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

Bronchial artery blood flow index (BFI) was measured in an unanesthetized sheep model using a chronically implanted ultrasonic flow probe. The bronchial circulation was monitored during changes of the concentrations of oxygen and carbon dioxide in inhaled air. Control BFI was 15.9 +/- 3.8 ml/min/m2 during normoxic breathing with 0% CO2 (n = 6) and 18.0 +/- 1.6 ml/min/m2 while breathing 28% O2 and 0% carbon dioxide (n = 6). Hypoxia (FIO2 = 0.10) significantly increased BFI to 25.8 +/- 4.9 ml/min/m2 with a decrease in the bronchovascular resistance index (BVRI) from a baseline of 7.85 +/- 1.73 to 4.75 +/- 0.86 mm Hg/(ml/min)/m2. Hyperoxia (FIO2 = 1.0) raised BFI to 30.5 +/- 10.1 ml/min/m2 without a significant decrease in BVRI. Changing the inhaled carbon dioxide concentration from 0 to 10% resulted in a significant increase in BFI from 18.0 +/- 1.6 to 43.6 +/- 10.3 ml/min/m2 and a decrease in BVRI from 5.56 +/- 0.44 to 4.63 +/- 2.18 mmHg/(ml/min)/m2 (not significant). The change in BFI varies directly with lymph flow for hypoxia and hypercarbia. This is consistent with changes in cardiac index, indicating probable changes in surface area being perfused in the lung. Changes in BFI with hyperoxia did not follow changes in systemic vascular resistance or cardiac index. Similarly, lymph flow elevation did not occur during hyperoxia. These data suggest that BFI changes with hyperoxia are not related to changes in total systemic vascular resistance, or cardiac index, and a different mechanism may control bronchovascular flow for this condition.
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PMID:Bronchial blood flow during changes in inhaled oxygen and carbon dioxide concentrations in conscious sheep. 158 3

Ventilatory acclimatization (VA) to hypoxia alters cerebrovascular responses to arterial blood gas perturbations. For example, after VA, cerebral blood flow (CBF) is elevated, at a given arterial CO2 tension (PaCO2), compared to CBF before VA. This experiment examined the effects of VA to 72 h of normobaric hypoxia [arterial O2 tension (PaO2) approx. 40 mmHg, O2 saturation in arterial blood approx. 50%] on total and regional cerebrovascular resistance (CVR and rCVR) and cerebral O2 extraction fraction (OEF) in 32 conscious sheep. Four different O2-CO2 gas combinations were sequentially administered to each sheep before and after VA. CVR and rCVR were calculated from CBF (radiolabeled microspheres) and arterial and cerebral downstream pressures; OEF was calculated from arterial and cerebral venous O2 contents. After VA, during hyperoxia, CVR and rCVR tended to be lower during both hypocapnia and hypercapnia. During hypoxia, although CVR and rCVR were slightly less during hypocapnia, CVR and rCVR during hypercapnia were surprisingly increased. The post-VA increases in mean CVR and mean rCVR during hypoxic gas combinations differed from the post-VA decreases during hyperoxic gas combinations (0.04 less than or equal to P less than or equal to 0.11). In contrast, although VA decreased OEF during three of four gas combinations (P less than or equal to 0.003), there was a greater mean post-VA decrease in OEF during hypercapnic gas combinations than during hypocapnic gas combinations (P = 0.025); decreases in OEF were correlated with decreases in cerebral O2 consumption. The post-VA CVR responses may reflect altered neurocirculatory control by the arterial chemoreflex; the OEF responses suggest relative cerebral hyperperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acclimatization to hypoxia alters cerebral convective and diffusive O2 delivery. 161 32

A new in vivo model for studying brain metabolic and haemodynamic oscillatory phenomena during ischaemia is described. In this model acute or chronic occlusion of one or two carotid arteries in the rat is performed. Due to the partial ischaemia developed, oscillations in the level of intramitochondrial pyridine nucleotides (NADH) as well as flavoproteins (Fp) were recorded from the brain by monitoring the fluorescence of these respiratory chain components. The two fluorescent signals (NADH and Fp) were measured by using the time sharing or DC fluorometer/reflectometer. The changes in the reflected light at the excitation wavelengths (366 and 450 nm) were recorded simultaneously. Bilateral carotid artery occlusion induced immediate oscillations (6-9 waves per min) in the mitochondrial redox state as well as in tissue blood volume in both hemispheres. To verify the accuracy of the NADH monitoring system, including the correction technique for haemodynamic and other artifacts, we used the intracarotid artery saline bolus injection approach. The results could be summarized as follows: (1) unilateral carotid artery occlusion resulted in delayed development of oscillations, particularly in the ipsilateral hemisphere; (2) the oscillation phenomenon was reversible if recirculation restarted within 5 min. Occlusion for more than 30 min resulted in irreversible oscillations; (3) the oscillation appearances and intensities were affected by various physiological conditions. Vasoconstriction, induced by hyperoxia, stimulated the oscillations while vasodilation, induced by hypercapnia, depressed them. Anoxia, hypoxia and spreading depression (SD) abolished the oscillations. Glucose injection was not effective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oscillations of cortical oxidative metabolism and microcirculation in the ischaemic brain. 167 46

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

Carotid body chemosensory response to hypoxia is attenuated as a result of prolonged normobaric hyperoxia (NH) in the cat. The effect of NH is likely to be due to high cellular PO2 and O2-related free radicals. Accordingly, the effect would be less if O2 delivery to the chemoreceptor tissue could be compromised. The aortic bodies, which appear to have less of a circulatory O2 delivery, as suggested by their vigorous responses to a slight compromise of O2 flow compared with those of the carotid body, could provide a suitable testing material for the hypothesis. We tested the hypothesis by studying both aortic and carotid body chemoreceptors in the same cats (n = 6) which were exposed to nearly 100% O2 for about 60 h. These chemoreceptor organs were also studied in 6 control cats which were maintained in room air at sea-level. The cats were anesthetized and their carotid and aortic chemosensory fibers were identified by the usual procedure, and their responses to hypoxia and hypercapnia and to bolus injections (i.v.) of cyanide and nicotine were measured. In the NH cats, the carotid but not aortic chemosensory responses to hypoxia and cyanide were attenuated and to hypercapnia (both onset and steady state) augmented. The aortic chemoreceptors were stimulated by hypoxia, hypercapnia, cyanide and nicotine both in the NH and the control cats similarly. The results support the hypothesis that it is presumably a higher tissue blood flow and hence a higher concentration of O2-related free radicals which ultimately led to the specific attenuation of O2 chemoreception in the carotid body.
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PMID:Aortic and carotid body chemoreception in prolonged hyperoxia in the cat. 178 Jun 2

Reactive astrocytosis is a process by which astrocytes respond to brain injury by showing an increase in glial fibrillary acidic protein (GFAP) staining that is associated with hypertrophy and/or hyperplasia of these cells. Because spreading depression (SD) is a perturbation uncomplicated by neuronal necrosis and is seen in both in vivo and in vitro neural structures, we sought to determine whether SD was a sufficient stimulus to induce enhanced GFAP staining. SD was elicited in anesthetized rats by application of KCI to parietal cortex for 3 hr; equimolar NaCI was applied to contralateral cortex. SD was confirmed by monitoring DC potentials in frontal neocortices. Animals were allowed to recover for 48 hr, and their brains were processed for semiquantitative and computer-based analyses of GFAP staining intensity. Experimental GFAP staining was referenced to contralateral control levels. Neocortical SD (13-37 SDs) was associated with a significant (p less than 10(-4)), 43% increase in GFAP staining intensity, which remained statistically greater than normal for more than 2 weeks. If SD was inhibited by combined hyperoxia and hypercarbia, only a nonsignificant (p greater than 0.20), 7% increase in GFAP staining was seen. Thus, SD may be a useful physiologic process with which to begin to explore the cellular mechanisms that induce the transformation of normal astrocytes into reactive species.
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PMID:Spreading depression increases immunohistochemical staining of glial fibrillary acidic protein. 190 91

This study assessed the effects of experimentally elevated plasma catecholamine levels on gill ventilation in rainbow trout (Oncorhyncus mykiss) exposed to various external ventilatory stimulants. Trout were exposed to hypoxia (water PO2 (PwO2) = 90 Torr) or hypercapnia (water PCO2 (PwCO2) = 4.5 Torr) for 30 min. These conditions caused gill ventilation volume (Vw) to increase by 2.3- and 1.5-fold, respectively, but did not stimulate release of catecholamines into the blood. While the stimulus (hypoxia or hypercapnia) was maintained, fish were given a bolus injection (0.3 ml), followed by intra-arterial infusion (0.6 ml.h-1), of a catecholamine mixture (2 x 10(-5) mol.l-1 adrenaline + 5 x 10(-6) mol.l-1 noradrenaline) to mimic the physiological concentrations and ratios of these catecholamines observed under more severe hypoxic or hypercapnic conditions. In hypoxic fish, this treatment caused a significant, but transient (5 min) depression of ventilation while during hypercapnia, the administration of exogenous catecholamines caused a more prolonged hypoventilatory response. These hypoventilatory responses occurred despite a catecholamine-induced blood acidosis (a potential ventilatory stimulant). To assess the importance of initial Vw and/or blood respiratory status on catecholamine-mediated hypoventilation, these experiments were repeated under hyperoxic (PwO2 = 640 Torr) hyperoxic hypercapnic (PwO2 = 510 Torr, PwCO2 = 4.8 Torr) or normoxic (PwO2 = 151 Torr) conditions in which Vw was either depressed (3.9-fold during hyperoxia) or unaffected. Intra-arterial infusion of catecholamines did not affect Vw under either of these experimental conditions. These results demonstrate that during a respiratory challenge, such as hypoxia or hypercapnia, physiologically relevant levels of circulating catecholamines can depress Vw and therefore do not support a stimulatory role for circulating catecholamines in the control of ventilation in fish.
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PMID:The effects of catecholamines on ventilation in rainbow trout during hypoxia or hypercapnia. 190 29

We investigated the mechanisms responsible for oxygen-induced hypercarbia in ventilator-dependent patients with advanced chronic obstructive pulmonary disease (COPD). To quantitate the effects of oxygen (O2) on respiratory drive, we determined the CO2 recruitment threshold (PCO2 RT) in 10 mechanically ventilated patients under normoxic (PaO2 = 67 +/- 7 mm Hg) and hyperoxic (PaO2 = 370 +/- 67 mm Hg) conditions. PCO2 RT is a measure of the CO2 responsiveness of the mechanically unloaded respiratory system and, as such, is independent of mechanical impedance and respiratory muscle strength. After O2 supplementation, PCO2 RT increased from 42 +/- 6 to 45 +/- 6 mm Hg (p less than or equal to 0.05), indicating a suppression of so-called hypoxic respiratory drive. The effect of hyperoxia on the dead space to tidal volume ratio (VD/VT) and CO2 elimination (VCO2) was studied in 6 patients. Measurements were made at identical ventilator settings, thus eliminating breathing pattern- and respiratory work-related effects on these variables. VD/VT rose from 0.49 +/- 0.09 to 0.55 +/- 0.06 (p less than or equal to 0.05), but VCO2 remained constant at 0.21 L/min. We discuss why measuring O2-induced changes in minute ventilation, VCO2, PaO2, and VD/VT in spontaneously breathing patients is insufficient to distinguish between gas exchange- and respiratory drive-related mechanisms for hypercarbia. Based on the O2-induced increase in PCO2 RT, we conclude that so-called suppression of hypoxic drive plays an important role in the pathogenesis of this disorder.
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PMID:Oxygen-induced hypercarbia in obstructive pulmonary disease. 190 46

Sleep apnea and other respiratory diseases produce hypoxemia and hypercapnia, factors that adversely affect skeletal muscle performance. To examine the effects of these chemical alterations on force production by an upper airway dilator muscle, the contractile and endurance characteristics of the geniohyoid muscle were examined in situ during severe hypoxia (arterial PO2 less than 40 Torr), mild hypoxia (PO2 45-65 Torr), and hypercapnia (PCO2 55-80 Torr) and compared with hyperoxic-normocapnic conditions in anesthetized cats. Muscles were studied at optimal length, and contractile force was assessed in response to supramaximal electrical stimulation of the hypoglossal nerve (n = 7 cats) or geniohyoid muscle (n = 2 cats). There were no significant changes in the twitch kinetics or force-frequency curve of the geniohyoid muscle during hypoxia or hypercapnia. However, the endurance of the geniohyoid, as reflected in the fatigue index (ratio of force at 2 min to initial force in response to 40-Hz stimulation at a duty cycle 0.33), was significantly reduced by severe hypoxia but not by hypercapnia or mild hypoxia. In addition, the downward shift in the force-frequency curve after the repetitive stimulation protocol was greater during hypoxia than hyperoxia, especially at higher frequencies. In conclusion, the ability of the geniohyoid muscle to maintain force output during high levels of activation is adversely affected by severe hypoxia but not mild hypoxia or hypercapnia. However, none of these chemical perturbations affected muscle contractility acutely.
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PMID:Effects of hypoxia and hypercapnia on geniohyoid contractility and endurance. 193 46

Chemical control of respiration in cats after chronic normobaric hyperoxia (NH; inhalation of 100% O2 for 60-67 h) was compared with that of control rats, anesthetized with pentobarbital. After chronic hyperoxia, induction of moderate hypoxia (PaO2 = 50-60 Torr) increased inspiratory time (TI) often without increasing tidal volume (VT). More intense hypoxia (PaO2 = 40-50 Torr) depressed tidal volume and further increased TI, diminishing the respiratory drive (VT/TI). Hypercapnia, on the other hand, increased tidal volume and shortened respiratory cycle time; but these responses were subnormal. The normal stimulatory effects of intravenous nicotine and inhibitory effect of dopamine on carotid chemo-receptor activity and ventilation were preserved in the NH cats. Cyanide, however, did not stimulate carotid chemoreceptor activity and ventilation. Thus, the changes in the carotid and aortic chemosensory activities elicited appropriate reflex ventilation responses, indicating that the central component of the chemoreflex was not impaired. The ventilatory depression during hypoxia despite an active chemosensory input is consistent with the lack of carotid chemosensory response to and a central depressant effect of hypoxia in the NH cats, and was presumably associated in part with an increased responsiveness of airway reflexes. We conclude that chronic hyperoxia selectively attenuated carotid chemosensory and chemoreflex responses to hypoxia.
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PMID:Chemical respiratory control in chronically hyperoxic cats. 207 96


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