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

21 patients with cirrhosis of the liver and 24 control patients were studied before and after a protein load (120 g protein per day during one week). An EEG was recorded and a visual assessment of frequency pattern was performed. Venous admixture was estimated during hyperoxia. According to the EEG frequency pattern the patient group with cirrhosis was subdivided into those with EEG slowing after the protein load (n = 7) and those without (n = 14). The following results were obtained: 1) Resting arterial blood gases did not change in either group. 2) There was a significant increase of the AaD02 (difference between alveolar p02 and peripheral arterial p02) in cirrhotics and controls. 3) The increase in AaD02 was significantly larger in those cirrhotics showing EEG slowing compared to those without EEG - slowing or to the controls. 4) Fractional venous admisture increased significantly in those cirrhotics showing EEG slowing. There was no significant change in those patients who did not show EEG changes or in the controls.
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PMID:Changes of EEG and pulmonary venous admixture during a protein load in patients with cirrhosis. 0 Feb 41

To determine the role of hypoxic pulmonary vasoconstriction in pneumococcal pneumonia, hemodynamic measurements were made in 16 dogs before, and within 36 hours after, intrapulmonary administration of type III pneumococcus. Ten dogs with one lobe or more of pneumonia increased their pulmonary vascular resistances and slightly decreased their arterial O2 tensions. Hypoxia increased and hyperoxia decreased their pulmonary vascular resistances. During O2 breathing, arterial PO2 was less during than before the pneumonia and increased when pulmonary perfusion was diverted away from the diseased lung. In 2 dogs breathing air, forcing the cardiac output through the diseased lung caused an increase in vascular resistance that could clearly be reduced by O2 breathing. In 5 dogs, lung mast cell counts showed no decrease in the lobes with pneumonia. In pneumococcal pneumonia, the hypoxic pulmonary pressor mechanism serves to decrease blood flow to the diseased lobes and, thus, to maintain the arterial PO2. Lung mast cells could participate in this response.
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PMID:Preservation of hypoxic pulmonary pressor response in canine pneumococcal pneumonia. 0 Sep 35

It has been shown experimentally that a 30-day exposure of white rats to hypokinesia and moderate hyperoxia decreases elimination of ammonia and increases the formation and release into an enclosed atmosphere of carbon monoxide, aldehydes and ketones. The level of metabolism of prophyrin and nitrogen containing compounds as well as of fats and carbohydrates is higher during a combined effect of hypokinesia and moderate hyperoxia than during their separate influences.
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PMID:[Effect of hyperoxia and hypokinesia on the formation and excretion of gaseous metabolic products in rats]. 0 3

10 Blood acid-base changes were studied at 17 degrees C in immersed crabs (Carcinus maenas) exposed to hypoxic and hyperoxic conditions, by measuring the pH and the CO2 partial pressure, PbCO2, and by calculating the bicarbonate concentration. 20 Hyperoxia first induces a marked respiratory acidosis with a rise of PbCO2. This acidosis is compensated thereafter by a non-ventilatory increase of the blood buffer base concentration. These results are discussed in relation to the general problems concerning the control of the blood acid-base balance in aquatic animals.
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PMID:[Blood acid-base changes produced by variations of water oxygenation in the crab Carcinus maenas (author's transl)]. 0 15

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

The respiratory system is described as a feedback control system. The controller consists of the peripheral chemoreceptors and the central chemosensitive structures, the respiratory centre in the medulla oblongata and the thorax-lung pump which they drive. The controlled system is comprised of three compartments (lung, brain and the remaining tissue) connected by the blood circulation. The controlled values are arterial pH and arterial O2 partial pressure and cerebral extracellular pH. Earlier models have been improved by: (1) the dead space description, (2) the thermodynamic formulation of the CO2 dissociation equation and the simple but accurate O2 dissociation equation of the blood, (3) the alteration of the CO2 dissociation equation for the brain and the remaining tissue to accommodate recent results, (4) the application of the one-receptor-theory of central chemosensitivity, (5) the pH dependence of brain circulation, (6) the bicarbonate exchange between blood and extracellular fluid of the brain and (7) the introduction of variable circulation times. Respiratory and metabolic disturbances of the respiratory system are analyzed. The mathematical formulation of the respiratory system is a differential difference equation system. In the steady state the experimental results are reproduced fairly well. A slight discrepancy is found in the simulation of metabolic acidosis. Apparently we have assumed the sensitivity of the peripheral chemoreceptors to be too large so that the respiratory response is not correctly predicted. In the numerical solution there is an overshoot in the on-transient and a damped oscillation in the off-transient of the alveolar CO2 partial pressure during respiratory acidosis. We have varied the parameters to make deviations small. The best agreement seems to result, if the central threshold is near the normal extracellular pH of the brain. A further deviation from experimental findings is that the cerebral CO2 and H+ concentration, the blood circulation of the brain, the alveolar O2 partial tension and the ventilation show a slight oscillation in the off-transient. Except for these discrepancies the experimental results, especially the stability of the extracellular pH of the brain, are reproduced fairly well. During hypoxia there are deviations form the experimental results if the central residual activity is constant and the central threshold deviates from the normal extracellular pH of the brain. But if the central residual activity is pH dependent and if the central threshold is equal to the normal extracellular pH of the brain, then the time course of VE and the other variables agree fairly well with experimental results. There is also a good correspondence between the theoretical and experimental data during hyperoxia. During metabolic acidosis the time constant of the bicarbonate exchange between blood and extracellular fluid of the brain is important. If a time constant of one minute is assumed, then the predicted and the experimental results correspond sufficiently well.
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PMID:[Mathematical simulation of the respiratory system (author's transl)]. 1 39

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

A review of anatomical and biochemical responses of the lung to high concentrations of oxygen leads us to postulate a biphasic adaptive response. The early phase entails a defense against life-threatening pulmonary edema engendered by destruction of oxygen susceptible cells forming most of the air-blood interface. This defense is brought about by type II alveolar cell replication to reform a continuous epithelial layer in the alveoli; its success would depend upon the rapidly with which this continuity can be reestablished. Factors favoring a successful defense would include an initial large population of type II cells or the ability of type II cells to divide fast enough to reestablish continuity before of oxygen-sensitive cells (type 1 alveolar epithelial and endothelial cells) proceeds to fatal pulmonary edema; both conditions probably exist in young animals, which are known to be more resistant to hyperoxia than old animals. The second phase of adaptation would require the development of increased tolerance of previously susceptible cells to continued exposure to high oxygen concentrations to prevent their total destruction. We postulate that here the development of new biochemical defenses or the augmentation of those previously present would play a major role.
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PMID:Biochemical and anatomical adaptation of the lung to oxygen-induced injury. 2 61

At high altitude, in resting conditions, no differences have been observed between High Altitude Natives (HAN) and acclimatized Sea Level Natives (SLN) in AaDO2, aADCO2 or venous admixture. In acclimatized SLN, AaDO2 is smaller than at sea level because of: (1) The minor effect on arterial oxygenation of the probably constant venous admixture. (2) The reduction of VA/Q inequality as shown by a smaller aADCO2. In HAN, DLCO is greater than in SLN; the contribution of DM or VC in this difference remains unsettled, mainly because of the difficulties of measurement of DM and VC in HAN suddenly exposed to acute hyperoxia. In SLN, in acute hypoxia, DLCO increased transitorily. Asynchronous mechanisms of adaptation to high altitude are evoked.
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PMID:Pulmonary gas exchange, diffusing capacity in natives and newcomers at high altitude. 3 Jan 30

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


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