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

The effect of hyperoxia on phagocytic defenses of neonatal rabbit lung was ascertained by exposure to a fractional inspired O2 concentration of 0.95 + or 0.21 for 48, 96, or 168 h. Intrapulmonary clearance of inhaled staphylococci was reduced by 67 and 74% after 96 and 168 h in hyperoxia (P less than 0.05). Impaired phagocytic killing was not due to diminished bacterial ingestion. Alveolar macrophages (AM) lavaged from pups reared in normoxia had a progressive ability to release superoxide (O-2) and showed increasing cyanide-sensitive O2 consumption during the 1st wk of life. Conversely, AM recovered from litters housed in hyperoxia for 48 h produced 190% more O-2 than normoxic controls (P less than 0.005), but this capacity to generate O-2 fell by 43% after 96 h of exposure (P less than 0.05). After 96 h of hyperoxia, AM had a significant shift toward cyanide-insensitive metabolism compared with normoxic cells (P less than 0.05). Polymorphonuclear leukocytes (PMN) entered the alveoli after 96 h of hyperoxia, and mortality rose abruptly in animals exposed for 168 h (16%) vs. 96 h (3%). Our findings indicate neonatal hyperoxia induces metabolic and bactericidal dysfunction in the primary pulmonary phagocyte, the AM, and this injury is followed by additional lung insult during PMN migration into the airways.
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PMID:Hyperoxia damages phagocytic defenses of neonatal rabbit lung. 355 28

The dependence of the carotid chemoreceptor responses to blood-borne stimuli on the ganglioglomerular nerve (GGN) activity was investigated in cats which were anesthetized, paralyzed and artificially ventilated. The activity of a few carotid chemoreceptor afferents from a slip or from the cut left carotid sinus nerve (CSN) and the activity of a few GGN fibers were recorded. The responses of the same chemoreceptor afferents to steady-state hypoxia at a constant paCO2 and to steady-state hypercapnia during hyperoxia were compared before and after the transection of the ipsilateral ganglioglomerular nerve (IGGN). Similarly the effects of IGGN transection on the responses of the same chemoreceptor afferents to graded doses of intravenous injections of sodium cyanide (20-60 micrograms) and nicotine (20-60 micrograms) at constant blood gas levels were studied. On the average, IGGN transection during normoxia only slightly changed the carotid chemoreceptor activity. Also, it did not significantly change the hypoxic and hypercapnic responses, and those to sodium cyanide and nicotine injections. Thus, the mean carotid chemoreceptor responses to physiological and pharmacological stimuli were largely independent of the GGN. However, certain GGN fibers were strongly stimulated by hypoxia and hypercapnia. Clearly, the total GGN traffic to the carotid body was not sufficiently strong to exert a significant control over the mean carotid chemoreceptor activity.
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PMID:Influence of ganglioglomerular nerve on carotid chemoreceptor activity in the cat. 395 Mar 26

The sensitivity of the brain to cyanide-induced histotoxic hypoxia and the protective effects of known cyanide antagonists, have been assessed in vivo by reflectance spectrophotometry. Cyanide-related changes in cytochrome a,a3 (cytochrome c oxidase) oxidation-reduction (redox) state, tissue hemoglobin saturation, and local blood volume were continuously monitored in cerebral cortex of rats. Noncumulative, dose-dependent inhibition of the in situ mitochondrial respiratory chain was evaluated directly by measuring increases in reduction levels of the terminal oxidase. These transient cytochrome a,a3 reductions were accompanied by increases in regional cerebral hemoglobin saturation and blood volume. Cytochrome redox responses were not altered either in magnitude or kinetics by hyperoxia; however, the cyanide-cytochrome dose-response curve was greatly shifted to the right by pretreatment with sodium nitrite, and the recovery rate of cytochrome a,a3 from cyanide-induced reduction was enhanced fourfold by pretreatment with sodium thiosulfate.
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PMID:Cyanide-induced cytochrome a,a3 oxidation-reduction responses in rat brain in vivo. 631 56

Rats exposed to 10 to 11 per cent oxygen for 7 days develop tolerance to hyperoxia and can survive for prolonged periods in 100 per cent oxygen. This preexposure to hypoxia is associated with a 180 per cent increase in the activity of the mangani superoxide dismutase but no increase in activity of copper-zinc superoxide dismutase, glucose-6-phosphate dehydrogenase, or the mitochondrial enzymes, cytochrome oxidase and succinate cytochrome c reductase. Cyanide-insensitive oxygen uptake is also increased after this exposure to hypoxia suggesting that an enhanced rate of production of partially reduced species of oxygen may occur. Morphometric and morphologic studies of lung structure demonstrate that no substantial change in cell population characteristics occur in the lungs of animals exposed to hypoxia, but there are ultrastructure changes in the cytoplasm of pulmonary capillary endothelial cells consistent with focal hypertrophy and enhanced metabolic activity of these cells.
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PMID:Structural and biochemical adaptive changes in rat lungs after exposure to hypoxia. 682 93

The present study was designed to analyze maturation of the respiratory response to hypoxia and hyperoxia in 41 newborn lambs aged 2-90 days. The O2 respiratory response was tested by progressive isocarbic hypoxia while minute ventilation (VE), tidal volume (VT), respiratory frequency (f), mean inspiratory flow (VT/TI), were measured. The occlusion pressure (P0.1) was also determined as an index of the neuromuscular output of the drive to breathe. The strength of the peripheral chemoreceptors was evaluated by the transient O2 100% inhalation test and by the early change in VE (delta VE) to cyanide (KCN) infusion. In all of the 2-, 10-, 30-, and 90-day groups of lambs, hypoxia induced a significant increase in P0.1 and in delta VE, delta VT, f, and VT/TI. The 2-day-old lambs showed a significantly lower response to hypoxia than did the older groups. Similarly, during the hyperoxia test and KCN infusion. Delta VE was smaller in the 2-day lambs than in the other lambs. We conclude that the postnatal maturation of the ventilatory response to O2 occurs in the first 10 days of life in newborn lambs and it is largely due to an increase in sensitivity of the O2 chemoreceptors.
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PMID:Postnatal maturation of the respiratory response to O2 in awake newborn lambs. 706 Dec 96

Because hyperoxia induces early injury to lung endothelial cells and since tolerance to hyperoxia is correlated with increased lung antioxidant enzyme activity, we measured superoxide dismutase, catalase and glutathione peroxidase in both fresh isolates and primary cultures of endothelial cells from pig pulmonary artery and aorta. Cultured endothelial cells were studied at confluency and up to 5 days thereafter under control or hyperoxic conditions. In both types of confluent cell, total and cyanide-insensitive superoxide dismutase increased when compared to fresh cells. The most conspicuous postconfluency change in both types of endothelial cell was a marked decrease in glutathione peroxidase, which could be prevented by the addition of selenomethionine to culture media. A 5-day exposure to hyperoxia resulted in a 2-fold increase in cyanide-insensitive superoxide dismutase in both aortic and pulmonary artery endothelial cells. In view of a similar decrease in DNA in both types of cells despite some differences in enzyme levels, oxygen cytotoxicity could not be related to a particular antioxidant enzyme profile.
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PMID:Effects of culture conditions and hyperoxia on antioxidant enzymes in pig pulmonary artery and aortic endothelium. 711 52

Because fetal rat lungs have lower baseline levels of both surfactant and antioxidant enzymes than full-term newborn rats, we questioned whether prematurely delivered rats might be more susceptible to O2 toxicity than those born at term. In the present studies, prematurely delivered rats (gestational d 21 of 22) and full-term rat pups were simultaneously put in > 95% O2 after birth. Surprisingly, we found that the preterm rats were not more susceptible to O2-induced lung damage and lethality than full-term newborns, but, in fact, the composite percentage of survival was even greater in the preterm pups from 7 to 9 d in hyperoxia and were similar thereafter up to 14 d in high O2. In addition, the preterm rats showed significantly decreased lung wet/dry weight ratios and consistently less severe pathologic evidence of pulmonary edema compared with term rats at 6 and 8 d of O2 exposure. The premature pups demonstrated the capability of inducing pulmonary antioxidant enzyme responses to hyperoxia by 3 d, and had significantly elevated copper-zinc superoxide dismutase, catalase, and glutathione peroxidase activities (and lung surfactant contents) at 6 d of O2 exposure compared with the term rats in O2. The rates of lung total O2 consumption and cyanide-resistant O2 consumption at d 6 in hyperoxia were not different for preterm versus term pups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative responses of premature versus full-term newborn rats to prolonged hyperoxia. 816 59

We previously demonstrated that chronic normobaric hyperoxia (NH) for 60-67 h attenuated the carotid chemosensory response to hypoxia, probably initiated by the generation of reactive oxygen species (ROS). Since biological systems are affected by oxygen in a dose-dependent manner, we hypothesized that hyperbaric oxygenation (HBO) would affect the cellular mechanisms of oxygen chemoreception in a shorter time. To test the hypothesis, we studied the effects of oxygen at 5 atmospheres absolute (ATA) on cats (n = 7) carotid body ultrastructure and chemosensory responses to hypoxia, hypercapnia, and to bolus injections of cyanide, nicotine and dopamine. Four control cats breathed room air at 1 ATA. At the termination of the experiments, carotid bodies from 4 cats in each group were fixed and prepared for electron microscopy and morphometry. On the average, HBO diminished the chemosensory responsiveness to hypoxia (P < 0.01, unpaired t-test) within about 2 h, supporting the hypothesis. The responses to hypercapnia or bolus injections of cyanide, nicotine and dopamine were normal. HBO did not diminish the distribution of the dense-cored vesicles but significantly increased the mean volume-density of mitochondria and decreased the cristated area per mitochondrion in the glomus cells. The latter suggests a link between oxidative metabolism and chemosensing, and the former excludes availability of neurotransmitters being the cause of the blunted chemosensory response to hypoxia.
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PMID:Hyperbaric oxygenation alters carotid body ultrastructure and function. 832 90

1. We sought to determine whether hypoxic stimulation of neurons of the rostral ventrolateral reticular nucleus (RVL) would elevate regional cerebral blood flow (rCBF) in anaesthetized paralysed rats. 2. Microinjection of sodium cyanide (NaCN; 150-450 pmol) into the RVL rapidly (within 1-2 s), transiently, dose-dependently and site-specifically elevated rCBF1 measured by laser Doppler flowmetry, by 61.3 +/- 22.1% (P < 0.01), increased arterial pressure (AP; +30 +/- 8 mmHg; P < 0.01)1 and triggered a synchronized 6 Hz rhythm of EEG activity. 3. Following cervical spinal cord transection, NaCN and also dinitrophenol (DNP) significantly (P < 0.05) elevated rCBF and synchronized the EEG but did not elevate AP; the response to NaCN was attenuated by hyperoxia and deepening of anaesthesia. 4. Electrical stimulation of NaCN-sensitive sites in the RVL in spinalized rats increased rCBF measured autoradiographically with 14C iodoantipyrine (Kety method) in the mid-line thalamus (by 182.3 +/- 17.2%; P < 0.05) and cerebral cortex (by 172.6 +/- 15.6%; P < 0.05) regions, respectively, directly or indirectly innervated by RVL neurons, and in the remainder of the brain. In contrast regional cerebral glucose utilization (rCGU), measured autoradiographically with 14C-2-deoxyglucose (Sokoloff method), was increased in proportion to rCBF in the mid-line thalamus (165.6 +/- 17.8%, P < 0.05) but was unchanged in the cortex. 5. Bilateral electrolytic lesions of NaCN sensitive sites of RVL, while not altering resting rCBF or the elevation elicited by hypercarbia (arterial CO2 pressure, Pa,CO2, approximately 69 mmHg), reduced the vasodilatation elicited by normocapnic hypoxaemia (arterial O2 pressure, Pa,O2, approximately 27 mmHg) by 67% (P < 0.01) and flattened the slope of the Pa,O2-rCBF response curve. 6. We conclude that the elevation of rCBF produced in the cerebral cortex by hypoxaemia is in large measure neurogenic, mediated trans-synaptically over intrinsic neuronal pathways, and initiated by excitation of oxygen sensitive neurons in the RVL.
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PMID:Contribution of oxygen-sensitive neurons of the rostral ventrolateral medulla to hypoxic cerebral vasodilatation in the rat. 886 63

1. The role of endogenous nitric oxide (NO) generated by neuronal nitric oxide synthase (NOS-1) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-1. 2. Experiments were performed on awake and anaesthetized mutant and wild-type control mice. Respiratory responses to varying levels of inspired oxygen (100, 21 and 12% O2) and carbon dioxide (3 and 5% CO2 balanced oxygen) were analysed. In awake animals, respiration was monitored by body plethysmograph along with oxygen consumption (VO2), CO2 production (VCO2) and body temperature. In anaesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Cyclic 3',5'-guanosine monophosphate (cGMP) levels in the brainstem were analysed by radioimmunoassay as an index of nitric oxide generation. 3. Unanaesthetized mutant mice exhibited greater respiratory responses during 21 and 12% O2 than the wild-type controls. Respiratory responses were associated with significant decreases in oxygen consumption in both groups of mice, and the magnitude of change was greater in mutant than wild-type mice. Changes in CO2 production and body temperature, however, were comparable between both groups of mice. 4. Similar augmentation of respiratory responses during hypoxia was also observed in anaesthetized mutant mice. In addition, five of the fourteen mutant mice displayed periodic oscillations in respiration (brief episodes of increases in respiratory rate and tidal phrenic nerve activity) while breathing 21 and 12% O2, but not during 100% O2. The time interval between the episodes decreased by reducing inspired oxygen from 21 to 12% O2. 5. Changes in arterial blood pressure and arterial blood gases were comparable at any given level of inspired oxygen between both groups of mice, indicating that changes in these variables do not account for the differences in the response to hypoxia. 6. Respiratory responses to brief hyperoxia (Dejours test) and to cyanide, a potent chemoreceptor stimulant, were more pronounced in mutant mice, suggesting augmented peripheral chemoreceptor sensitivity. 7. cGMP levels were elevated in the brainstem during 21 and 12% O2 in wild-type but not in mutant mice, indicating decreased formation of nitric oxide in mutant mice. 8. The magnitude of respiratory responses to hypercapnia (3 and 5% CO2 balanced oxygen) was comparable in both groups of mice in the awake and anaesthetized conditions. 9. These observations suggest that the hypoxic responses were selectively augmented in mutant mice deficient in NOS-1. Peripheral as well as central mechanisms contributed to the altered responses to hypoxia. These results support the idea that nitric oxide generated by NOS-1 is an important physiological modulator of respiration during hypoxia.
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PMID:Altered respiratory responses to hypoxia in mutant mice deficient in neuronal nitric oxide synthase. 967 81


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