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

Hyperoxia has been shown to disrupt certain membrane bound enzyme systems within the pulmonary endothelium which are responsible for the metabolism of several endogenous vasoactive compounds. This study was to evaluate whether the potential disruption of the prostaglandin dehydrogenase/reductase and angiotensin converting enzymes, as a consequence of hyperoxia, would alter the activation/deactivation of prostaglandins or the angiotensins (I and II) and thereby alter their peripheral cardiovascular actions. Two groups of anesthetized dogs, one group ventilated with ambient air and the other with 100% oxygen, were given bolus injections of angiotensin I, angiotensin II, prostaglandin E2, sodium nitroprusside, and phenylephrine before and during 8 h of exposure to air or oxygen. The hyperoxic animals demonstrated a significant increase in mean arterial pressure responsiveness to both angiotensin I and angiotensin II. The responsiveness to the drugs increased by 41% for angiotensin I and 43% for angiotensin II. The ambient air control dogs showed no significant changes for any compounds tested. These data indicate that with 8 h of hyperoxia the renin-angiotensin system's ability to influence cardiovascular function is augmented, whereas, the hemodynamic effects of prostaglandins are unaltered.
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PMID:Effects of 100 percent oxygen on the cardiovascular responses to vasoactive compounds in the dog. 386 38

The dependence of the carotid chemoreceptor responses to blood-borne stimuli on the ganglioglomerular nerve (GGN) activity was investigated in cats which were anesthetized, paralyzed and artificially ventilated. The activity of a few carotid chemoreceptor afferents from a slip or from the cut left carotid sinus nerve (CSN) and the activity of a few GGN fibers were recorded. The responses of the same chemoreceptor afferents to steady-state hypoxia at a constant paCO2 and to steady-state hypercapnia during hyperoxia were compared before and after the transection of the ipsilateral ganglioglomerular nerve (IGGN). Similarly the effects of IGGN transection on the responses of the same chemoreceptor afferents to graded doses of intravenous injections of sodium cyanide (20-60 micrograms) and nicotine (20-60 micrograms) at constant blood gas levels were studied. On the average, IGGN transection during normoxia only slightly changed the carotid chemoreceptor activity. Also, it did not significantly change the hypoxic and hypercapnic responses, and those to sodium cyanide and nicotine injections. Thus, the mean carotid chemoreceptor responses to physiological and pharmacological stimuli were largely independent of the GGN. However, certain GGN fibers were strongly stimulated by hypoxia and hypercapnia. Clearly, the total GGN traffic to the carotid body was not sufficiently strong to exert a significant control over the mean carotid chemoreceptor activity.
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PMID:Influence of ganglioglomerular nerve on carotid chemoreceptor activity in the cat. 395 Mar 26

Our earlier studies have shown that local cortical blood flow (CoBF) in the rabbit has been autoregulated in a narrow range of mean arterial blood pressure (MABP) and autoregulation of cortical oxygen tension (bPO2) has been maintained in a wider range (75-110 mmHg) than that of CoBF. In the present studies, bPO2, NAD/NADH redox state, and CoBF were measured under the various conditions of hypoxia and hyperoxia to discuss the critical level of cortical oxidative metabolism and autoregulation of CoBF in relation to oxidative metabolism. New Zealand white rabbits were anesthetized with pentobarbital sodium intraperitoneally and paralyzed with gallamine triethiodide intravenously. They were ventilated artificially maintaining normal blood gas analysis. NAD/NADH redox state was measured with a compensated fluorometer with a reflectance device to correct for hemodynamic artefacts and bPO2 was monitored continuously with the polarographical method. They were measured simultaneously. CoBF was monitored with the thermal diffusion cerebral blood flow monitor of Flowtronics. Hypoxia and hyperoxia were produced by decreasing or increasing the inspired oxygen concentration. Arterial blood samples were obtained for blood gas determination before and during the episode of hypoxia or hyperoxia. A definite reduction of NADH began at a 50% decrease of PaO2. It corresponded to 70 mmHg of PaO2. Below 50% decrease of PaO2, NADH was reduced largely. This was statistically significant (p less than 0.01). Although, the oxidation of NADH occurred in the moderate hyperoxic state, no oxidation of NADH occurred more than 6.1% of full scale even in the condition of higher PaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of hypoxia and hyperoxia on cortical oxidative metabolism in relation to cerebral blood flow autoregulation]. 396 89

Microwaves (2450 MHz) are shown to increase 22Na permeability of rabbit erythrocytes for exposures only within the narrow temperature range of 17.7 to 19.5 degrees C (Tc) which coincides with a nonlinearity in the Arrhenius plot reflecting an apparent membrane phase transition. Significantly, this response is not observed for cholesterol-loaded erythrocyte membranes which exhibit a linear Arrhenius plot and no apparent phase transition at Tc. The permeability increase at Tc is a nonlinear function of absorbed power but is a linear function of the internal electric field strength of the sample and saturates at approximately 400 mW/g and 600 V/m, respectively. The permeability increase was found to be reversible and transient in that immediately following termination of exposure sodium influx is significantly reduced but returns to normal within 60 min. Extracellular factors exert a significant influence on the microwave effect. The presence of plasma markedly potentiates the increase in 22Na permeability at Tc. Oxygen also modulates the microwave effect with relative hypoxia (5 mm Hg) and hyperoxia (760 mm Hg) enhancing the permeability increase. In contrast, the presence of two antioxidants, ascorbic acid or mercaptoethanol, inhibits the effect. These findings raise important questions about the physical and chemical nature of microwave interactions with cell membranes and also shed light on earlier studies reporting either positive or negative effects on membrane permeability.
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PMID:Microwaves and the cell membrane. II. Temperature, plasma, and oxygen mediate microwave-induced membrane permeability in the erythrocyte. 407 May 42

The sensitivity of the brain to cyanide-induced histotoxic hypoxia and the protective effects of known cyanide antagonists, have been assessed in vivo by reflectance spectrophotometry. Cyanide-related changes in cytochrome a,a3 (cytochrome c oxidase) oxidation-reduction (redox) state, tissue hemoglobin saturation, and local blood volume were continuously monitored in cerebral cortex of rats. Noncumulative, dose-dependent inhibition of the in situ mitochondrial respiratory chain was evaluated directly by measuring increases in reduction levels of the terminal oxidase. These transient cytochrome a,a3 reductions were accompanied by increases in regional cerebral hemoglobin saturation and blood volume. Cytochrome redox responses were not altered either in magnitude or kinetics by hyperoxia; however, the cyanide-cytochrome dose-response curve was greatly shifted to the right by pretreatment with sodium nitrite, and the recovery rate of cytochrome a,a3 from cyanide-induced reduction was enhanced fourfold by pretreatment with sodium thiosulfate.
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PMID:Cyanide-induced cytochrome a,a3 oxidation-reduction responses in rat brain in vivo. 631 56

Hyperbaric air and hyperbaric hyperoxia, which have been shown to decrease both liver plasma flow and plasma volume in dogs, may potentially affect the disposition of drugs whose distribution and/or elimination are dependent upon those actions. This study examined the effects of those conditions on the disposition of salicylic acid, using the dog as a model. The drug was administered to six mixed-breed dogs as a 10 mg sodium salicylate/kg i.v. bolus at 1 ATA breathing air (control), at 2.8 ATA breathing 100% O2, and at 6 ATA breathing air, followed by serial blood sampling for 8 h. Statistical analysis showed a significant increase (p less than 0.05) in salicylate clearance at 2.8 ATA compared to control with a subsequent, although not statistically significant, increase in elimination half-life. There were no significant differences between the values observed at 6 ATA and either control or 2.8 ATA. As 100% O2 at 2.8 ATA is used during hyperbaric oxygen medical therapy and during decompression, this change in disposition of this commonly used agent may have implications in man. Studies in man must be conducted, however, to determine if the same conclusions apply.
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PMID:Salicylate pharmacokinetics in the dog at 6 ATA in air and at 2.8 ATA in 100% oxygen. 662 74

Plasma ionic status and renal excretion of acidic equivalents and electrolytes were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control); 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. Plasma [Cl-] progressively declined in approximate equivalence to the rise in [HCO-3] which compensated the respiratory acidosis of hyperoxia, while [Na+] increased only slightly. [Ca2+] and [K+] rose, [phosphate] declined, and [NH+4] was unchanged. During normoxic recovery, the [Na+], [Cl-] and [HCO-3] changes were reversed, [K+] and [Ca2+] showed further elevations, and [NH+4] increased sharply . Renal acid output increased greatly during hyperoxia with elevations in both NH+4 and titratable components, though the latter predominated due to a marked elevation of phosphate excretion. Renal efflux rates of other electrolytes were generally homeostatic for ECF composition, with increased Na+, K+, and Ca2+ effluxes, and decreased Cl- efflux. Clearance calculations indicated that net tubular reabsorption increased for Cl-, fell for Na+ and K+, and changed over to marked net secretion for phosphate, while net ammonia secretion increased. Most trends were reversed upon return to normoxia. The critical role of phosphate in urinary electrolyte balance and acid-base regulation is emphasized. The net renal excretion of acidic equivalents accounted for only 7-10% of the total compensation observed for the whole animal during hyperoxia. The kidney contributed primarily in conserving ECF HCO-3 and secondarily in balancing branchial exchanges.
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PMID:The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. II. The role of the kidney. 672 70

Fluxes of both acidic equivalents (JH+net) and electrolytes across the gills were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control), 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. A highly negative JH+net (i.e., excretion) was responsible for over 90% of the compensation of respiratory acidosis induced by hyperoxia in the whole animal. Similarly, a highly positive JH+net (i.e., uptake) accounted for virtually all the compensation of metabolic alkalosis induced by normoxic recovery. Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was associated with large net losses of Na+ and net gains of Cl-, effects reflected in ECF composition. Unidirectional flux analyses with radiotracers (22Na, 36Cl) demonstrated that these net flux alterations resulted from rapid and complex changes in both influx and efflux components such that the difference between JNa+net and JCl-net was stoichiometrically equivalent to JH+net. The results support the concept that Na+ vs acidic equivalent (H+, NH+4) and Cl- vs basic equivalent (HCO-3, OH-) exchanges at the gill are dynamically adjusted in order to correct internal acid-base disturbances.
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PMID:The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. III. Branchial exchanges. 672 71

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

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.
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PMID:Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat. 681 27


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