory volume (at a fixed rate of 54 min-1) on cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in control pithed rats or during pressor responses to either the alpha 1-adrenoceptor agonist phenylephrine or the alpha 2-agonist xylazine. Phenylephrine was investigated in the presence of propranolol (3 mg kg-1). The rats were pithed under halothane anaesthesia. 2. A respiratory volume of 15 ml kg-1 produced modest hypercapnia (PaCO2 = 47 mmHg), hypoxia (PaO2 = 60 mmHg) and acidosis (pH = 7.35) relative to control animals respired at 20 ml kg-1 (PaCO2 = 32 mmHg; PaO2 = 77 mmHg; pH = 7.47). In rats respired at 15 ml kg-1, total peripheral resistance was lower, and cardiac output greater (due to increased stroke volume), than in the controls. Lowering respiratory volume reduced distribution of cardiac output to the kidneys, increased it to the large intestine and also increased blood flow through the gastrointestinal tract, skin and spleen. A respiratory volume of 30 ml kg-1 gave mild hypocapnia (PaCO2 = 19 mmHg), hyperoxia (PaO2 = 101 mmHg) and alkalosis (pH = 7.59) compared to 20 ml kg-1 but had no effect on cardiac output distribution or organ blood flow although heart rate was 29% greater at 30 ml kg-1. 3. Xylazine (500 micrograms bolus followed by 100 micrograms min-1 infusion) at all three respiratory volumes gave well-sustained mean pressor responses of 62-64 mmHg by increasing both total peripheral resistance and cardiac output (resulting from increased stroke volume). It increased the proportion of cardiac output passing to the liver, reduced that going to the spleen and gastrointestinal tract and increased cardiac, renal and hepatosplanchnic blood flows. 4. The secondary, relatively sustained, pressor effect of phenylephrine (5 micrograms bolus followed by 0.4 micrograms min-1 infusion, i.v.) varied at the 3 respiratory volumes with mean values from 32 to 53 mmHg. This response was due to both increased total peripheral resistance and cardiac output (resulting from greater stroke volumes and/or heart rates). Phenylephrine increased the proportion of cardiac output passing to the gastrointestinal tract, heart, kidneys and hepatosplanchnic bed and increased cardiac, hepatosplanchnic, renal and gastrointestinal blood flows. 5. Respiratory volume had no effect on the cardiovascular effects of xylazine. However, respiratory volume modified the effects of phenylephrine on heart rate and changed the relative contributions of stroke volume and heart rate to the increased cardiac output. It also influenced the effects of phenylephrine on cardiac output distribution to the liver, epididimides and hepatosplanchnic bed and on blood flow through skeletal muscle and the large intestine. 6. Changes in respiratory volume of air ventilated pithed rats thus influence cardiac output, its distribution and regional blood flows. Such changes can also differently influence the responses of various vascular beds to phenylephrine whilst having no effect on their responses to xylazine.
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PMID:Effect of artificial respiratory volume on the cardiovascular responses to an alpha 1- and an alpha 2-adrenoceptor agonist in the air-ventilated pithed rat. 289 57

The recovery velocity of the acido-alkaline state of the intraocular fluid depended upon the ocular hemodynamics in the rabbit intraocular chamber. Oppressive action of hyperoxia and substitute hypocapnia on intraocular blood circulation was revealed. The RQ reduction described in some eye diseases and after intraocular operations can be connected with changes in gaseous composition of the intraocular fluid.
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PMID:[Role of the gas composition of intraocular fluid in the regulation of intraocular circulation]. 302 75

The relationship between the activity of the buccal force pump, expressed as the time integral of positive buccal pressure, and PaO2 was investigated in conscious toads, Bufo marinus, unidirectionally ventilated at a high flow rate (240-260 ml/min). The high ventilatory flow rate meant that PaO2 was largely independent of the animal's ventilatory activity so that the relationship between pulmonary ventilation and PaO2 was effectively open-loop. The hypoxemic threshold (PaO2) for lung ventilation was 54.2 mm Hg in hypocapnia (PaCO2 = 4.7 +/- 0.3 mm Hg), 82.6 mm Hg in normocapnia (PaCO2 = 11.6 +/- 0.2 mm Hg), and 137.9 mm Hg in hypercapnia (PaCO2 = 20.1 +/- 0.1 mm Hg). Unidirectional ventilation with 20% O2 in N2, a condition in which the toads were normoxic but hypocapnic, stopped pulmonary ventilation cycles. Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which PaCO2 is elevated this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad. Bilateral denervation of the carotid labyrinths decreased pulmonary ventilation in absolute terms, but did not reduce the proportionate increase in pulmonary ventilation in response to normocapnic hypoxia, suggesting that chemoreceptors within the carotid labyrinth may contribute to, but are not solely responsible for, the hypoxemic ventilatory drive.
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PMID:Hypoxemic threshold for lung ventilation in the toad. 312 Feb 66


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