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

Crayfish, Astacus leptodactylus, for several hours breathed water equilibrated either with a hypoxic gas mixture, or air, or oxygen. The hydrostatic pressure in the right epibranchial cavity was recorded and the left epibranchial water sempled from time to time. The higher the water oxygenation, the less the duration of ventilation, the frequency of the scaphognathite beats which ensure water convection, the negative of the water hydrostatic pressure relative to ambient water pressure, and the respired water flow. The water convection per unit quantity of oxygen consumed decreased by a factor of about 20 when the animal passed from hypoxic water at PO2 of 72 torr to hyperoxic water at PO2 of 697 torr. Prolonged hyperoxia, up to 100 days, results in a hypercapnic acidosis of the prebranchial blood. pH decreased about 0.2 unit, PCO2 increased from 2.5 torr to a value of 6 torr, and [HCO-3] from 6 to a value of 9 meq-L-1. This hypercapnic acidosis remained uncompensated during several weeks exposure to hyperoxia. Observations on the fresh water crayfish, a marine crab, and several species of fish, suggest that in aquatic animals (1) the ventilatory activity depends greatly on the degree of water oxygenation: the higher the water oxygenation, the lower the ventilation; (2) the change of ventilation may be accompanied by a new equilibrium of the blood acid-base status, quite different from that observed in normoxia.
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PMID:Crayfish respiration as a function of water oxygenation. 1 99

In cats air embolism of the brain was produced by injecting 0.6 ml blood foam into the innominate artery proximal to the origin of both common carotid arteries. Air embolism caused transient ischemia of the brain, reaching a maximum within 1 min after injection. Resolution of the air embolism began a few minutes later and was completed within 15 min in the center and within 30 min in the border zone of the main supplying arteries. During this phase tissue perfusion was inhomogenous with reduced flow rates in some areas and reactive hyperemia up to 300% in others. This resulted in venous hyperoxia and a decrease of arteriovenous oxygen difference to as low as 2 ml/100 ml blood. Reactive hyperemia was accompanied by brain swelling and an increase in intracranial pressure from 3.6 +/- 1.2 to 12.3 +/- 2.0 mm Hg. The reason for hyperemia was a decrease of cortical pH which fell from 7.33 +/- 0.03 to 7.03 +/- 0.05, and which caused a dilation of pial arteries up to 260%. Immediately after embolism, the EEG flattened and oxygen consumption decreased. After normalization of flow, oxygen consumption returned to normal, but EEG only partially recovered. Air embolism had little effect on the water and electrolyte content of the brain, and produced very little damage to the blood-brain barrier.
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PMID:Arterial air embolism in the cat brain. 4 47

Recent data demonstrate that the magnitude of the heat loss that occurs from the respiratory tract during exercise correlates with the degree of post-exertional obstruction that develops in asthmatics. Respiratory heat loss relates directly to the minute ventilation and heat capacity of the inspired gas and inversely to its water content and temperature. Because it has been shown that inhaling 100% oxygen during exercise blunts the obstructive response, we wondered if this effect could be accounted for by differing values of heat exchange with air and oxygen breathing. To examine this question, we studied 10 asthmatics by measuring multiple aspects of pulmonary mechanics before and after four bouts of exhausting leg work during which the subjects inhaled either air or oxygen conditioned to provide widely differing thermal burdens on their airways. Under all inspired gas conditions, oxygen breathing produced significantly less obstruction than air. Minute ventilation was also significantly less with oxygen as was the total heat lost. As the latter fell, so did the magnitude of the postexercise obstruction. When the differences in ventilation and respiratory heat loss between air and oxygen were eliminated by eucapnic hyperventilation, the differences in the obstructive responses also disappeared. Thus, the effects of hyperoxia on exercise-induced asthma can be accounteed for solely by alterations in heat exchange.
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PMID:A critical assessment of the mechanism by which hyperoxia attenuates exercise-induced asthma. 45 67

Water-insoluble proteins of rat brain were studied as affected by hyperbaric oxygenation (oxygen pressure 6 at.ga. convulsion state). Solubilization of proteins under effect of hyperoxia and triton X-100 increases by 32-81%. Changes in the amino acidic composition of proteins extracted by 0.5% triton X-100 are characterized by an increase in the amount of aspartic acid, cystin, leucine and isoleucine and by a decrease in the amount of histidine, arginine and methionine. Electrophoresis in 7.5% polyacrylamide gel of proteins in the 0.5% triton X-100 extract showed changes in the number and mobility of protein bands.
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PMID:[Effect of hyperoxia on water-insoluble proteins of the brain]. 68 68

Rats (200-260 g) were exposed in sealed, recycling chambers continuously for 2-30 days to gas mixtures designed to maintain the same alveolar PO2 in the presence or absence of inert gas. Mixtures with inert gas (N2, He, or Ne) were at ground level; those without inert gas (100 percent O2) were in an altitude chamber. The O2 categories were: I-100 percent O2 at 747 torr; II-74 percent O2 + 26 percent inert and 566 torr 100 percent O2; III-47 percent O2 + 53 percent inert and 381 torr 100 percent O2; IV-21 percent O2 + 79 percent inert and 197 torr 100 percent O2. One of the two room-air controls was "restricted-fed" to the level of the lowest intake group. Measurements included body, pituitary, and thyroid weight, food and water intake, plasma volume and hematocrit, pituitary and plasma TSH, and plasma PBI. Severe depression in all variables and over 50 percent mortality was seen in I by day 4. All variables were depressed in II, but there was no mortality to 20 days. Pituitary-thyroid function appeared to be particularly sensitive to depression by hyperoxia, with plasma TSH levels reduced between 42 and 60 percent in II and III. No effect was attributable to the inert gas, whether it was N2, He, or Ne, nor was any specific effect traceable to the presence or absence of inert gas.
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PMID:Pituitary-thyroid function of rats in hypobaric oxygen-inert gas environments. 80 43

Prolonged exposure to hyperoxia can result in significant lung injury and has been associated with the development of bronchopulmonary dysplasia. Leukotrienes (LT) recruit polymorphonuclear leukocytes (PMN) to the lung, increase vascular permeability, and have therefore been postulated to play a role in the pathogenesis of hyperoxic lung injury. This study investigates ICI 198,615 (ICI), an LTD4 and LTE4 receptor antagonist in preventing hyperoxic lung injury in newborn rabbits. Matched littermates of 7-day-old rabbits received ICI (0.1 or 1.0 microM/kg/h) or vehicle alone, were exposed to greater than 95% O2, and sacrificed after 48, 72, 84 and 96 h of exposure. Bronchoalveolar alveolar lavage fluid (BAL) of the left lung was analyzed for white cell count, differential, absolute number of PMNs, total protein, and cyclooxygenase products 6-keto-PGF1 alpha, and thromboxane B2. Lung water was quantified utilizing the right lung. Results demonstrated no significant differences between the ICI groups or between the ICI groups and controls. In conclusion, the administration of the LTD4 and LTE4 receptor antagonist ICI 198,615 was insufficient to reduce the formation of pulmonary edema, reduce mortality or attenuate hyperoxic lung injury. These experiments suggest that a number of other mediators may be involved in the hyperoxic lung injury process and that the functional inhibition of a portion of the arachidonic acid cascade was not sufficient to either prevent or attenuate hyperoxic lung injury in newborn rabbits.
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PMID:Evaluation of a leukotriene receptor antagonist in prevention of hyperoxic lung injury in newborn rabbits. 131 78

Persistent pulmonary hypertension of the newborn (PPHN) characterised by right to left shunting with intense cyanosis is difficult to manage, and in the best of centres carries a 40-60 percent mortality. We report our one year's experience of managing six neonates with PPHN. There were 5 males and 1 female with mean birth weight of 2.59 +/- 0.487 kg and gestation period 39 +/- 2.0 wks and 1 minute Apgar score 2.8 +/- 2.1. Four to six babies were born by cesarean section and 3-6 babies had aspiration pneumonia. All babies presented within 12 hours of age (mean 5.08 +/- 5 hrs) with intense cyanosis and respiratory distress. Diagnosis were confirmed in all by (a) hyperoxia test, (b) simultaneous determination of preductal and postductal paO2 (c) contrast echocardiography and (d) hyperoxia-hyperventilation test. Babies were managed with hyperventilation using mean ventilatory rates of 100 +/- 45 per minute, an inspired oxygen concentration of 100%, peak inspiratory pressures 27 +/- 9 cm of H2O, and expiratory pressures 5 +/- 1.6 cms of H2O, and mean air way pressures of 10.4 +/- 2.7 cms H2O. Alkali therapy was used in 3 of the six babies whereas low dose dopamine was infused in all six babies. Inspite of aggressive ventilatory therapy, only 3 out of 6 babies could be salvaged.
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PMID:Persistent pulmonary arterial hypertension of the newborn. 134 Aug 63

Prolonged apnea and cardiovascular changes have been elicited in infant animals by the application of water to the laryngeal mucosa. Previous reports have produced conflicting evidence in regard to the possible role of arterial chemoreceptors in modulating this reflex. The present study was designed to determine the effect of carotid body stimulation or suppression on the duration of apnea and severity of cardiovascular changes in response to water in the larynx of piglets. The role of swallowing in terminating the apnea was also investigated. Hypoxia and isoproterenol, both carotid body stimuli, caused decreased apnea duration. Hyperoxia was associated with prolonged apnea duration; however, dopamine, which inhibits carotid body chemoreceptors, produced no significant change. Hypotension and bradycardia were only observed after prolonged apnea or chemoreceptor stimulation, supporting the concept that the cardiovascular component of the laryngeal chemoreflex is a result of changes in blood gas concentration rather than a direct response to laryngeal chemostimulation. The interval between water application and initiation of swallowing was not significantly affected by hypoxia or carotid body stimulation and swallowing did not always occur before resumption of breathing.
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PMID:Arterial chemoreceptor influences on the laryngeal chemoreflex. 147 Apr 57

The effect of hyperoxia on the arousal response to airway occlusion during non-rapid eye movement (NREM) sleep was studied in six normal male subjects with a mean age (+/- SD) of 23.5 +/- 8.7 yr by testing the response to the occlusion of a face mask covering the nose and mouth. Occlusion trials while the subjects breathed room air (room air condition) were alternated with trials in which subjects breathed a mixture of room air and oxygen adjusted to maintain a sleeping baseline arterial oxygen saturation of 98% (hyperoxic condition). The time to arousal (mean +/- SEM) was significantly longer during oxygen administration (4.1 +/- 4.5 versus 28.9 +/- 4.6 s; p < 0.002). The maximal deflections in airway pressure were measured at a supraglottic location during airway occlusion to reflect the degree of inspiratory effort. The maximal airway suction pressure preceding arousal did not differ between the room air (27.4 +/- 5.4 cm H2O) and hyperoxic conditions (26.6 +/- 5.9 cm H2O). Conversely, the rate of increase in inspiratory effort (maximal pressure) during occlusion was decreased by oxygen administration. We conclude that hyperoxia prolongs the time to arousal after airway occlusion by decreasing the rate of increase in the magnitude of inspiratory efforts, but it does not change the arousal threshold.
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PMID:Effect of hyperoxia on the arousal response to airway occlusion during sleep in normal subjects. 148 20

Cardiopulmonary responses to prolonged hyperoxia and their relationships to the development of lung pathology have not been fully characterized in primates. In this study, circulatory hemodynamics and pulmonary function, vascular permeability, and leukocyte sequestration were measured in male baboons after 100% O2 exposure and related to ultrastructural changes of lung injury by electron microscopy. Three groups of animals were exposed to 100% O2 in an exposure cage for 40, 66, and 80 h, respectively. A fourth group of animals was exposed in a cage for 80 h and then anesthetized and ventilated with 100% O2 for additional time. These animals were exposed for a total duration of 110 h or until death from the injury. Physiological responses to hyperoxia were characterized by decreases in total lung capacity and inspiratory capacity at 80 and 110 h. A significant increase in pulmonary leukocyte accumulation was noted by 80 h. Extravascular lung water and permeability surface-area product increased at 80 and 110 h. Cardiac output and stroke volume also decreased, and systemic vascular resistance increased after 80 and 110 h of hyperoxia. Histopathological changes were present in the lungs of all but the 40-h exposure group. Animals exposed for 66 h showed endothelial injury and neutrophil accumulation. By 80 h, animals showed endothelial cell destruction, interstitial edema, and type I cell injury. At 110 h, animals showed substantial destruction of endothelial and type I epithelial cells, exposure of alveolar basement membrane, congestion of capillaries, and substantial interstitial edema. The data indicate that histological changes by electron microscopy precede physiological responses to hyperoxic pulmonary injury in baboons by as much as 14 h and that the physiological responses to early hyperoxic injury are relatively insensitive to the pathological injury.
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PMID:Responses of baboons to prolonged hyperoxia: physiology and qualitative pathology. 177 33


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