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

This study was designed to characterize the ventilatory interaction between central and carotid body (CB) chemoreceptor stimulation in awake goats undergoing selective CB perfusion. This model allowed us to expose central and CB chemoreceptors to separate blood gas conditions in an animal that is conscious and not systemically hypoxic. Systemic CO2 ventilatory response curves, performed by progressively increasing FICO2 in systemic hyperoxia, were completed in 7 goats during CB perfusion with hypercapnic-hypoxic blood and normocapnic-normoxic blood, and in 3 goats without CB perfusion. The slopes of the curves done with perfusion were not significantly different (P greater than 0.05) in CB hypercapnic hypoxia and CB normocapnic normoxia for VE, VT, f and VT/TI, and the coefficients of variation of slopes generated with and without perfusion were similar. Our data indicate there is addition of central and CB chemoreceptor input in respiratory control, and we conclude that the previously demonstrated stimulus interaction at the CB is the primary source of the hyperadditive hypercapnic-hypoxic ventilatory interaction in an animal unaffected by anesthetics or brain hypoxia.
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PMID:Central-peripheral chemoreceptor ventilatory interaction in awake goats. 250 45

PaO2, PaCO2 and pHa were measured via an extracorporeal loop in conscious snapping turtles (Chelydra serpentina) breathing air or hypoxic (10, 15% O2), hyperoxic (30% O2), or hypercapnic (2% CO2) gases. Turtles breathed into an inverted funnel ventilated with the test gas. Breathing was recorded with a differential pressure transducer. In all turtles, nonventilatory periods were interrupted by breathing episodes containing multiple breaths. In normoxia, PaO2 at the end of nonventilatory periods ranged from 22-128 mm Hg, although PaCO2 showed a less than 5 mm Hg variation about the mean. There was a positive correlation between PaCO2 at the end of the nonventilatory period and the number of breaths in the succeeding period of ventilation. PaCO2 at the end of nonventilatory periods did not change significantly in hyperoxia, although mean PaO2 was significantly increased. In hypoxia, on the other hand, mean PaO2 was significantly reduced and PaCO2 at the end of the nonventilatory period was slightly, but significantly lower. Nonventilatory periods were shorter when turtles breathed 15% O2 (9.3 +/- 1.2 min) or 10% O2 (5.5 +/- 0.3 min) than when they breathed air (17.6 +/- 3.4 min). The results indicate that, in undisturbed turtles, the most important stimulus triggering a breathing episode is the rise in PaCO2 to a critical value during the preceding nonventilatory period. An increase in hypoxic drive shortens the nonventilatory period. However, in normoxia, PaO2 at the end of many nonventilatory periods probably does not fall sufficiently to stimulate O2-sensitive chemoreceptors.
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PMID:Factors terminating nonventilatory periods in the turtle, Chelydra serpentina. 250 23

Cultured type II pneumocyte responses to in vitro normoxia (95% air:5% CO2) or hyperoxia (95% O2:5% CO2) were quantified. Normoxic culture (0 to 96 h) of rabbit type II cells resulted in enhanced cell-monolayer protein and DNA content. During this same time, cellular activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH Px) decreased. Compared to cultures maintained in normoxia, hyperoxic exposure of cultures resulted in decreased cell-associated protein and DNA content. Exposure to hyperoxia also resulted in cytotoxicity as demonstrated by elevated cellular release of DNA, lactate dehydrogenase (LDH), and preincorporated 8-[14 C]adenine. Cellular catalase and GSH Px activities in hyperoxic cells decreased similarly to normoxic controls. In contrast, cellular SOD activity in hyperoxic cells decreased less than in normoxic cultures. Cellular SOD activity in hyperoxic cultures, when normalized for cellular protein, but not DNA, was greater than normoxic values after 24 to 96 h of exposure. Unlike the decrease in cellular antioxidant enzymes during normoxic and hyperoxic culture, cellular LDH activity increased during both these exposures. Cellular LDH activity in 24 to 96 h hyperoxia-exposed cells increased to a lesser extent than normoxic controls. The extent of depression in LDH activity was dependent on whether the activity was normalized for cellular protein or DNA. Type II pneumocytes, which normally undergo hyperplasia and hypertrophy during hyperoxia in vivo, exhibited oxygen sensitivity in vitro. Exposure of type II cells to hyperoxia in vitro resulted in alterations in cellular SOD and LDH activities, but recognition of such changes were dependent on whether enzymatic activities were normalized for cellular DNA or protein.
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PMID:Responses of type II pneumocyte antioxidant enzymes to normoxic and hyperoxic culture. 250 12

We have tested the ability of hyperoxia (98% O2-2% CO2 at 2.8 atmospheres absolute [ca. 284.6 kPa]) to enhance killing of Escherichia coli (serotype O18 or ATCC 25922) by nitrofurantoin, sulfamethoxazole, trimethoprim, gentamicin, and tobramycin. We have also looked for interactions between hyperoxia and the aminoglycosides against Pseudomonas aeruginosa ATCC 27853. Hyperoxia significantly enhanced bacteriostatic activity of nitrofurantoin and trimethoprim as measured by MIC testing. The possibility exists that these effects might be due to the method required to tests MICs under hyperoxic conditions rather than to the effect of hyperoxia itself. In addition, hyperoxia enhanced killing of bacteria by trimethoprim as measured by MBC testing. Hyperoxia decreased numbers of E. coli by 1.3 log10 and P. aeruginosa by 2.7 log10 in cation-supplemented Mueller-Hinton broth medium. The bacteriostatic effects of hyperoxia did not affect MICs of gentamicin or tobramycin. The lack of interaction between hyperoxia and gentamicin or tobramycin was confirmed by determining the number of viable bacteria remaining after 24 h of exposure to hyperoxia by using a pour plate method. We conclude that hyperoxia potentiates the antimicrobial activity of the reduction-oxidation-cycling antibiotic tested (nitrofurantoin) and of one of the antimetabolites tested (trimethoprim). Hyperoxia does not enhance the bactericidal effects of gentamicin and tobramycin, which require oxidative metabolism for transport into bacterial cells.
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PMID:Hyperoxia and the antimicrobial susceptibility of Escherichia coli and Pseudomonas aeruginosa. 251 May 93

Contribution of autonomic nervous system activity to the heart rate and blood pressure responses during chemoreceptor excitations by systemic hypoxia and hypercapnia and to hyperoxia and hypocapnia was analyzed in the urethane-anesthetized, artificially ventilated rats. Systemic hypoxia induced a co-activation of two antagonistic nerves: an increase in cardiac sympathetic and in cardiac vagal efferent nerve discharges. Increased heart rate was due to predominance of the cardiac sympathetic over the cardiac vagal activation. In spite of a marked reflex increase in the renal and cardiac sympathetic nerve activities, the local vasodilator effect of hypoxia prevented consistent changes in arterial blood pressure. Bilateral section of the carotid sinus nerves (CSN) mostly abolished autonomic nerve responses and produced a profound decreases in the blood pressure during hypoxia. Hyperoxia elicited a pressor response due to peripheral vasoconstriction with no significant change in the autonomic nerve activities except for a decrease in the cardiac sympathetic nerve discharges. Hypercapnia significantly increased blood pressure and renal nerve sympathetic activity. In contrast to hypoxia, hypercapnia excited cardiac sympathetic and inhibited cardiac vagal activity. This reciprocal effect did not elicit neurogenic cardioacceleration, because it was masked by the local inhibitory action of CO2 on the heart rate. The increase in sympathetic activities and in blood pressure during hypercapnia persisted after bilateral CSN section indicating that the responses were mediated by central rather than by peripheral chemoreceptors. Hypocapnia produced a significant increase in cardiac vagal discharges yet a cardioacceleratory response occurred due to the local effect upon heart rate. The present results indicate that in the rat, autonomic nervous responses differ depending on the type, i.e. hypoxic or hypercapnic, chemoreceptor stimuli. Reflex heart rate and blood pressure responses do not follow the autonomic nerve activities exactly. Circulatory responses are greatly modified by local peripheral effects of hypoxic, hyperoxic, hypocapnic or CO2 stimuli on the cardiovascular system. Species differences characterizing the autonomic nerve responsiveness to chemical stimuli in the rat are described.
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PMID:Autonomic nerve and cardiovascular responses to changing blood oxygen and carbon dioxide levels in the rat. 251 Dec 37

1. Respiratory sensation during exercise is generally considered to be related to respiratory mechanical factors which may be manifest as an abnormal relationship between the force applied to the lungs and chest wall and the resulting motion (if any); that is, a 'length-tension' inappropriateness (Campbell & Howell, 1963). This suggests that there should be a direct correlation between ventilation (VE) and the associated intensity of the perceived sensation, such that the sensation associated with a particular level of VE should remain essentially constant regardless of the source of respiratory stimulation. 2. In order to establish whether certain respiratory stimuli might be 'dyspnoeagenic' (i.e. capable of evoking an intensity of respiratory sensation out of proportion to their influence on VE), we investigated the influence of both peripheral chemoreflex activation (induced by isocapnic hypoxia) and central chemoreflex activation (induced by hypercapnic hyperoxia) on the intensity of respiratory sensation in seven healthy adults during moderate cycle ergometer exercise (i.e. below the lactate threshold, theta 1ac). 3. In each test, an 'isopnoea' was established for which a particular level of VE was sustained over a prolonged period (approximately 30 min) while the proportional contributions to the ventilatory drive from either exercise and the peripheral chemoreflex or from exercise and the central chemoreflex were slowly altered to new stable levels, without the subject's knowledge, VE, tidal volume, inspiratory and expiratory durations, mean inspiratory flow, and end-tidal PCO2 and PO2 (PET,CO2, PET,O2) were monitored breath-by-breath. The intensity of respiratory sensation was rated with a visual analogue scale. 4. Isopnoeic ratings of respiratory sensation were systematically greater for peripheral chemoreflex activation by isocapnic hypoxia during exercise at 50% theta 1ac (for which the degree of peripheral chemoreflex activation, estimated by hyperoxic transition or 'Dejours' testing, averaged approximately 23% of the total VE), compared to 90% theta 1ac during isocapnic hyperoxia. Ratings during exercise at 50% theta 1ac for central chemoreflex activation by hypercapnic hyperoxia were not systematically different from 90% theta 1ac during isocapnic hyperoxia, however. 5. As VE was stable throughout each isopnoea and the MVV (maximum voluntary ventilation) was uninfluenced by the test condition, the dyspnoea index (VE x 100/MVV) was not affected. Breathing pattern was also unaffected. 6. We conclude that in normal subjects exercising moderately, activation of the peripheral chemoreceptors by isocapnic hypoxia evokes an intensity of respiratory sensation which is out of proportion to that evoked by an isopnoeic stimulation of the central chemoreceptors with hypercapnic hyperoxia at the same level of exercise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of peripheral and central chemoreflex activation on the isopnoeic rating of breathing in exercising humans. 251 73

1. The ventilatory response to changes in end-tidal carbon dioxide tension during hyperoxia, obtained with Read's rebreathing method and a steady-state technique, were compared. 2. In ten young male subjects, forty successful rebreathing and thirteen steady-state experiments were performed on thirteen different morning sessions. 3. In all subjects the ventilatory CO2 sensitivities obtained with the rebreathing method (Sr) were appreciably larger than the steady-state CO2 sensitivities (Ss). The ratio Sr/Ss ranged from 1.40 to 2.59 with a mean value of 1.85. 4. We argue that these results can be explained by considering the effect of changes in cerebral blood flow upon increasing the arterial CO2 tension during rebreathing and the steady state. 5. We conclude that in general the CO2 sensitivity obtained with Read's rebreathing method does not represent the steady-state CO2 sensitivity.
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PMID:The ventilatory CO2 sensitivities from Read's rebreathing method and the steady-state method are not equal in man. 251 74

We studied the steady state responses of heart rate (HR) to carbon dioxide inhalation under hyperoxic, euoxic, and hypoxic conditions in 9 healthy men. With increasing end-tidal PCO2, HR generally increased slightly. On the other hand, distinct increment in VE in response to step increase in end-tidal PCO2 was observed in all three different conditions. Significant positive correlation between hypercapnic VE and HR responsiveness was found in both hyperoxic and hypoxic conditions, whereas no such tendency was seen in euoxic condition. We suggest that the effect of CO2 inhalation on HR is mainly determined by the pulmonary inflation reflex in hyperoxia, the pulmonary inflation reflex plus peripheral chemoreceptor activity in euoxia, and the additional sympathetic and humoral factors in hypoxia, respectively.
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PMID:Carbon dioxide-heart rate responses during hyperoxia, euoxia, and hypoxia. 251 28

The effects of almitrine bismesylate (initial intravenous dose 0.6 mg.kg-1 followed by continuous infusion of 0.4 mg.kg-1.h-1) on the ventilatory response to CO2 during hyperoxia and hypoxia were determined in 6 anaesthetized cats with the use of the dynamic end-tidal CO2 forcing technique. It was found that almitrine almost doubled the peripheral ventilatory sensitivity to CO2 during hyperoxia (mean PETO2 45.6 kPa) and also during mild hypoxia (mean PETO2 8.7 kPa). The apnoeic threshold (B) was in both cases shifted to substantially lower values than those of the control measurements. No significant effects of almitrine were found on the central ventilatory sensitivity to CO2 either during hyperoxia or during hypoxia. It is argued that the decrease of the apnoeic threshold may be due to an inhibitory effect of almitrine on the carotid body dopaminergic activity, and that the increase of the sensitivity to CO2 stems from a "hypoxia mimetic" mechanism.
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PMID:Almitrine and the peripheral ventilatory response to CO2 in hyperoxia and hypoxia. 251 70

The ventilatory and hemodynamic responses to hypoxia, hyperoxia, and hypercapnia before and during sufentanil infusion were studied in 16 chronically tracheostomized dogs anesthetized with two concentrations, 1 and 0.5 minimal alveolar concentration (MAC) of isoflurane. Sufentanil was infused at a rate to obtain a constant end-tidal carbon dioxide (PETCO2) of approximately 50 mm Hg for each isoflurane level. Before the sufentanil infusion, the PETCO2 was increased to 50 mm Hg by adding CO2 to the inspired gas, to allow comparisons at isocapnic conditions. Sufentanil caused only minor hemodynamic changes but significantly reduced ventilation during both levels of isoflurane. The ventilatory response to hypercapnia decreased substantially, but there were no significant alterations in the ventilatory response to hypoxia. After sufentanil infusion, hyperoxia caused a larger decrease in minute ventilation and caused apnea in four dogs. These results suggest that administering sufentanil during isoflurane anesthesia causes a reduction in the contribution of the central chemoreflexes to ventilatory drive and, consequently, a relative increase in the contribution from the peripheral chemoreflexes.
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PMID:Ventilatory and cardiovascular responses to sufentanil infusion in dogs anesthetized with isoflurane. 252 4


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