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

Central respiratory drive responding to pH changes was eliminated by bilateral coagulation or cold block of area S (intermediate area) on the ventral medullary surface in 7 anaesthetized cats. Arterial pH, PCO2, and PO2 (4 cats) and the respiratory response to hypoxia and hypercapnia (6 cats) were observed before and after coagulation. After coagulation in hyperoxia the arterial pH dropped from 7.30 to 7.09, the arterial PCO2 was elevated from 4.80 kPa to 8.17 kPa (6 cats). Ventilation increased by 477 ml at a PCO2a of 6.58 kPa when PO2a was reduced from 39.5 kPa to 8.5 kPa before coagulation, after coagulation ventilation increased by 241 ml (4 cats). The peripheral chemoreceptors guaranteed spontaneous breathing even in hyperoxia. The data reveal that the loss of respiratory homeostasis by elimination of the S areas is due to the loss of central chemosensitive drive with concomitant reduction of peripheral chemoreceptor effect.
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PMID:Respiratory response to hypoxia and hypercapnia after elimination of central chemosensitivity. 4 38

To investigate the influence of variations in arterial oxygen tensions (PaO2), arterial carbon dioxide tensions (PaCO2), and arterial pH on long bone medullary pressures, seven anaesthetized dogs were investigated. Comparing the control medullary pressures, i.e. the mean medullary pressures obtained at the normal range of PaO2 (75--110 mmHg) with the mean medullary pressures corresponding to the range of PaO2 of less than 75 mmHg, statistically significant (P less than 0.05) decreases were seen in both epiphyseal, metaphyseal and diaphyseal medullary pressures, from 27.6 +/- 5.0 to 15.5 +/- 3.6 mmHg, from 23.5 +/- 2.9 to 13.9 +/- 2.3 mmHg and from 27.7 +/- 3.9 to 18.3 +/- 2.5 mmHg (all mean values +/- s.e. mean), respectively. Hyperoxia, hypocapnia, hypercapnia or metabolic acidosis had no effect on medullary pressures in any of the regions studied.
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PMID:Observations on long bone medullary pressures in relation to arterial PO2, PCO2 and pH in the anaesthetized dog. 4 59

Pulmonary ventilation (V) and alveolar gas composition (PACO2, PAO2) were studied in 12 healthy men who performed gradual muscular work under conditions of controlled hypercapnia, hypoxia, hyperoxia or their combinations. The respiratory response was estimated by absolute values of ventilation at the given PACO2 value and by its rise by 1 mm Hg of increased PACO2 (delta V/delta PACO2) under rest and under transitional and steady-state exercise. The exercise on-switch was accompanied by displacement to the top and an increased slope of the response curve (delta V/delta PACO2) not related to the work load. These changes suggest multiplicative interaction of the neurogenic and hypercapnic drives in the load switch-on. During steady-state exercise an important role of the hypoxic drive was revealed: hypoxemia induced a shift of the delta V/delta PACO2 response curve to a higher level, especially with the great work load. Thus the positive interaction between the hypercapnic and hypoxic respiratory drive augments with muscular exercise.
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PMID:[Relationship between hypercapnic and hypoxic stimuli of respiration during muscular activity]. 45 11

This study was undertaken to compare phrenic motoneuron responses to hypercapnia and isocapnic hypoxia. Efferent activity of single phrenic nerve fibers was recorded with that of the contralateral phrenic nerve in decerebrate cats which were vagotomized, paralyzed, and artificially ventilated. At normocapnia in hyperoxia, single phrenic fibers were distributed into approximately equal "early" and "late" populations according to their onset of activity relative to the period of the phrenic burst. Elevations of PACO2 or diminutions of PAO2 resulted in progressive increases in the number of spikes per respiratory cycle and decreases in the modal interspike interval for both early and late units. Moreover, either stimulus caused an onset of late unit activity at progressively earlier portions of inspiration. At equivalent levels of peak integrated phrenic discharge achieved at normocapnia or hypercapnia as compared to normoxia or hypoxia, there were no differences in activity patterns for either early or late units. It is concluded that hypoxia-induced alterations in the activity of single phrenic motoneurons are identical to those changes resulting from hypercapnia.
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PMID:Comparison of phrenic motoneuron responses to hypercapnia and isocapnic hypoxia. 46 30

Using ten normal dogs, the right upper lobe of the lung was isolated in vivo by a balloon catheter and was artificially ventilated with nitrogen, air, 60% oxygen in nitrogen, and 60% oxygen and 20% carbon dioxide in nitrogen, while the rest of the lungs maintained a spontaneous breathing of ambient air. Aminophylline did not show a vasodilating action under severe alveolar hypoxia (PAO2: ca. 40 mmHg); on the contrary, it seemed to potentiate hypoxic pulmonary vasoconstriction. When the regional alveolar oxygen tension became less hypoxic (PAO2: ca. 70 mmHg) or higher than that in the rest of the lungs which spontaneously breathed ambient air, aminophylline showed a definite vasodilating action. Aminophylline also showed a vasodilating action in alveolar hypercapnia in the presence of alveolar hyperoxia.
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PMID:Effect of aminophylline on regional perfusion distribution in the lungs. 48 2

Friedreich's Ataxia (F.A.) is a degenerative disease which commonly leads to premature death of cardiorespiratory origin. To explain the early death of these patients, previous investigations have established the existence of 1) a cardiomyopathy in nearly 100% of cases, 2) a restrictive pulmonary syndrome of scoliotic origin and 3) a mild hypoxemia associated with slight respiratory alkalosis and a normal oxyhemoglobin dissociation curve. To further assess the cause of early death in patients with such neuromyopathy, we evaluated, in eleven F.A. patients, the sensitivity of the respiratory centers to hypercapnia, hypoxia, and hyperoxia. Ventilatory (VE, VT, F, VT/Ti) and occlusion pressure (P0.1) responses were taken as indices of the respiratory centers output during progressive hypercapnia (Read's method) and isocarbic hypoxia (Weil's method). We studied 11 Friedreich's Ataxia patients and 11 age, sex, and armspan matched controls. The responses of patients to hypercapnia were significantly greater than controls but their responses to hypoxia were similar to controls. Our study establishes that the respiratory centers are functioning adequately in early Friedreich's Ataxia and do not contribute to cardio-respiratory insufficiency in such neuromyopathy.
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PMID:Regulation of respiration in Friedreich's ataxia. 48 4

The influence of regional alveolar oxygen and carbon dioxide tensions on the distribution of lung blood flow and gas exchange was studied in unanaesthetised sheep. Right apical lobe (RAL) hypoxia, induced by administering nitrogen or nitrogen/oxygen mixtures to the lobe, stimulated a prompt, graded and well sustained reduction in lobar blood flow. Maximum hypoxia was accompanied by an approximate 65% reduction in perfusion, a significant fall in RAL carbon dioxide tension and output, a reversal of lobar oxygen flux and an average 13 Torr fall in arterial oxygen tension. The reduction in perfusion and gas exchange persisted in the face of elevated systemic oxygen tensions produced by giving pure oxygen instead of air to the remainder of the lung (RL). Mild RAL hypercapnia potentiated the hypoxia-induced change in perfusion and gas exchange. During lobar hypoxia RL blood flow and gas exchange increased to maintain total pulmonary gas exchange at an essentially constant level. RAL hyperoxia did not significantly alter the distribution of perfusion or gas exchange.
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PMID:Regional alveolar gas composition and lung function in sheep. 49 47

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

The measurement of pressure in the mouth 0.1 sec after the initiation of an occluded inspiratory effort (P0.1) has been proposed as an index of activity of medullary inspiratory neurons. If changes in FRC can be interpreted as important changes in the length-tension curve of the diaphragm or the total respiratory musculature, then changes in FRC from one occlusion pressure measurement to another can complicate such an interpretation of the P0.1 measurement. Forty-five subjects divided into three different groups were seated in a variable volume body plethysmograph. They had their FRC, P0.1, VT and VE measured while breathing air, 100% oxygen, 11% oxygen balance nitrogen, and 4% carbon dioxide in 20% oxygen balance nigrogen. All 45 showed a decrease in FRC during hyperoxia (-12%); 40 of 43 showed increases in FRC during hypoxia (14%); 42 of 43 showed an increased FRC during hypercapnia (15%). Changes in VE were small as were changes in P0.1 values. These latter changes generally followed the same pattern of changes as FRC though the magnitude of the changes showed more variability. We were unable to demonstrate a significant correlation between changes in FRC and changes in P0.1 under the conditions of our experiments.
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PMID:The effect of hyperoxia, hypoxia and hypercapnia on FRC and occlusion pressure in human subjects. 69 49

To determine the relationship of ventilatory responsiveness to hypoxia and hypercapnia to exercise hyperpnea, these responses and steady-state exercise ventilation (VE) were measured in 16 athletes during light (1/3 VO2 max) and heavy (2/3 VO2 max) exercise. Both the hypoxic and hypercapnic ventilatory responses correlated positively with VE per unit metabolic rate (VE/VCO2) at both exercise levels (P less than 0.05). The contribution of the hypoxic response to normoxic exercise VE was quantified by comparing VE in normoxia to VE during a brief (1 min) exposure to high O2 (PAO2 = 200 Torr). High O2 reduced normoxic exercise VE by a mean of 20% at either exercise intensity. Among individuals this reduction was directly dependent upon the intensity of the hypoxic response, and ranged from 7 to 42% of normoxic VE. After the variable reduction of normoxic VE by hyperoxia, all correlations of ventilatory response with exercise VE were lost except for the correlation of hypercapnic response with heavy exercise VE/VCO2. These findings indicate that the extent of VE in light or heavy exercise is modified by the strength of the hypoxic ventilatory response, and that the hypercapnic response independently correlates with VE during heavy exercise.
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PMID:Exercise ventilation correlates positively with ventilatory chemoresponsiveness. 71 73


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