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

In decerebrate, vagotomized cats, introduction of CO2 into the isolated laryngeal airway while systemic PCO2 is held constant evokes dose-related reflex changes in ventilatory activity. Because systemic hypoxia is known to exaggerate ventilatory responses to other types of laryngeal chemostimulation in neonates, we have compared the responses of phrenic and hypoglossal nerve activities to ventilation of the larynx with 10% CO2 during systemic hyperoxia (FIO2 = 1.00) to those during hypoxia (FIO2 = 0.12). Compared with the hyperoxic baseline condition, hypoxia stimulated phrenic activity but attenuated the reduction in phrenic activity evoked by intralaryngeal CO2. Hypoglossal activity was increased by intralaryngeal CO2 and this response appeared to be reduced by hypoxia, but neither of these findings was statistically significant. The response of phrenic activity to intralaryngeal CO2 during systemic hypercapnia was similar to that during hypoxia. The increase of phrenic activity in response to hypoxia was prevented by carotid body resection. Similarly, the hypoxic attenuation of the phrenic response to intralaryngeal CO2 appeared to be absent after carotid body resection, although this finding was not established statistically. These results differ from previous reports of exaggerated laryngeal chemoreflex responses during hypoxia. The difference may reflect differences in the receptors and synaptic mechanisms of the reflexes, the severity and time course of hypoxia or the presence or depth of general anesthesia or sleep.
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PMID:Influence of hypoxia on ventilatory responses to intralaryngeal CO2 in cats. 802 21

High fractions of inspired oxygen are commonly used during general anesthesia in birds. Observations in ducks anesthetized with halothane or pentobarbital indicated that high fractions of inspired oxygen depress ventilation. The purpose of this study was to test the hypothesis that ducks hypoventilate when breathing high fractions of inspired oxygen, compared with the same ducks breathing low fractions of inspired oxygen. Respiratory variables were recorded in 7 ducks anesthetized with 1.4% isoflurane in oxygen. Four concentrations of oxygen (21, 40, 70, and > 90%) were used for each duck. Respiratory rate decreased as the fraction of inspired oxygen increased, but not significantly. There was a significant decrease in tidal volume as PaCO2 increased. Hyperoxia was observed to contribute to hypoventilation in ducks anesthetized with isoflurane in oxygen.
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PMID:Effects of low and high fractions of inspired oxygen on ventilation in ducks anesthetized with isoflurane. 819 65

The pulmonary vascular effects of inhaled anesthetics have been reported variably. We compared the effects of intravenous anesthesia (propofol) and inhalational anesthesia (isoflurane) on multipoint mean [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (PpaO)]/cardiac output (Q) plots and on pulmonary vascular impedance (PVZ) spectra in eight dogs alternatively ventilated in hyperoxia [inspired O2 fraction (FIO2) 0.4] and in hypoxia (FIO2 0.1). Q was altered by a manipulation of venous return. During propofol, hypoxia increased (Ppa-PpaO) by an average of 2-3 mmHg over the entire range of Q studied, from 1 to 2.5 l.min-1 x m-2. This hypoxic pulmonary vasoconstriction (HPV) was associated with insignificant changes in PVZ. Decreasing Q in hypoxia and hyperoxia did not affect PVZ. Compared with propofol, isoflurane decreased (Ppa-PpaO) by an average of 2-5 mmHg at all levels of Q studied in both hypoxia and hyperoxia but did not affect HPV. During isoflurane anesthesia, 0 Hz PVZ was lower (P < 0.01) in hypoxia, but otherwise the PVZ spectrum was not different from that recorded during propofol anesthesia. We conclude that, in dogs, 1 degree general anesthesia with isoflurane alone decreases pulmonary vascular tone without inhibition of HPV and that 2 degrees pressure/Q plots in the time domain are more sensitive than those in the frequency domain to subtle hemodynamic changes induced by hypoxia or isoflurane at the periphery of the pulmonary vasculature.
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PMID:Pulmonary vascular impedance vs. resistance in hypoxic and hyperoxic dogs: effects of propofol and isoflurane. 833 47

The aim of the present study was to examine whether hypoxic pulmonary vasoconstriction (HPV) is preserved during one-lung ventilation combined with thoracic epidural anesthesia (TEA) in dogs. Using a separately ventilated left lower lobe (LLL) in situ, the pressure-flow (P-Q) curve was obtained. The HPV response was assessed by the shift of the P-Q curve, changes in blood flow diversion rate (FDR) and decrease in PaO2 during hypoxic gas ventilation of LLL. In the control group (n = 7), the shift of P-Q curve, changes in FDR, and decrease in PaO2 remained constant during four consecutive hypoxic stimulations. In the TEA group (n = 6), the P-Q curve shifted to the left during hyperoxia, but the magnitude of the shift during hypoxia was unchanged. FDR and decrease in PaO2 were significantly reduced compared with baseline values (P < 0.05 with analysis of variance). TEA reduced heart rate, cardiac output, mean arterial pressure, mean pulmonary arterial pressure, and mixed venous oxygen tension. Our results suggest that TEA did not affect the primary pulmonary vascular tone at baseline or during lobar hypoxia, but enhanced the diversion of blood flow and arterial blood oxygenation during lobar hypoxia. This enhanced HPV response probably reflects hemodynamic changes, such as decreased cardiac tension, due to sympathetic nerve activity blockade by TEA.
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PMID:The effect of thoracic epidural anesthesia on hypoxic pulmonary vasoconstriction in dogs: an analysis of the pressure-flow curve. 861 Aug 66

The present study was designed to determine whether neurons near the ventral medullary surface (VMS) that are important to control of breathing in adult mammals are also important to control of breathing in neonates. In 7-day-old goats (n = 22), the VMS was surgically exposed under halothane anesthesia. Stainless steel thermodes (2 x 2 mm) were used to cool (20 degrees C) and thereby create neuronal dysfunction of discrete VMS sites. Bilateral cooling under anesthesia 0-2 or 2-4 mm lateral to the midline between the exit of cranial nerves VI and XII resulted in a reduction (P < 0.05) of breathing and most often in apnea. Cooling caudal or rostral to this area did not have a consistent effect on breathing. In 7-day-old goats (n = 8), 3 x 3-mm thermodes were chronically implanted bilaterally on the VMS surface between the exit of cranial nerves VI and XII. The goats recovered and were studied over several days thereafter. VMS cooling while the goats were awake caused breathing to decrease (P < 0.05), but apnea was never observed. The decrease was less (P < 0.05) than while the goats were anesthetized. After 10 s of cooling, the hypopnea while the goats were awake was uniform during eupnea, hypercapnia, hyperoxia, and hypoxia, but after 10 s of cooling, the decrease was relatively greater (P < 0.05) during hyperoxia and hypercapnia. These effects of VMS cooling are qualitatively the same as in adult goats; thus the data are consistent with mature VMS contribution to the control of breathing in neonatal goats.
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PMID:Effect on breathing of ventral medullary surface cooling in neonatal goats. 880 99

To assess the role of diaphragmatic activity at the end of expiration (DE) in the control of end-expiratory lung volume (EELV), 1) these two parameters were correlated in anesthetized cats breathing different gas mixtures; and 2) expiratory flow volume curves in normoxia and hypoxia together with changes in esophageal pressure were measured. The influence of volume feedback on DE control was tested by applying positive end-expiratory pressure (PEEP). The effect of anesthesia was determined by measuring DE in unanesthetized cats. In hyperoxia, DE (but not EELV) decreased. In hypocapnic hypoxia (12, 10, and 8% O2), both DE and EELV gradually increased, and these changes were significantly correlated. When normocapnia was restored in 8% O2, DE and EELV decreased but remained higher than in air. Hypercapnia affected neither DE nor EELV. PEEP blocked the hypoxia-induced increase in DE. Hypoxia decreased expiratory flow and esophageal pressure. Finally, the increases in DE at 12 and 10% O2 were more pronounced when the cats were unanesthetized. These results suggest that the increase in diaphragmatic activity induced by hypocapnic hypoxia during expiration affects expiratory flow and thoracic volume and, therefore, plays a major role in increasing EELV. This phenomenon may also be controlled by volume feedback.
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PMID:Changes in end-expiratory lung volume and diaphragmatic activity during hypoxia and hypercapnia in cats. 884 51

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

Alveolar fluid resorption occurs by active epithelial sodium transport and is accelerated by terbutaline in healthy lungs. We investigated the effect of terbutaline on the rate of alveolar fluid resorption from rat lungs injured by hyperoxia. Rats exposed to > 95% O2 for 60 h, sufficient to increase wet-to-dry lung weight and cause alveolar edema, were compared with air-breathing control rats. After anesthesia, the animals breathed 100% O2 for 10 min through a tracheostomy. Ringer solution was instilled into the alveoli, and the steady-state rate of volume resorbed at 6 cmH2O pressure was measured via a pipette attached to the tracheostomy tubing. Ringer solution in some animals contained terbutaline (10(-3) M), ouabain (10(-3) M), or both. Normoxic animals resorbed 49 +/- 6 microliters.kg-1.min-1; ouabain reduced this by 39%, whereas terbutaline increased the rate by 75%. The effect of terbutaline was blocked by ouabain. Hyperoxic animals absorbed 78 +/- 9 microliters.kg-1.min-1; ouabain reduced this by 44%. Terbutaline increased the rate by a mean of 39 microliters.kg-1.min-1, similar to the absolute effect seen in the normoxic group, and this was blocked by ouabain. Terbutaline accelerates fluid resorption from both normal and injured rat lungs via its effects on active sodium transport.
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PMID:Terbutaline stimulates alveolar fluid resorption in hyperoxic lung injury. 890 92

It is not clear if ventilation with oxygen increases brain tissue oxygen pressure (PO2) during ischaemia. We have measured brain tissue PO2, carbon dioxide pressure (PCO2) and pH during baseline anaesthesia and oxygen ventilation in non-ischaemic control patients (n = 9), patients with cerebral occlusive disease (n = 11) and patients with arteriovenous malformations (AVM, n = 12). The same anaesthetic treatment was given to all groups and anaesthesia was constant during the study. Arterial pressure, brain temperature and arterial blood-gas tensions were similar between groups. Under baseline conditions, brain tissue PO2 was mean 4.2 (SD 1.4) kPa in the controls and was 70% lower in patients with ischaemia and AVM. Patients with occlusive disease also had elevated tissue PCO2 and acidosis. During oxygen ventilation, PO2 increased to 7.5 (2.9) kPa in controls and this was 50% greater than the increase in the ischaemia and AVM patients. The results showed that baseline tissue oxygenation and increases in PO2 during hyperoxia were attenuated in patients with ischaemia or AVM.
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PMID:Brain tissue oxygenation in patients with cerebral occlusive disease and arteriovenous malformations. 906 35

Exposure to high concentrations of oxygen is known to induce changes in lung function through effects on several pulmonary cell types, including alveolar macrophages (AM). In this study, we studied the in vitro effects of hyperoxia on the release of proinflammatory cytokines and the expression of surface receptors in AM obtained from cynomolgus monkeys by bronchoalveolar lavage under general anesthesia. AM were exposed for 24 h to moderate (50% O(2)) or severe (95% O&sub2) hyperoxia in the absence or presence of LPS, and the release of IL-1beta, IL-6, and TNF-alpha was measured in culture supernatants by ELISA. In addition, the expression of the surface molecules HLA-DR, CD14, and CD11b was assessed by flow cytometry. Exposure to 95% O2 activated resting AM to produce significantly increased amounts of IL-1beta and IL-6. Moreover, hyperoxia amplified the release of TNF-alpha by LPS-stimulated AM in an oxygen tension-dependent manner. Finally, exposure to 95% O2 upregulated the expression of the adhesion molecule CD11b on AM, whereas the expression of HLA-DR and CD14 was not affected. These findings support the view that hyperoxia-induced activation of AM may represent an initial event in the proinflammatory sequence caused by hyperoxia.
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PMID:Hyperoxia induces upregulation of CD11b and amplifies LPS-induced TNF-alpha release by alveolar macrophages. 911 Sep 20


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