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

Exposure of the elasmobranch Scyliorhinus stellaris to environmental hyperoxia (PO2 of 500 mm Hg) resulted in a considerable rise of arterial PCO2 from 1.9 mm Hg during normoxia to about 11 mm Hg after 6 days as an expression of the primarily oxygen-oriented regulation of gill ventilation. In contrast to the typical pattern during environmental hypercapnia, however, arterial plasma pH was hardly affected by the considerable hyperoxia-induced hypercapnia. At elevated arterial PO2 values (200-300 mm Hg) gill ventilation was apparently not adjusted exclusively for the oxygen demands of the organism, but was matched to the requirements of acid-base regulation such that the rise in PCO2 could be compensated for by a net gain of bicarbonate-equivalent ions from the environment. This fine adjustment of gill ventilation to the bicarbonate-equivalent uptake rate extended the process of adaptation to about 6 days and resulted in an almost complete pH compensation during the entire process of PCO2 increase. These data suggest that during conditions of reduced oxygen-related respiratory drive the regulation of gill ventilation is primarily dependent upon the acid-base parameters.
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PMID:Regulation of ventilation and acid-base status in the elasmobranch Scyliorhinus stellaris during hyperoxia-induced hypercapnia. 312 38

We evaluated a new combined sensor for monitoring transcutaneous carbon dioxide tension (PtcCO2) and oxygen tension (PtcO2) in 20 critically ill newborn infants. Arterial oxygen tension (PaO2) ranged from 16 to 126 torr and arterial carbon dioxide tension (PaCO2) from 14 to 72 torr. Linear correlation analysis (100 paired values) of PtcO2 versus PaO2 showed an r value of 0.75 with a regression equation of PtcO2 = 8.59 + 0.905 (PaO2), while PtcCO2 versus PaCO2 revealed a correlation coefficient of r = 0.89 with an equation of PtcCO2 = 2.53 + 1.06 (PaCO2). The bias between PaO2 and PtcO2 was -2.8 with a precision of +/- 16.0 torr (range, -87 to +48 torr). The bias between PaCO2 and PtcCO2 was -5.1 with a precision of +/- 7.3 torr (range, -34 to +8 torr). The transcutaneous sensor detected 83% of hypoxia (PaO2 less than 45 torr), 75% of hyperoxia (PaO2 greater than 90 torr), 45% of hypocapnia (PaCO2 less than 35 torr), and 96% of hypercapnia (PaCO2 greater than 45 torr). We conclude that the reliability of the combined transcutaneous PO2 and PCO2 monitor in sick neonates is good for detecting hypercapnia, fair for hypoxia and hyperoxia, but poor for hypocapnia. It is an improvement in that it spares available skin surface and requires less handling, but it appears to be slightly less accurate than the single electrodes.
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PMID:Transcutaneous carbon dioxide and oxygen tension in newborn infants: reliability of a combined monitor of oxygen tension and carbon dioxide tension. 313 91

Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration (TE) in chloralose-urethan-anesthetized dogs. Surgical removal of the carotid bodies abolishes this interaction. Since halothane anesthesia in hyperoxia greatly impairs peripheral chemoreflexes, experiments were conducted to determine whether hypercapnia would attenuate the effects of Paw on f and TE in halothane-anesthetized dogs (approximately 1.5 minimum alveolar concentration). Integrated activity of the phrenic nerve was monitored as a function of Paw (2-12 cmH2O) in a vascularly isolated left lung at varied levels of arterial PCO2 (PaCO2; 38-80 Torr) controlled by inspired gas concentrations ventilating the denervated but perfused right lung. Halothane was administered only to the right lung. The results were as follows: 1) integrated phrenic amplitude increased with PaCO2 but was unaffected by Paw; 2) f decreased as Paw increased but was not affected by PaCO2; 3) the inspiratory duration (TI) increased as PaCO2 increased but was unaffected by Paw; 4) TE increased as Paw increased but was unaffected by PaCO2; and 5) there was no phrenic response to intravenous sodium cyanide (50-100 micrograms/kg). Thus, unlike chloralose-urethan-anesthetized dogs, hypercapnia does not attenuate the effect of lung inflation on f or TE in halothane-anesthetized dogs. Furthermore, hypercapnia increases TI during halothane anesthesia, an effect found after carotid denervation but not found in intact chloralose-urethan-anesthetized dogs. It is suggested that these differences between chloralose-urethan- and halothane-anesthetized dogs may be due to functional carotid chemoreceptor denervation by halothane.
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PMID:Ventilatory responses to lung inflation and arterial CO2 in halothane-anesthetized dogs. 313 47

1. The role of chemoreceptors in the control of heart rate and behaviour during diving activity in the tufted duck was investigated in two ways. In a closed-loop experiment, ducks were exposed to ambient gas mixtures of varied composition during diving activity in an indoor tank. Characteristics of diving behaviour, heart rate and deep body temperature were monitored under hypoxic, hyperoxic and hypercapnic conditions and compared with those in air. Secondly, in an open-loop experiment the role of the carotid body (CB) chemoreceptors in the control of the responses to altered inspired gas composition and in the cardiac responses to extended and enclosed dives (Stephenson, Butler & Woakes, 1986) was investigated by chronic bilateral denervation of these receptors. 2. Heart rate during submersion was unaffected by inspired gas composition in control (data from intact and sham-operated ducks combined) and CB-denervated ducks, though diving behaviour was significantly modified in both groups of animals in response to altered inspired gas composition. Hypoxia and hypercapnia resulted in an increase in the proportion of total diving time spent breathing at the surface. The main effect of hypoxia (9-10% O2) was to reduce dive duration in control ducks and this effect was almost completely abolished after CB denervation. Hypercapnia (5-6% CO2) reduced dive duration less markedly than hypoxia but it greatly increased the duration of the inter-dive interval, effects which were not significantly influenced by CB denervation. Hyperoxia (40-45% O2) had very little effect on either behaviour or heart rate during diving, although deep body temperature was significantly elevated in this gas mixture during diving activity. There was also a less marked, but nevertheless significant, apparent hyperthermia during diving activity in air on an indoor tank but not on an outdoor pond. Conversely, there was a significant apparent hypothermia during diving activity under hypoxic conditions. 3. The CB chemoreceptors were shown to play a role in cardiac control during diving under certain circumstances. The duration of pre-dive tachycardia was significantly increased in hypoxia and this increase was abolished after CB denervation. The rate of development of bradycardia during extended and enclosed dives was slowed following CB denervation, though the initiation of the responses in extended and enclosed dives and the eventual attainment of sub-resting heart rates in enclosed dives were not prevented, indicating that other, as yet unidentified, sensory inputs are involved in cardiac control under these conditions.
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PMID:Chemoreceptor control of heart rate and behaviour during diving in the tufted duck (Aythya fuligula). 313 33

1. We have studied the effects of intravenous infusions of 0.1 mmol/min KCl (raising arterial potassium from ca. 3.2 to 6.0 mM) on the steady-state responses of carotid body chemoreceptors to end-tidal PCO2 and PO2 in the pentobarbitone-anaesthetized cat. 2. The excitatory effect of these KCl infusions was enhanced by hypoxia and reduced or abolished by hyperoxia. 3. Hypercapnia did not enhance, and usually reduced, excitation by KCl. 4. When similar control discharge frequencies were established by hypoxia or by hypercapnia, a KCl infusion excited the hypoxic discharge by about twice as much as it did the hypercapnic discharge. 5. These observations are not inconsistent with the idea that the mechanism underlying hypoxic excitation of arterial chemoreceptors is one that controls extracellular potassium concentration near the afferent nerve ending. 6. Insofar as potassium-induced excitation of chemoreceptor discharge is abruptly reduced by hyperoxia it behaves like Asmussen and Nielsen's postulated 'anaerobic work substance' and it may therefore contribute to the increased importance of the arterial chemoreflex reported in exercise.
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PMID:Effects of potassium, oxygen and carbon dioxide on the steady-state discharge of cat carotid body chemoreceptors. 313 72

In patients with obstructive apnea, it was hypothesized that stimulation of the ventilatory system by hypercapnia during sleep would increase pharyngeal inspiratory muscle activity and thereby increase upper airway caliber. We predicted that this increase in caliber would decrease the number of apneas and sleep time spent apneic. In contrast, suppression of the ventilatory system activity with hyperoxia was predicted to decrease both inspiratory muscle activity and pharyngeal caliber and thereby increase the number of apneas and apnea time. In all 7 patients with symptomatic obstructive sleep apnea studied, 3 with upper airway narrowing obvious during wakefulness, inhalation of 3 to 6% CO2 preferentially stimulated upper airway inspiratory muscle tonic electrical activity relative to the activity of chest wall inspiratory muscles and diminished periodic breathing. Apnea time decreased from 60 +/- 2% (mean +/- SEM) of sleep time during ambient air inhalation to 12 +/- 3% during CO2 inhalation; 50% O2 had the reverse effect on inspiratory muscle tonic electrical activity and increased apnea time to 75 +/- 5% of sleep time. We conclude that manipulation of inspiratory muscle tonic activity and alteration of the pattern of breathing by CO2 and O2 inhalation lead to significant changes in the pattern of upper airway inspiratory collapse during sleep. We speculate that physiologic variables related to the control of upper airway inspiratory muscle function are instrumental in the pathophysiology of obstructive sleep apnea.
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PMID:Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations. 314 3

In three groups of subjects we studied heart rate (HR) and ventilatory responses to progressive eucapnic hypoxia, steady-state hypercapnia with and without hypoxia, and hyperoxic and hypoxic breathholding (BH). Groups were six subjects about 25 years after bilateral carotid body resection (BR), eight subjects of an equally long period after unilateral resection (UR), and three control subjects similar to the study groups in age and pulmonary function (C). During progressive hypoxia, HR increased more in BR than in UR and C subjects. Ventilatory response was lowest in BR subjects (as expected). Steady-state hypoxic hypercapnia (end-tidal PO2, 60 Torr) depressed HR significantly more in C than in BR and UR subjects. Again, ventilatory response was lower in BR than in C subjects. HR progressively increased during BH initiated in hyperoxia (end-tidal PO2, 200 Torr) and hypoxia (end-tidal PO2, 70 Torr). In the BR group, the HR increment during hypoxia was significantly larger than that during hyperoxia. No such difference was apparent in UR and C groups. Thus, hypoxia with or without hypercapnia tends to accelerate HR in BR subjects whereas either less tachycardia or slowing is seen in UR and C subjects.
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PMID:Bilateral carotid body resection in man enhances hypoxic tachycardia. 324 70

We investigated the mechanism of hyperoxic-induced hypercapnia in 17 stable patients with moderate to severe chronic obstructive pulmonary disease (mean FEV1 = 0.95 L and FVC = 2.43 L). Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia were measured with standard rebreathing techniques. In a randomized, single-blind fashion, we studied the effect of 15 min of hyperoxia or air on transcutaneous carbon dioxide (PtcCO2), CO2 production (VCO2), total minute ventilation (VE), and calculated dead space to tidal volume ratio (VD/VT). With O2, the PtcCO2 (p less than 0.01) and VD/VT (p less than 0.02) increased. The change in PtcCO2 with O2 was not significantly related to the indices of respiratory drive, nor to the baseline PtcCO2 or SaO2, but was related to the FEV1 (p less than 0.05). The O2 caused a slight decrease in mean VE and mean VCO2, but the effects in individual patients were variable. Both substantial increases or decreases in VE (delta VE) occurred, but these were accompanied by changes in VCO2 (delta VCO2) in the same direction. The effect of changes in VE on PaCO2 is shown to be almost completely cancelled by the concomitant changes in VCO2. Thus, the major portion of the change in PaCO2 was due to changes in VD/VT. We conclude that hyperoxic-induced hypercapnia is primarily due to impairment in gas exchange rather than to depression of ventilation. A reduced FEV1 appears to be a significant risk factor, whereas indices of respiratory drive are not likely to play a major role.
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PMID:Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease. 356 37

The carotid chemoreceptor discharge responses to hypoxia and hypercapnia were quantitatively compared between normotensive (NTR) and spontaneously hypertensive rats (SHR). For this purpose we recorded afferent mass discharges from the carotid sinus nerve (CSN) at various levels of end-tidal O2 and CO2 concentrations (FetO2, FetCO2 (%)) in the urethane-anesthetized, vagotomized and artificially ventilated rats. The CSN chemoreceptor discharge was evaluated by subtracting the small activity remaining in acute hyperoxia (chemoreceptor inactivation), which was estimated as baroreceptor in origin, from the large total CSN activity. The CSN chemoreceptor discharges at various levels of FetO2 or FetCO2 were expressed as the percent of control activity measured in normoxic and normocapnic conditions (FetO2, 15-16%; FetCO2, 4.5-5.1%). There was an exponential increase in the CSN chemoreceptor discharge as FetO2 was decreased from hyperoxic to various hypoxic levels (maximally 6%) at a maintained FetCO2 (normocapnia). The relationship between the CSN chemoreceptor discharge and the hypoxic stimulus was quantitatively assessed by the regression analysis using an exponential function. Exponential increases in the CSN chemoreceptor discharge by hypoxia and the parameters in the exponential function reflecting the sensitivity to hypoxia were significantly higher in the SHR than in the NTR, which indicated a high carotid chemoreceptor discharge response to hypoxia in the SHR. The CSN chemoreceptor discharge was increased linearly by increasing the FetCO2 from the normocapnic level up to about 10% at a maintained FetO2 (normoxia). Increases in discharge produced by severe hypercapnia were, however, much smaller than that caused by hypoxia. The slope of the CO2 stimulus-CSN chemoreceptor discharge response line was almost the same in NTR and SHR. The results demonstrated that the responsiveness of rat carotid chemoreceptor to hypoxia is augmented in the SHR. The role of carotid chemoreceptor afferents in ventilatory reflex responses to hypoxia and their alterations in the SHR are discussed.
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PMID:Carotid chemoreceptor discharge responses to hypoxia and hypercapnia in normotensive and spontaneously hypertensive rats. 359 46

The time-dependent effects of hypoxia on the discharge rate carotid chemoreceptors were measured in anesthetized cats. Hypoxic exposure of two different durations were used: a short-term exposure (2-3 h) was used to measure the response of the same carotid chemoreceptors; and a long-term exposure (28 days at inspired PO2 of 70 Torr) to study carotid chemoreceptor properties in one group of cats relative to those of a control group. In the chronically hypoxic and control groups, determinations were made of the 1) steady-state responses to four levels of arterial PO2 (PaO2) at constant levels of arterial PCO2; 2) steady-state responses to acute hypercapnia during hyperoxia; and 3) maximal discharge rates during anoxia. We found that the acute responses of carotid chemoreceptor afferents to a given level of hypoxia (PaO2 = 30-40 Torr) did not significantly change within 2-3 h. After long-term exposure the carotid chemoreceptor responses to hypoxia significantly increased, with no significant changes in the hypercapnic response and in the maximal discharge rate during anoxia. We conclude that isocapnic hypoxia may not elicit a sufficient cellular response within 2-3 h in the cat carotid body to sensitize the O2 responsive mechanism, but hypoxia of longer duration will sensitize such a mechanism, thereby augmenting the chemosensory activity.
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PMID:Time-dependent effect of hypoxia on carotid body chemosensory function. 365 28


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