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

The influence of arterial O2 and CO2 tensions on electroconvulsive seizure duration was investigated in five mongrel dogs under consistent anaesthetic conditions. Seizure durations were measured in a randomized protocol of nine possible combinations of arterial gas tension spanning increased, normal or decreased levels of PaO2 and PaCO2. Seizure duration was directly related to PaO2 (p less than 0.00001) and inversely related to PaCO2 (p less than 0.0001). A significant synergism was evident at the extremes of PaO2 and PaCO2, with seizure duration being greater than predicted for hyperoxia-hypocapnia and hypoxia-hypercapnia and shorter than predicted for hypoxia-hypocapnia and hyperoxia-hypercapnia. We conclude that arterial gas tensions strongly influence ECT-induced seizure duration and through this may influence the therapeutic efficacy of electroconvulsive therapy.
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PMID:Arterial PaO2 and PaCO2 influence seizure duration in dogs receiving electroconvulsive therapy. 366 9

We used mechanical ventilation of the fetal lungs in utero on 11 fetal lambs at 140-145 days gestation to alter fetal blood gases and thus separate the influences of PaO2 and PaCO2 on extrauterine breathing after cord clamping. The fetus was delivered either into a 40 degrees C saline bath or onto a cold table. Mechanical ventilation was stopped 2 min after delivery and the time to onset of continuous air breathing was observed. Also two fetuses were ventilated in utero 5 or more days after chronic instrumentation at 127 days gestation; in these animals the time to onset of breathing (diaphragm EMG) was recorded after stopping the ventilator and occluding the cord. We conclude: (a) hypercapnia is a stimulus to breathing even in hyperoxia and at 40 degrees C; (b) hypocapnia delays the start of extrauterine breathing in hyperoxia at 40 degrees C; (c) hypoxia inhibits breathing in the absence of hypercapnia or cold; (d) cold overrides the effects of hypocapnia in normoxia or moderate hypoxia.
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PMID:Determinants of the onset of continuous air breathing at birth. 366 76

O2 and CO2 partial pressures in end-tidal gas (PA) and carotid artery blood (Pa) were measured during non-steady-state gas exchange in unanesthetized dogs. In 5 experiments (A), low O2 breathing in open circuit preceded prolonged rebreathing during maintained normoxia. In 6 experiments (B), steady-state hypoxia and hypercapnia were followed by rebreathing CO2 in hyperoxia which caused PAO2 to rise and then fall while PACO2 increased. Negative (Pa-PA)CO2, averaging -5 torr, were observed 10 sec after starting rebreathing in B and values between -1 and -2 torr were noted later in A and B. (PA-Pa)O2 showed considerable transient increases for 2 min in A and 20 sec in B. This behavior of (PA-Pa)O2 could be explained by a lung model with unequal distribution of alveolar ventilation and perfusion to alveolar volume. The negative (Pa-PA)CO2 values observed during rebreathing with rapidly increasing PACO2 were in part attributable to such unequal distribution effects, in part to lung-to-carotid artery transit time effects.
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PMID:Transient PO2 and PCO2 differences between end-tidal gas and arterial blood during rebreathing in awake dogs. 392 16

We investigated the response of renal nerve activity (RNA) to hypercapnia and assessed the contribution of the peripheral chemoreceptors to the response of RNA in anesthetized and artificially ventilated cats. RNA and arterial pressure were recorded at four levels of PETCO2 with hyperoxia in intact and in peripheral chemoreceptor denervated cats. In intact cats, RNA increased progressively with increasing PETCO2, while no consistent change in arterial pressure was observed. In peripheral chemoreceptor denervated cats, the response of RNA to increasing PETCO2 was totally abolished. These results suggest that the peripheral chemoreceptors play an important role in increasing RNA during hypercapnia.
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PMID:Effects of hypercapnia on renal nerve activity. 393 28

The dependence of the carotid chemoreceptor responses to blood-borne stimuli on the ganglioglomerular nerve (GGN) activity was investigated in cats which were anesthetized, paralyzed and artificially ventilated. The activity of a few carotid chemoreceptor afferents from a slip or from the cut left carotid sinus nerve (CSN) and the activity of a few GGN fibers were recorded. The responses of the same chemoreceptor afferents to steady-state hypoxia at a constant paCO2 and to steady-state hypercapnia during hyperoxia were compared before and after the transection of the ipsilateral ganglioglomerular nerve (IGGN). Similarly the effects of IGGN transection on the responses of the same chemoreceptor afferents to graded doses of intravenous injections of sodium cyanide (20-60 micrograms) and nicotine (20-60 micrograms) at constant blood gas levels were studied. On the average, IGGN transection during normoxia only slightly changed the carotid chemoreceptor activity. Also, it did not significantly change the hypoxic and hypercapnic responses, and those to sodium cyanide and nicotine injections. Thus, the mean carotid chemoreceptor responses to physiological and pharmacological stimuli were largely independent of the GGN. However, certain GGN fibers were strongly stimulated by hypoxia and hypercapnia. Clearly, the total GGN traffic to the carotid body was not sufficiently strong to exert a significant control over the mean carotid chemoreceptor activity.
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PMID:Influence of ganglioglomerular nerve on carotid chemoreceptor activity in the cat. 395 Mar 26

We evaluated mechanisms underlying changes in discharge frequencies of medullary respiratory neurons. This evaluation was made by determining variations in antidromic latencies; these variations reflect changes in membrane potentials. In decerebrate, vagotomized, paralyzed, and ventilated cats, activities of the phrenic nerve and single respiratory neurons were monitored in hyperoxic normocapnia, hyperoxic hypercapnia, and/or normocapnic hypoxia. Axonal projections were defined as bulbospinal or laryngeal by antidromic activation. At normocapnic hyperoxia, antidromic latencies fell to minima during periods of spontaneous neuronal activity, with maxima occurring between neuronal bursts. In hypercapnia or hypoxia, these minima were not altered, whereas maximum latencies typically rose for neurons whose discharge frequencies increased. However, the increased frequencies most strongly correlated with increases in the difference between maximum and minimum latencies. No such correlation was evident for neurons whose discharge frequencies declined. We conclude that the overall change of membrane potential primarily defines neuronal discharge frequencies. Changes in membrane potentials induced by peripheral and central chemoreceptor afferents and by direct actions of hypercapnia and hypoxia are discussed.
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PMID:Changes in antidromic latencies of medullary respiratory neurons in hypercapnia and hypoxia. 405 99

1. The effects of moderate degrees of hypercapnia in hypoxia and in hyperoxia on the baroreceptor-cardiodepressor reflex have been studied in nine normal men.2. The beat-by-beat relation between pulse interval (I) and systolic pressure (P) during transient elevations of arterial pressure induced by intravenous injections of angiotensin II and phenylephrine was used to assess the sensitivity (DeltaI/DeltaP) and setting (I at a single reference arterial pressure) of the reflex.3. There was no consistent change in reflex sensitivity in any of the conditions studied.4. In hyperoxia (P(A, O2) approximately 200 torr) hypercapnia was associated with significant re-setting of the reflex in the direction of tachycardia. The extent of the re-setting was correlated with the degree of hypercapnia and with the accompanying increase in breathing.5. When hyperoxia with hypercapnia was replaced by hypoxia (P(A, O2) approximately 55 torr) with hypercapnia (which causes substantial arterial chemoreceptor activity), pulse interval at constant arterial pressure was further decreased.6. The tachycardia of hypoxia could not be accounted for by change of arterial pressure, P(A, CO2) or pulmonary ventilation, since it was most clearly demonstrable at constant values of pressure and either P(A, CO2) or ventilation.
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PMID:The effects of hypercapnia, hypoxia and ventilation on the baroreflex regulation of the pulse interval. 432 95

1. The effects of changes in ventilation and/or alveolar P(CO2) on the baroreflex control of heart rate have been studied in seven experiments on six young men and women who had been trained to control tidal volume and respiratory frequency at various levels independent of alveolar P(CO2), during hyperoxia.2. Intravenous phenylephrine provoked transient rises of directly measured arterial pressure during which individual systolic pressures (P) were linearly related to the following pulse interval (I). Baroreflex sensitivity was expressed as the slope of the regression of I on P, and reflex setting (I(ref)) as I at a single reference arterial pressure (= mean P for the experiment).3. Voluntary control of breathing had little effect on heart rate and arterial pressure (baroreflex setting), but diminished reflex sensitivity.4. Hypercapnia regularly caused tachycardia at the reference pressure (i.e. baroreflex setting lowered). The response was completely or partly reproduced by change of P(A, CO2) at constant ventilation in four subjects but not in two others; in them change of ventilation at constant P(A, CO2) completely mimicked the effect of free-breathing hypercapnia.5. Values of baroreflex sensitivity were relatively scattered. Hypercapnia caused a fall in baroreflex sensitivity in three subjects whether ventilation was fixed or free to rise. After separating the effect of voluntarily controlling ventilation, ventilation per se was without effect on reflex sensitivity.6. It is concluded that hypercapnia and hyperpnoea have separate effects on the baroreflex, the relative magnitudes of which differ from one subject to another. Baroreflex setting and sensitivity vary independently in response to change of ventilation and of P(A, CO2).
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PMID:The effects of raising alveolar PCO2 and ventilation separately and together on the sensitivity and setting of the baroreceptor cardiodepressor reflex in man. 444 70

1. Foetal breathing movements, electrocortical activity, arterial pressure and heart rate were recorded continuously in chronically catheterized sheep, 97-145 days pregnant.2. With increasing gestational age there was a fall in heart rate of 0.67 beats/day and a rise in arterial pressure of 0.46 mmHg/day.3. Hypoxaemia in the foetus was induced by allowing the ewe to breathe low oxygen mixtures, 9% O(2) with 3% CO(2) in N(2). In the younger foetuses there was an initial rise in heart rate whereas in the older foetuses there was a fall. After the end of hypoxia there was a persistent tachycardia in both groups. In the older foetuses there was a rise of arterial pressure.4. Two vagotomized older foetuses showed cardiovascular responses similar to those of the younger foetuses.5. Foetal breathing movements were abolished by hypoxaemia in twenty-two of twenty-five experiments. In the three exceptional experiments there was a small rise in P(a, CO2).6. The proportion of time occupied by low voltage electrocortical activity in the foetus was reduced by hypoxaemia.7. Hypercapnia was induced by giving the ewe 4-6% CO(2) with 18% O(2) in N(2) to breathe. After an initial slight fall the foetal heart rate increased and there was a small rise in foetal arterial pressure.8. The proportion of time occupied by low voltage electrocortical activity and breathing movements was increased by hypercapnia.9. Maternal hyperoxia, induced by giving 50% O(2) in N(2), did not significantly increase foetal breathing movements unless the ewe was in labour. In labour the foetuses had lower P(a, O2) values initially and a reduced incidence of foetal breathing, both of which were increased by maternal hyperoxia.
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PMID:Foetal respiratory movements, electrocortical and cardiovascular responses to hypoxaemia and hypercapnia in sheep. 447 94

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
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PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76


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