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

Blood flow to subunits of the lung was studied in the duck by use of radioactive microspheres. In spontaneously breathing, unanesthetized animals (series I) neopulmo was slightly better perfused than the average lung and along the paleopulmonic parabronchi, blood flow was found to decrease in the direction of ventilatory gas flow and thus of decreasing PO2 and increasing PCO2 in lung gas. The effects of respiratory gases on regional lung perfusion were investigated in unidirectionally ventilated animals (series II) in which gas mixtures offered to both lungs could be controlled independently. Local hypoxia resulted in reduction of local blood flow, whereas effects from hyperoxia or CO2 could not be substantiated. Reversal of the direction of unidirectional ventilatory flow (series III), and thus reversal of the profiles of respired gas concentrations along the parabronchi, suggest that the inhomogeneity in blood flow observed in spontaneously breathing animals of series I can only in part be explained as an acute adjustment to the local hypoxia. Calculations show that this inhomogeneity of blood flow constitutes an only minor impairment of the overall gas exchange efficacy of the parabronchial lung.
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PMID:Blood flow distribution in the duck lung and its control by respiratory gases. 62 69

Dopamine is present in the carotid body and has been postulated to be an inhibitory neurotransmitter. The purpose of this study was to determine the effects of dopamine on ventilation in man and to examine its mechanism of action. Dopamine (0.5-10 mug/kg per min) was infused in eight normal men at different levels of arterial chemoreceptor activity, produced by varying the inspired Po(2). During normoxia dopamine produced a small decrease in minute ventilation (Ve) and an increase in arterial Pco(2). When arterial chemoreceptors were stimulated by hypoxia, infusion of dopamine produced a marked initial depression of Ve followed by a sustained although less pronounced decrease in Ve. An increase in Pa(co) (2) and a decrease in Pao(2) were also observed. When arterial chemoreceptor activity was suppressed by hyperoxia, infusion of dopamine did not affect ventilation. Subjects also breathed a hypercarbic, hyperoxic gas mixture. The hypercarbia produces hyperventilation by stimulating central chemoreceptors, whereas the hyperoxia suppresses peripheral chemoreceptors. Dopamine did not alter ventilation while the subjects were breathing this gas mixture. These studies suggest that dopamine suppresses ventilation in man through an action on the arterial chemoreceptor reflex. These findings support the hypothesis that dopamine is an inhibitory neurotransmitter in the carotid body, and that release of dopamine may modulate the sensitivity of peripheral arterial chemoreceptors.
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PMID:Depression of ventilation by dopamine in man. Evidence for an effect on the chemoreceptor reflex. 64 Nov 49

Neonatal rats (4--7 days old) and adult rats (approximately 80 days old) were continuously exposed to either 96--98% oxygen or air. Examination of the lungs of neonatal rats, who survived 5 days of oxygen exposure with no evidence of respiratory distress, showed significant increases in the pulmonary superoxide dismutase (SOD) activity (peak value: 144% of air-exposed controls), glutathione peroxidase (GP) activity (126%), glutathione reductase (GR) activity (122%), reduced glutathione (GSH) level (176%), and glucose-6-phosphate dehydrogenase activity (151%). Adult rats, most of whom succumbed within 3 days of oxygen exposure, did not show any significant increase in the activities of pulmonary SOD, GP, GR, and the level of GSH as compared to the air-exposed adult animals. Glucose-6-phosphate dehydrogenase was significantly elevated in the 72-hr oxygen-exposed adult rats. It is concluded that increases in the lung complement of SOD, GR, GP, and GSH in the neonatal rat during oxygen challenge may provide the mechanism(s) for their increased tolerance to hyperoxia-induced lung injury as compared to the adults.
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PMID:Oxygen toxicity: comparison of lung biochemical responses in neonatal and adult rats. 64 79

The results of the studies on the gas composition and acid-base equilibrium of the blood in patients operated upon under epidural anesthesia have proved the rise of venous hyperoxia and the drop of the gas utilization percentage both in anesthetized and non-anesthetized regions. At the level of the whole organism, however, no essential changes of oxygen metabolism are noted.
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PMID:[Gas composition and acid-base equilibrium of blood of patients operated on under conditions of epidural anesthesia]. 64 85

Resting respiratory parameters and respiratory responses to acute changes in end-tidal O2 and CO2 pressure (PETO2 and PETCO2) were investigated in Peru in 23 newborn and 4 older infants at 3.850 m and in 13 newborns at 800 m. The study was done with the subjects asleep in a thermoneutral environment. The transient increase in ventilation in both high- and low-altitude newborns was followed by a decrease in response to acute hypoxia. During hyperoxia the two groups showed a slight but not clearly significant decrease in ventilation, whereas older high-altitude infants showed a sustained decrease. All subjects showed a prompt and clear response to CO2 inhalation during hyperoxia. We conclude that ventilatory peripheral chemoreflex is not fully developed in newborns regardless of altitude. The weak link in the reflex arc may reside in the afferent component because CO2 response was not impaired. Since hypoxic response became persistent in older infants its blunting in adult high-altitude natives is not a legacy of newborns.
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PMID:Regulation of breathing in newborns at high altitude. 64 68

Normal and iron-deficient rats were exposed to 90% O2 at 760 Torr for 24 or 48 h. Erythrocyte response to hyperoxia was monitored by potassium (rubidium) influx studies, by storage stress, and by ultrastructural studies. Normal rat erythrocytes exhibited morphological changes and decrease of ouabain-sensitive potassium influx compared to unexposed controls. Both components of erythrocyte potassium influx were affected by iron deficiency. Erythrocytes from unexposed iron-deficient rats showed a 50% increase in ouabain-sensitive potassium influx compared to controls. Iron-deficient rats exposed to hyperoxia for 24 or 48 h, had erythrocytes with morphological changes. Erythrocytes of iron-deficient rats exposed for 24 h showed no influx change; those exposed for 48 h showed a decrease of ouabain-sensitive influx compared to erythrocytes of controls.
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PMID:Response of the iron-deficient erythrocyte in the rat to hyperoxia. 64 73

Ventilation and Pa(CO2), were measured in six subjects after 10-12 min of breathing 1-2% CO2 during hyperoxia and hypoxia. These inspired CO2 concentrations were achieved in two ways: by enriching the inspirate with CO2 and by having the subjects breathe through dead spaces of 100-400 cm3. Breathing through dead space gave the same results as CO2 enrichment of the inspirate when the effect of the dead spaces on mean inspired CO2 was allowed for. During hyperoxia all subjects demonstrated isocapni hyperpnea in response to mean inspired CO2 concentrations of 1%; ventilation increased without change in PA(CO2). When mean inspired CO2 concentration approximated 1.5% two subjects showed isocapnic hyperpnea, and one subject demonstrated isocapnic hyperpnea in response to mean inspired CO2 concentrations of 2%. The increase in PA(CO2) observed in each subject in response to 2% CO2 in O2 correlated negatively with the slope of that subject's rebreathing CO2 response curve. Hypoxia (PA(O2Y = 45-50 mm Hg) depressed the response to 1% CO2 in that, while hypoxic, no subject showed isocapnic hyperpnea in response to 1% CO2. The isocapnic hyperpnea we observed was chiefly due to increased tidal volume, and was therefore not analogous to the isocapnic hyperpnea observed by others in dogs in response to increases of CO2 in lung gas. When low levels of CO2 produced an increase in PA(CO2) the associated change in ventilation (delta Ve/delta PA(CO2)was much less than that observed while rebreathing 7% CO2. Isocapnic hyperpnea in response to low levels of CO2 is common among normal individuals, and is depressed by hypoxia; the stimulus responsible for this response is unknown.
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PMID:Ventilatory response to low levels of CO2. 66 46

Effect of hypoxia and hyperoxia on some indexes of energy metabolism was studied in the brain of intact rats and those with preliminarily administered hydrocortisone. So hypoxia (8 and 5.5% of oxygen in the medium) increases considerably the lactate and pyruvate content and has no effect on the oxidation and photophosphorylation in the brain mitochondria. The hyperoxic medium (1 at. abs. for 3-5h) inhibits consumption of oxygen and inorganic phosphate by the brain mitochondria, does not effect the lactate content and lowers the pyruvate level. The preliminary administration of hydrocortisone (1 mg per 100 g) under conditions of hypoxia and hyperoxia leads to the further intensification of the glycolysis independently of the initial level of the process. At the same time hormone administration favours normalization of the oxidative processes in the brain tissue under conditions of hyperoxia.
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PMID:[Characteristics of the intensity of glycolytic and oxidative processes in rat brain tissue under hypoxia and hyperoxia]. 66 25

Activity of glutaminase (both phosphate-dependent and phosphate-independent forms of the enzyme) as well as glutamate decarboxylase activity were studied in hyperoxia (6 ati) and under conditions of protection by means of arginine from the effect of hyperoxia. In hyperoxia activity of phosphate-dependent and phosphate-independent forms of glutaminase was decreased by 45% and 51%, respectively. At the same time, glutamate decarboxylase activity was decreased by 32%. Arginine showed a protective effect, delaying the time of oxygen convulsions onset by 2.5-fold. The low activities of glutaminases were maintained but the glutamate decarboxylase activity was increased and even exceeded the control level by 29%. A mechanism of the protective effect of arginine is discussed.
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PMID:[Protective effect of arginine in hyperoxia. Activity of cerebral glutaminase and glutamate decarboxylase]. 66 82

The breathing patterns after voluntary hyperventilation were determined in 14 healthy young subjects under four different conditions: (1) normoxia, (2) hyperoxia, (3) hypoxia, and (4) sudden administration of oxygen against a background of hypoxia to evaluate the effect of hypoxia on the pattern of the posthyperventilation breathing. Under hypoxia the ventilation in the immediate posthyperventilation period was depressed although no decreased ventilation was observed under hyperoxia or normoxia in this period. Sudden administration of oxygen depressed further the decreased ventilation in the posthyperventilation period.
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PMID:The effect of hypoxia on posthyperventilation breathing. 66 17


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