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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

In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, lowered PaO2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolar PCO2 was uncontrolled or kept constant at the hyperoxic control. The V-PaO2 response was to a greater extent due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolar PCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, when PACO2 was not controlled, but a distinct decrease in ventilation, when PACO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, lowered PaO2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways--and possibly also to a lack of O2--, mainly shortening respiratory cycle duration.
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PMID:The role of the vagus nerves in the ventilatory response to lowered PaO2 with intact and eliminated carotid chemoreflexes. 57 48

Impedance plethysmography was used to measure resting cardiac stroke volume (SV) and thoracic conductive volume (TCV) in four divers at intervals during a prolonged dry saturation dive (17 days at 18.6 ATA and 7 days' decompression). Resting heart rate (HR), blood pressure (BP), and pulmonary minute ventilation (VE) were measured 4 times per day for the duration of the 30-day experiment. The vital capacity (VC) and its subdivisions IC and ERV were measured by spirometry every 3 days. In nonsmokers, VC fell significantly with time (r = 0.64), while VC in smokers increased nearly 400 ml during the first week at pressure before tending to fall with time. Compared to predive, the mean ERV was increased 629 ml at pressure, while VE and respiratory rate were not changed. The increased ERV did not persist postdive and was probably the result of the increased work of breathing a dense gas (4.1 g/liters). Residual volume (RV) measured by nitrogen dilution before and after the dive increased 38% and remained significantly increased (22%) even after one year in 4 divers. It is suggested that hyperoxia (0.3 ATA PO2) combined with increased gas flow resistance caused the VC to fall and RV to increase. The major cardiovascular findings were a transient bradycardia associated with increased stroke volume leading to a significant increase in resting cardiac output associated with an increased rate of rapid ventricular filling, TCV, and BP at depth. Lowering the ambient temperature for 3 days did not re-establish the bradycardia, suggesting that hyperbaric bradycardia is not due to a subtle cold stress.
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PMID:Hana Kai II: a 17-day dry saturation dive at 18.6 ATA. IV. Cardiopulmonary functions. 91 Mar 17

We asked what effects hyperoxia may have on the metabolic response to cold of the newborn rat. Whole body gaseous metabolism (VO2 and VCO2) was measured in 2-day old rats by open flow respirometry at ambient temperatures (Tamb) between 40 and 20 degrees C, changed at a rate of 0.5 degrees C/min during normoxia and hyperoxia (100% O2 breathing). In normoxia, the thermoneutral range was very narrow, at Tamb = 33-35 degrees C. A decrease in Tamb at first stimulated VO2; a further drop in Tamb below 28 degrees C reduced metabolic rate. The metabolic response to cold was not sufficient to maintain body temperature (Tb). In hyperoxia average values of VO2 were above the normoxic values at all Tamb, but the difference was mostly apparent at low Tamb; at 20 degrees C, hyperoxic VO2 averaged 73% more than in normoxia. This metabolic increase determined a significant but small rise of Tb. We conclude that in the 2-days-old rat hyperoxia has a stimulatory effect on metabolism which is Tamb-dependent, being much more apparent in the cold. This supports the concept that the normoxic VO2 of the newborn is limited by the supply of O2. However, the fact that in the cold, even in hyperoxia, VO2 did not reach very high values, and Tb was not maintained, suggests that not only O2 availability, but also the rate of O2 utilization limits the aerobic metabolic response of the newborn.
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PMID:Effects of hyperoxia on the metabolic response to cold of the newborn rat. 146 Feb 49

The causes of the adenosine monophosphate (AMP) deamination increase in rat brain mitochondria under conditions of hyperoxia, hypoxia and cold stress were studied. Data from the inhibitory analysis suggest that the increased intensity of AMP deamination under hypoxia is conditioned by the alterations in the substrate specificity of type A monoamine oxidase which acquires the ability to deaminate AMP. The enhancement of AMP deamination under hyperoxia and cold stress is due to the activation of true AMP deaminase in the mitochondrial fraction. The cytoplasmic AMP deaminase activity remains unchanged thereby. The effects of the AMP deaminase specific effectors, ATP and inorganic phosphate, were investigated.
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PMID:[Deamination of adenosine monophosphate in the rat brain in hyperoxia, hypoxia, and cold stress]. 152 39

Interactions between the control of thermogenesis and ventilation were studied during normoxia, hyperoxia, and ambient or CO hypoxia in adult anesthetized intact or carotid-denervated cats. Shivering, metabolic and ventilatory responses to cold stress were studied. In addition, the effects of transient pharmacological stimulation (NaCN) or inhibition (Dopamine) of arterial chemoreceptor activity were studied under different levels of oxygenation. In intact animals, cold exposure provoked increases in VO2 and ventilation which were directly proportional to the intensity of shivering. During ambient or CO hypoxia, VO2 was less than in normoxia for all values of shivering intensity, suggesting that a non-shivering thermogenesis component may also be inhibited by hypoxia. The decrease in VO2 was associated with a smaller decrease in ventilation in ambient than in CO hypoxia because of the presence of the chemoreflex drive during ambient hypoxia. Pharmacological changes in chemoreceptor activity induced transient and opposite changes in ventilation and shivering intensity, confirming their role in the control of thermogenesis. After carotid denervation, when the drug effects were inconsistent or absent, changes in levels of oxygenation were still followed by changes in shivering activity and associated changes in VO2 and ventilation. We conclude that control of thermogenesis and ventilation and their interaction may be mediated by chemoreceptors as well as by direct effects upon central, possibly diencephalic structures.
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PMID:Control of metabolic and ventilatory responses to cold in anesthetized cats. 160 55

Respiratory muscle EMG responses to transient, specific carotid body excitation (NaCN, hypoxia) and inhibition (dopamine, hyperoxia) were studied in 7 unanesthetized standing dogs while intact (N = 7) and during bilateral cold block of the vagi (N = 3). In all dogs carotid body excitation augmented the EMG activities of both expiratory muscles (triangularis sterni, TS; transversus abdominis, TA) and the (inspiratory) crural diaphragm (CR); carotid body inhibition significantly reduced phasic EMG activities in all muscles. With vagal blockade the response of the TS to carotid body stimulation was increased; that of the TA was essentially unchanged from the intact state. In all dogs expiratory muscle recruitment in response to carotid body excitation/inhibition could either precede or follow that of the CR. We conclude that in response to specific, transient carotid body excitation or inhibition: (1) Changes in CR, TS and TA EMGs are qualitatively similar. (2) Vagal feedback is strongly inhibitory to TS and excitatory to TA. (3) Changes in expiratory muscle EMGs do not require preceding changes in the CR. Carotid body stimulation contributes significantly to the generation of phasic expiratory activity during eupnea.
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PMID:The influence of carotid body chemoreceptors on expiratory muscle activity. 227 Mar 59

Oxygen consumption (VO2) and shivering movements were recorded in adult, conscious cats in a thermoneutral (24-27 degrees C) and in a cold (3-8 degrees C) environment during normoxia, hypoxia, or hyperoxia for 55 min. In the cold environment, VO2 correlated with shivering index (SI) under conditions of normoxia or ambient hypoxia (FIO2 = 0.12). During normoxia, VO2 was 63% higher in the cold than the thermoneutral environment. Ambient hypoxia acutely reduced VO2 in cold and thermoneutral environments, the decrement being greater for the former than the latter. Similarly, the variation in VO2 for unit change in SI was greater in hypoxia than normoxic conditions, suggesting that hypoxia influenced nonshivering as well as shivering components of cold-induced VO2. Hypoxia induced by CO (FICO = 0.002) also reduced VO2 and SI, a result that is consistent with previous results indicating that carotid body chemoreceptors do not mediate the suppression of shivering by ambient hypoxia. Hyperoxia increased VO2 and SI in the cold, and the effects of both hypoxia and hyperoxia in the cold were antagonized by increasing FICO2 to 0.03. The results demonstrate that hypoxia suppresses VO2 in the cold by reducing the intensity of shivering and, probably, by an action on metabolic rate that is unrelated to cold-induced calorigenesis.
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PMID:Effects of hypoxia on metabolic rate of conscious adult cats during cold exposure. 275 60

It has been established that white rats adapted to the low temperature of the environment (45 days 2-4 degrees C) in contrast to the animals undergoing such action during 3 days (cold stress) show resistance to the toxic action of the high oxygen pressure. The considerable removal of convulsions under the action of oxygen, the absence of increase of erythrocyte membrane permeability in the preconvulsive stage of hyperoxia and prevention of changes in the substrate specificity of type A monoamine oxidase both in preconvulsive and convulsive periods of oxygen intoxication are their characteristics.
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PMID:[Biochemical indices of the sensitivity of cold-adapted animals to hyperoxic exposure]. 343 32

The activity and kinetic properties of monoaminoxidase, the level of histamine and polyamines are studied under three extreme factors--hyperoxia, hypoxia and cold stress. The similarity of the metabolic responses of the organism to the investigated extreme factors is shown. All studied parameters indicate that the selected regime of hyperoxia has the most negative effect on the organism; hypoxia has the slightest effect and cold stress takes an intermediate position.
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PMID:[Monoamine oxidase activity and brain levels of histamine and polyamines in various extreme exposures]. 357 28


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