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

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

The ventilatory effects of prolonged oxygen administration were examined in seven dogs during thiopentone anaesthesia. Ventilation, tidal volume (VT), ventilatory rate (f), minute ventilation (VE), inspiratory time (TI), expiratory time (TE), period (Ttot), TI/Ttot and mean inspiratory flow (VT/TI) were measured during the inhalation of room air, after 30 min of oxygen inhalation, and finally after a return to breathing room air. Arterial blood-gas tensions were measured before and after 5, 10, 20 and 30 min of oxygen administration and 15 min after return to breathing room air. Oxygen administration produced an immediate, significant and persistent decrease in ventilation, principally from a decrease in ventilatory rate and changes in ventilatory times. This was in contrast to what occurred in awake animals. Modifications in ventilatory mechanics or suppression of an hypoxic stimulus to ventilation were probably not involved. Anaesthesia may modify centrally mediated ventilatory responses to hyperoxia.
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PMID:Ventilatory effects of oxygen in the dog under thiopentone anaesthesia. 335 42

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.
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PMID:Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2. 339 90

Chronic sequelae of neonatal hyperoxia was studied in male rats exposed to 0.96-1.0 FiO2 for the first 8 days of life. At 58 days of age functional and morphologic cardiopulmonary changes were compared with controls. Right ventricular systolic pressure was measured percutaneously under anesthesia and was increased in the O2 group (29.5 mm Hg +/- 3.1 versus 23.2 mm Hg +/- 3.5, p less than 0.001). Lung and heart weights were similar between groups. Right ventricular weights however were increased in the O2 group (0.197 g +/- 0.023 versus 0.175 g +/- 0.020, p less than 0.001). Air pressure-volume curves were similar but in the O2 rats saline deflation curves were shifted left and maximal fluid lung volumes were greater (14.1 +/- 1.2 versus 12.0 +/- 0.7 ml, p less than 0.001). Pulmonary arteries were perfused at 100 cm H2O with a barium-gel mixture and lungs were fixed at 25 cm H2O with formalin. Microscopic examination of lungs revealed dysplastic changes of alveolar architecture which included irregularly enlarged alveoli and incomplete alveolar septation. Morphometric studies of the lungs showed that the O2 rats had an increased volume proportion of parenchyma (0.865 +/- 0.020 versus 0.850 +/- 0.019, p less than 0.05), increased mean linear intercept (72.3 microns +/- 9.5 versus 53.6 microns +/- 5.0, p less than 0.001), decreased number of alveoli per mm2 (207 +/- 34 versus 319 +/- 39, p less than 0.001) and fewer small arteries (20-200 microns) per mm2 (8.7 +/- 1.3 versus 14.9 +/- 2.4, p less than 0.001). The number of small arteries/100 alveoli was similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic vascular pulmonary dysplasia associated with neonatal hyperoxia exposure in the rat. 364 29

Effects of mechanical ventilation of the lungs of fetal lambs in utero are described. Feasibility studies were performed acutely on four fetuses at 140-142 days gestational age. Five fetuses were prepared for chronic experiments at 122-128 days gestation. Mechanical ventilation was used to produce changes in fetal blood gases for periods of up to 24 h in acute preparations or for repeated periods of 3-9 h on consecutive days in chronic preparations. This technique permits the study of fetal lambs in utero under conditions which normally occur after birth without producing maternal changes or using anesthesia and whilst the umbilical circulation remains open. Four situations were examined using ventilation in these chronic preparations: (1) expansion of the lungs whilst maintaining fetal normoxia and normocapnia; (2) fetal normoxia and hypocapnia; (3) hyperoxia and normocapnia; (4) hyperoxia and hypocapnia. None of these situations produced continuous fetal breathing, either during ventilation or after switching off the ventilator. We conclude that they do not provide appropriate stimuli to mimic those which normally produce continuous breathing after birth.
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PMID:Breathing activity in fetal sheep during mechanical ventilation of the lungs in utero. 366 75

Because the H2-receptor antagonist cimetidine has been shown to inhibit drug metabolism, the effects of cimetidine on anesthetic metabolism and toxicity were investigated in a rat model. Cimetidine decreased inorganic plasma fluoride production after methoxyflurane administration both in 21% oxygen (P less than 0.001) and in 100% oxygen (P less than 0.001). Phenobarbital produces an increased fluoride formation after methoxyflurane anesthesia, and this fluoride formation is also reduced by cimetidine (P less than 0.005). There was no significant difference between the plasma fluoride levels in rats anesthetized with halothane or enflurane. Although cimetidine inhibited the in vivo defluorination of methoxyflurane, fluoride levels were still within the nephrotoxic range, and cimetidine is not likely to play a role as part of a preanesthetic regimen that would permit the increased clinical use of methoxyflurane. Cimetidine also inhibited the oxidative metabolism of halothane; cimetidine decreased (P less than 0.05) trifluoroacetic acid concentrations after halothane anesthesia in 21% oxygen and in 100% oxygen and decreased (P less than 0.05) bromide concentrations after halothane anesthesia in 100% oxygen. Trifluoroacetic acid levels were less (P less than 0.02) after halothane anesthesia in 14% oxygen as compared with 100% oxygen, indicating a reduction in oxidative metabolism under hypoxic conditions. However, bromide concentrations were maximal after halothane anesthesia in 21% oxygen, and significantly (P less than 0.001) less after halothane anesthesia in 14% and 100% oxygen. Bromide production, therefore, seems to be inhibited by both hypoxia and hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of cimetidine on anesthetic metabolism and toxicity. 396 34

The effects of progressively increasing hyperoxia from 0.22 to 1 on the ventilatory action of a ventilatory analeptic with a peripheral action, almitrine, were studied in six dogs under deep anaesthesia by Alfatesine administered at a constant flow rate. At FiO2 = o.22, almitrine partially corrected hypoventilation. From FiO2 o.30 to FiO2 0.50, initial hypoventilation was unaltered. At FiO2 = 1, it was worsened. This preliminary study will need to be completed by examination of the interference almitrine-FiO2 at different levels of anaesthesia and of respiratory depression, by study of the effects of different levels of FiO2 on the respiratory depression caused by Alfatesine and by study of the effects of the sudden administration of pure oxygen.
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PMID:[Effect of different FiO2 on the ventilatory action of almitrine in the anesthetized dog. Preliminary study]. 610 90

Changes in lung endothelial metabolic function, determined in vitro, have been proposed as sensitive indexes of hyperoxic lung damage. However, it is unclear whether these changes are also seen in vivo. We studied the possibility, using conscious rabbits in which jugular and carotid catheters had previously been placed under halothane anesthesia. Approximately 24 h later, test animals were exposed to normobaric hyperoxia (96 +/- 2%), while a second group was maintained in room air. Multiple indicator dilution methods were used to study (1) metabolism of 3H-benzoyl-phe-ala-pro (BPAP), a synthetic substrate for angiotensin converting enzyme (ACE), and (2) removal of 14C-5-hydroxytryptamine (5-HT) during a single transpulmonary passage in conscious animals. Determinations were made serially during exposure (room air or hyperoxia) or until death occurred in the oxygen-treated animals. Lungs of air-exposed animals hydrolyzed 81 +/- 2% of injected BPAP (0.1 to 0.15 nmoles) during a single passage. Percent metabolism was unaltered during the next 72 h. However, in test animals, ACE activity, as reflected by BPAP metabolism, was significantly reduced after 16 h of exposure to oxygen (77 +/- 2%, p less than 0.01) and continued to decrease to a nadir of 66 +/- 3% at 40 h. Single-pass lung uptake of 14C-5-HT (77 +/- 2%) was unchanged throughout the 72-h period in air-exposed rabbits. In test animals, 14C-5-HT removal decreased to 65 +/- 4% (p less than 0.01) after 24 h of oxygen exposure; 5-HT removal remained depressed compared with the 0 h control determination for the oxygen group at all subsequent measurement intervals. Light and electron microscopy of lungs from oxygen-exposed rabbits demonstrating reduced 5-HT removal and ACE activity at 24 h revealed normal endothelial and type I cell morphologic features. We conclude that exposure to 100% oxygen produced significant reduction in pulmonary 5-HT removal and BPAP metabolism prior to the onset of morphologic damage.
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PMID:Early detection of oxygen-induced lung injury in conscious rabbits. Reduced in vivo activity of angiotensin converting enzyme and removal of 5-hydroxytryptamine. 628 9

Healthy parturients with uterine displacement received oxygen inhalation before and during spinal anesthesia for elective cesarean section. Oxygen was administered through a mask (group OH2 : 20 cases) or via a nasal cannula (group OH1: 20 cases) for 33 to 69 minutes. All patients were in the right lateral position prior to spinal block and were in the left tilt after the anesthesia. The fetal blood-gas values were relatively evaluated among the OH2, OH1 and OH groups which received oxygen via a cannula for 9 to 17 minutes. The maternal artery PO2 values for the OH2 group (the mean: 491.7 +/- 61.4mmHg) were significantly higher than those for the OH1 and OH groups (244.5 +/- 28.0 and 225.0 +/- 62.9mmHg, respectively). The umbilical vein PO2 (46.1 +/- 7.5mmHg) and SO2 (87.6 +/- 6.3%) of the OH2 group were also significantly greater than those of the other groups (PO2: 36.1 +/- 4.1mmHg, SO2: 77.3 +/- 6.0% in the OH1 group and PO2: 37.5 +/- 6.4mmHg, SO2: 77.6 +/- 10. 3% in the OH group, respectively). The Apgar scores and both the maternal and fetal acid-base values for all groups were excellent. The umbilical vein to artery PO2 and SO2 gradients of the OH2 group were significantly greater than those of the other groups. It is emphasized that maternal hyperoxia with uterine displacement improves fetal oxygenation without adversely affecting the fetal acid-base state, even if it is excessive and maintained for 60 minutes.
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PMID:[The influence of maternal oxygen inhalation for 30 to 60 minutes on fetal oxygenation]. 650 71

In decerebrate, vagotomized, paralyzed, and ventilated cats, phrenic and respiratory-related hypoglossal discharges were evident at normocapnic normoxia or hyperoxia. Both increased progressively in hypercapnia or hypoxia. With increasing drive, onset of inspiratory hypoglossal activity began earlier relative to phrenic onset; an early expiratory hypoglossal burst was also observed. Following subanesthetic doses of chloralose, halothane, ketamine, or pentobarbital, hypoglossal activity was depressed much more than phrenic discharge. In moderate hypercapnia or hypoxia, phrenic activity increased more than hypoglossal, whereas, at high drive, the latter rose more sharply in some cats. Electromyograms of the diaphragm and genioglossus were recorded in intact awake cats to determine if their responses and those of decerebrates are comparable. Respiratory-related genioglossal discharge was evident in normocapnia. We conclude that anesthesia suppresses hypoglossal motor activities much more than those of the bulbospinal-phrenic system. Data for decerebrate cats and unanesthetized cats or humans provide no evidence of a differential distribution of chemoreceptor afferents on hypoglossal and bulbospinal-phrenic neurons, as suggested by results in anesthetized animals.
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PMID:Respiratory-related hypoglossal nerve activity: influence of anesthetics. 662 15


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