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

In six healthy male volunteers at sea level (PB 747-759 Torr), we measured pH and PCO2 in cerebrospinal fluid (CSF), and in arterial and jugular bulb blood; from these data we estimated PCO2 (12) and pH for the intracranial portion of CSF. The measurements were repeated after 5 days in a hypobaric chamber (PB 447 Torr). Both lumbar and intracranial CSF were significantly more alkaline at simulated altitude than at sea level. Decrease in [HCO3-] IN lumbar CSF at altitude was similar to that in blood plasma. Both at sea level and at high altitude, PCO2 measured in the lumbar CSF was higher than that estimated for the intracranial CSF. At altitude, hyperoxia, in comparison with breathing room air, resulted in an increase in intracranial PCO2, and a decrease in the estimated pH in intracranial CSF. With hyperoxia at altitude, alveolar ventilation was significantly higher than during sea-level hyperoxia or normoxia, confirming that a degree of acclimatization had occurred. Changes in cerebral arteriovenous differences in CO2, measured in three subjects, suggest that cerebral blood flow may have been elevated after 5 days at altitude.
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PMID:Alkaline shift in lumbar and intracranial CSF in man after 5 days at high altitude. 0 73

In peripherally chemodenervated and vagotomized cats and rabbits, either spontaneously breathing or artificially ventilated, we studied the reaction of the respiratory control system to changes in the extracellular fluid (ECF) pH at the ventral surface of the medulla oblongata. The brainstem ECF-pH was varied either by alternating periods of hypoxia and hyperoxia or by intravenous infusion of lactic acid to achieve endogenous or exogenous lactacidosis, respectively. Additionally, the arterial PCO2 was changed by varying the inspiratory CO2-fraction or the respirator's pumping rate. When pulmonary ventilation or central respiratory drive (in terms of phrenic nerve activity) was related to brainstem ECF-pH, no unique function resulted for respiratory (CO2-induced) and metabolic (lactic acid induced) acid-base changes, thus contradicting the "reaction theory" for central respiratory chemosensitivity. Under steady state conditions, there was no ventilatory reaction to endogenous or exogenous metabolic brainstem acidosis at all. However, the apneic threshold was shifted towards the acid range, although the sensitivity of the respiratory system to CO2 remained nearly unchanged, no matter whether CO2 was inhaled or increased by acetazolamide. This points to a dominating role of CO2 or at least carbonic acid over fixed acids for the central chemosensitive control of pulmonary ventilation.
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PMID:Hypoxia and the "reaction theory" of central respiratory chemosensitivity. 128 96

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

Reported is a system of apparatures to control characteristic changes of cardiorespiratory function during different methods of endoscopic ventilation. The aim of the study is to measure and record simultaneously and continuously ECG, thoracic movement, tracheal pressure, pulmonary artery pressure and arterial oxygen pressure using transcutaneous technique. Measurements of arterial blood pressure and blood gas analysis (PaO2, PaCO2, BE, HCO3-, pH) are carried out in intervals. Four different methods of injector-ventilation are compared with the conventional laryngoscopic ventilation on the basis of a test program. Laryngoscopic ventilation as well as injectorventilation by CARDEN-Tubus make it possible to achieve a hyperoxaemic situation by normofrequent ventilation. Despite of hyperventilation it is not possible in every case to achieve an increased capillary oxygen pressure of 200 to 300 mm Hg by injector-ventilation with Venturi effect because of a smaller oxygen proportion. In jet-ventilation with N2O/O2-mixture (3:1) there is no appreciable hyperoxia, but a small reduction of systemic arterial blood pressure. With all techniques of mechanical respiration usual middle intratracheal pressure of respiration was not exceeded. Traumatic pressure of jets was only indirectly shown in steep rises of pressure by the applied technique of measurement.
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PMID:[Monitoring respiratory and circulatory parameters in comparing various jet ventilation procedures]. 211 91

The purpose of this study is to examine effects of hyperoxic gas mixtures on changes of blood indices during bicycle exercise of human. Oxygen-enriched gases (30% O2) were inspired during the ramp load exercise of 25 watt/min. Changes of blood indices were analyzed with Sequential Multiple Analyzer with the computer (SMAC). The improvement of exercise performance were discussed about relationship between function of hyperoxic gas and physiological mechanism. Three experimental conditions were set as follows (I) 30% O2 +N2 gases balance, (II) air (21% O2), and (III) 30% O2 +2% CO2 +N2 gases balance. Arterial blood were sampled from the radial artery of the forearm in order to analyze following items; 1) pH level, PaO2, PaCO2, and HCO3 of these blood gases, 2) Blood sugar, TG, and F-CH of the blood contents, 3) red blood corpuscle, white blood corpuscle, Hb, and Ht values, 4) LDH, CK, GOT, and GPT of the blood enzymes, 5) TP, ALB, Na, K, Ca and Cl of the electric ions. In the case of inspiring hyperoxic gases, the recovery rate of blood indices increased after this ramp load exercise remarkably, and the whole exercise metabolism were removed from acidosis tendency to alkalosis value of the resting condition significantly. At hyperoxic experimental conditions, the blood sugar and oxygen consumption were much more decreased than these at normal oxygen content one during both states of exercise and recovery times. These data of the blood indices would support strongly to the hypothesis that improvement of oxygen delivery should be depended upon the enhanced performance with the hyperoxic gases. There might be effects of the hyperoxia on the cellular metabolism and on function of the vascular muscle during those aerobic exercise.
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PMID:[Effects of breathing high concentrations of oxygen on changes in blood indices during bicycle exercise]. 238 13

In the unanesthetized dogfish, Scyliorhinus canicula, oxygen and carbon dioxide partial pressures and concentrations in inspired and expired water and the acid-base balance of arterial blood, pHa and PcCO2, were determined. Each dogfish was exposed to waters differing in oxygenation and in CO2 levels, which was controlled with a pH-CO2-stat device, for successive 2- to 3-h periods. The four ambient conditions were: normoxia-normocapnia (inspired PO2, PIO2 ca 160 Torr; PICO2 ca 0.3 Torr), hyperoxia-normocapnia (PIO2 ca 730 Torr), hyperoxia-hypercapnia (PICO2 ca 1.0 Torr); normoxia-hypercapnia. At both low and high ambient CO2, the inspired-expired O2 and CO2 concentration differences increased in hyperoxia. Ventilation was depressed, and concomitantly, PACO2 increased and the arterial plasma pH decreased. The hypercapnic acidosis was rapidly but only partially compensated by an increase of the plasma bicarbonate concentration. Due to the buffer action of carbonate in sea water, low and high ambient CO2 levels corresponded respectively to high and low values of the CO2 capacitance coefficient, betaWCO2. At both ambient oxygenation levels, the expired-inspired PCO2 difference was greater at low than at high betaWCO2. At a given ambient CO2 level, expired PCO2, PECO2, wash higher in hyperoxia than in normoxia; an effect more marked at low than at high betaWCO2. Thus, the water capacitance coeffcient betaWCO2 is an important factor determining PECO2 values and probably arterial blood acid-base balance. As a general conclusion, the acid-base balance of the arterial blood in the dogfish is very much dependent on the conditions of the oxygenation and acid-base balance of the ambient water which consequently should be carefully controlled.
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PMID:Blood acid-base balance as a function of water oxygenation: a study at two different ambient CO2 levels in the dogfish, Scyliorhinus canicula. 677 56

Six subjects rode a bicycle ergometer on three occasions breathing 17, 21, or 60% oxygen. In addition to rest and recovery periods, each subject worked for 10 min at 55% of maximal oxygen uptake (VO2 max) and then to exhaustion at approximately 90% VO2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, and pH were measured. VO2, carbon dioxide output, [H+]a, and [HCO3-]a were calculated. Performance times were longer in hyperoxia than in normoxia or hypoxia. However, VO2 was not different at exhaustion in normoxia compared with hypoxia or hyperoxia. During exercise, hypoxia was associated with increased lactate levels and decreased [H+]a, PCO2, and [HCO3-]a. The opposite trends were generally associated with hyperoxia. At exhaustion, [H+]a was not different under any inspired oxygen fraction. These results support the contention that oxygen is not limiting for exercise of this intensity and duration. The results also suggest that [H+] is a possible limiting factor and that the effect of oxygen on performance is perhaps related to control of [H+].
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PMID:Oxygen uptake, acid-base status, and performance with varied inspired oxygen fractions. 677 81

Hemolymph acid-base variables (pH, PCO2 and CCO2), hemolymph Ca2+ and Na+ concentrations, and osmolality were measured in unrestrained crabs, Cancer productus, before, during and following 4 hr emersion and 43 hr hyperoxia (460-510 Torr), both at 10 degrees C. Emersion and hyperoxia provoked an acidosis associated with elevation of hemolymph CCO2 and PCO2, yet attempts to calculate PCO2 from measured pH and CCO2 always resulted in values greater than those measured directly. This discrepancy between measured and calculated PCO2, was associated with base excess, and was eliminated upon in vitro equilibration of the hemolymph and more slowly in vivo, suggesting that metabolic compensation for the acidosis occurred more rapidly than could acid-base equilibration. During emersion, increases of CCO2 and [Ca2+] provide evidence that the internal CaCO3 stores, possibly from the exoskeleton, were mobilized during acid-base compensation. Hyperoxia provoked no such increase in Ca2+, and branchial uptake of HCO3- may make a major contribution to the elevation of CCO2 during hyperoxia. It is suggested that shell buffering by aquatic crustaceans provides a means of compensation for acidosis under conditions during which branchial function is impaired.
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PMID:Non-equilibrium acid-base status in C. productus: role of exoskeletal carbonate buffers. 678 8

Blood acid-base balance, blood gases, respiration, ventilation, and renal function were studied in the rainbow trout during and following sustained environmental hyperoxia (PIO2 = 3.50-650 Torr). Animals were chronically fitted with dorsal aortic cannulae for repetitive blood sampling, oral membranes for the measurement of ventilation, and bladder catheters for continuous urine collection. Hyperoxia caused a proportional increase in arterial O2 tension and a stable 60% reduction in ventilation volume (Vw), the latter mainly due to a decrease in ventilatory stroke volume. O2 consumption exhibited a short-term elevation. Arterial CO2 tension (PaCO2) rose within 1 h, causing an immediate drop in arterial pH (pHa), and continued to increase gradually thereafter, reaching a value 2-4x the normoxic control level after 96-192 h. Compensation of the associated acidosis by the accumulation of [HCO3-] in the blood plasma started within 5-6 h, and was complete by 48 h. Therefore, further compensation occurred simultaneously with the gradual rise in PaCO2. The kidney played an important active role in this compensation by preventing excretion of the accumulated [HCO3-]. Upon reinstitution of normoxia, PaCO2 dropped to control levels within 1 h, and restoration of blood acid-base status by reduction of [HCO3-] had commenced by this time. A complete return to control values occurred within 20 h. During hyperoxia, an experimental elevation of the depressed Vw above control normoxic levels caused only a minor and transient reduction in PaCO2 and no change in pHa, but injection of branchial vasodilator 1-isoprenaline (10 mumol/kg) produced a large drop in PaCO2 and rise in pHa. It is concluded that the rise in PaCO2 during hyperoxia is mainly due to internal diffusive and/or perfusive limitation associated with branchial vasoconstriction, rather than to external convective limitation associated with the decreased Vw.
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PMID:Blood acid-base regulation during environmental hyperoxia in the rainbow trout (Salmo gairdneri). 678 12

When mixed venous blood is oxygenated in alveolar air with higher PCO2, the PCO2 within the red cell is though to exceed the alveolar PCO2 due to the Haldane effect and to block the inward CO2 diffusion. If the direction of the CO2 diffusion is not reversed during the contact time, the HCO2-gain in the plasma will not exceed the amount estimated from venoalveolar PCO2 difference by using a CO2 dissociation curve of separated plasma. In order to clarify the validity of the above thought, the venoarterial CO2 content difference was measured by using a van Slyke apparatus and a PCO2 electrode at various alveolar PCO2 levels in rebreathing dogs. The HCO3-rise in the whole blood was obviously reduced when acute hypercapnia was administered in both normoxia and hyperoxia. Quantitatively, the decrease of CO2 content under hypercapnia corresponded to the difference in CO2 content between the true and separated plasma. The reduction, however, was slightly stronger in normoxia than in hyperoxia with alveolar PO2 of 300 to 420 mmHg. These data seem to support the following explanation: When venous blood was oxygenated in normoxic air with PCO2 higher than true venous, the inward CO2 diffusion was inhibited by the Haldane effect and the reversed diffusion after the oxygenation could also be disregarded during the contact time. Because the oxygenation was accelerated in hyperoxia and the direction of the CO2 diffusion was reversed earlier than in normoxia, the plasma CO2 content became higher in hyperoxia than in normoxia.
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PMID:Relationship between venoarterial CO2 content difference and venoalveolar PCO2 difference in acute hypercapnia in dogs. 679 75


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