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

If 100% O2 produces hyperventilation by increasing central CO2 due to cerebral vasoconstriction or dimished reduction of oxyhemoglobin, then, there should be a parallel decrease in alveolar and CSF PCO2 during O2 breathing in neonates. To test this hypothesis, we measured ventilation, alveolar PCO2 and CSF PCO2, pH and HCO2 before and 10-20 min after infants began breathing 100% O2. With 100% O2, minute ventilation increased from 0.193 +/- (SE) 0.013 (n = 7) to 0.252 +/- 0.013 liter/min/kg (p less than 0.015), PACO2 decreased from 42 +/- 2 to 38 +/- 2 mm Hg (p less than 0.005), CSF PCO2 decreased from 51 +/- 1 to 44 +/- 1 mm Hg (p less than 0.015), and pH increased from 7.308 +/- 0.013 to 7.354 +/- 0.013 (p less than 0.05). CSF bicarbonate decreased, but not significantly. These findings, showing a trend toward alkalosis, suggest that the neonate, like the adult man, induces hyperventilation during hyperoxia via an increase in PCO2 at the central level.
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PMID:Effect of inhaling 100% O2 on ventilation and acid-base balance in cerebrospinal fluid of neonates. 677 Sep 13

An extracorporeal circulation in combination with a stop­flow technique was used to characterize the acid­base disequilibrium in the arterial blood of rainbow trout Oncorhynchus mykiss during environmental hypoxia, hyperoxia or hypercapnia. Arterial blood was routed from the coeliac artery through an external circuit in which pH (pHa), partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were monitored continuously. The stop­flow condition was imposed by turning off the pump which drove the external loop. Water PO2 or PCO2 was adjusted to give the experimental conditions by bubbling N2, O2 or CO2 through a water equilibration column supplying the fish. During normoxia, the arterial blood exhibited a positive acid­base disequilibrium of approximately 0.04 pH units; that is, pH increased over the stop­flow period by 0.04 units. The extent of the imbalance was increased significantly by hypoxia (final PaO2=2.7­3.7 kPa; deltapH=0.05 units). In fish exposed to hyperoxia (final PaO2=47­67 kPa), the direction of the disequilibrium was reversed; pHa declined by 0.03 units. During hyperoxia, CO2 excretion was impaired by 63 % and the PCO2 of postbranchial blood was higher than that of prebranchial blood. It is therefore conceivable that a reversal of the normal, outwardly directed, diffusion gradient for CO2 accounted for the negative disequilibrium; CO2 uptake at the gills would drive plasma CO2/HCO3-/H+ reactions towards CO2 hydration and H+ formation. During hypercapnia, fish exhibited a twofold increase in the positive pH disequilibrium (deltapH=0.06 units). The results of this study confirmed the existence of an acid­base disequilibrium in the arterial blood of rainbow trout and clearly demonstrated that the extent and/or direction of the disequilibrium are influenced by the respiratory status of the fish.
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PMID:THE EFFECTS OF HYPOXIA, HYPEROXIA OR HYPERCAPNIA ON THE ACID-BASE DISEQUILIBRIUM IN THE ARTERIAL BLOOD OF RAINBOW TROUT 931 84

The purpose of this study was to determine if baseline oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in brain tissue adjacent to an arteriovenous malformation (AVM) is different from measures in control patients. In addition, PO2, PCO2, and pH changes were measured during the course of AVM resection. Two groups were studied. Group 1 (n = 8) were non-ischemic patients scheduled for cerebral aneurysm clipping. Group 2 (n = 13) were patients undergoing neurosurgery for AVM resection. Following craniotomy, the dura was retracted and a PO2, PCO2, pH sensor inserted into non-ischemic brain tissue in Group 1. In Group 2, the sensor was inserted into tissue adjacent to the AVM. Following equilibration, tissue gases and pH were measured during steady state anesthetic conditions in Group 1 and during AVM resection in Group 2. The results show that under baseline conditions before the start of surgery, tissue PO2 was decreased in AVM compared to control patients but PCO2 and pH were not changed. During AVM resection, PO2 increased, PCO2 decreased, and pH increased compared to baseline measures. These parameters did not change in control patients over a similar time period. The results suggest that chronic cerebrovascular adaptation occur in AVM patients with decreased tissue perfusion pressure as an adjustment for decreased oxygen delivery. During AVM resection, this adaptation produces a hyperemic environment with relative tissue hyperoxia, hypocapnia, and alkalosis which is not corrected by the end of surgery.
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PMID:Increased brain tissue oxygenation during arteriovenous malformation resection. 1023 2

Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO(3) infusion for 48 h were used to create chronic respiratory (RA) or metabolic acidosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alkalosis, urine pH increased, and [titratable acidity (TA) - HCO(-)(3)] and net H(+) excretion became negative (net base excretion) with unchanged NH(+)(4) efflux. During RA, urine pH did not change, but net H(+) excretion increased as a result of a modest rise in NH(+)(4) and substantial elevation in [TA - HCO(-)(3)] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H(+) excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA - HCO(-)(3)] and a smaller elevation in phosphate but a sevenfold greater increase in NH(+)(4) efflux. In urine samples of the same pH, [TA - HCO(-)(3)] was greater during RA (reflecting phosphate secretion), and [NH(+)(4)] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and plasma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only alanine aminotransferase increased. The differential responses to RA vs. MA parallel those in mammals; in fish they may be keyed to activation of phosphate secretion by RA and cortisol mobilization by MA.
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PMID:Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis. 1044 55

Hyperoxia and alkalemia, as a result of pulmonary hyperventilation and elevation of plasma DNA (pDNA), are seen during the first 24 h after ischemic stroke. In this study we have examined the correlation between pDNA and these blood parameters in health and stroke. Acid-base equilibrium, oxygen status, hemoglobin affinity to oxygen and concentration of pDNA in arterial blood were measured after the intravenous injection of homologous long-chain DNA to healthy rats and rats subjected to common carotid arterial occlusion. In addition the effect of adding homologous DNA to human and rat venous blood samples was studied in vitro. Hyperoxia, alkalemia, and an increase in hemoglobin affinity to oxygen were seen in rats with artificial stroke. A marked decrease in pulmonary hyperventilation and hemoglobin affinity to oxygen was observed after injection of homologous genomic DNA (10(-6) g/mL of blood). After the DNA injection, blood gas measurement and concentration of pDNA were correlated. Addition of DNA at a concentration of 10(-7) g/mL to venous blood samples in vitro increased oxygen saturation that disappeared when the dose of the DNA increased 10-fold. Thus, a change of pDNA concentration or size can alter acid-base equilibrium, oxygen status, and oxygen transport. These results may be important for a better understanding of the mechanisms of stroke and other diseases associated with the elevation of pDNA concentration, and they open the possibility of new therapeutic approaches.
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PMID:Influence of plasma DNA on acid-base balance, blood gas measurement, and oxygen transport in health and stroke. 1883 60