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

This study examined the effects of hyperoxic training on specific cardiorespiratory and metabolic responses. A group of 19 male subjects trained for 5 weeks on a cycle ergometer at 70 percent of hyperoxic or normoxic maximal heart rate, the hyperoxic group (HG) breathing 70 percent O2, the normoxic group (NG) breathing 21 percent O2. The subjects were tested pre- and post-training under both hyperoxia and normoxia. Measurements included cardiac output (Q(c)), stroke volume (SV), heart rate (HR), pulmonary ventilation (V(E)), oxygen consumption (VO(2)), partial pressure of oxygen (PO(2)), partial pressure of inspired carbon dioxide (PCO(2)), blood lactate concentration [La], and fiber type composition. The V(E) was significantly lower at submaximal work rates (P <0.05) and maximal V(E) increased after training in both groups for both test conditions; hyperoxic V(E) was lower than normoxic V(E) (P <0.05). The maximal V0(2) increased significantly (P <0.05) in both groups for both tests and was 11 percent - 12 percent higher during hyperoxia. Post-training maximal heart rate (HR(max)) was significantly decreased (P <0.05) at the same absolute work rate regardless of the training group or test type. The SV was increased at each work rate and Q c was unchanged. The maximal Q(c) increased significantly (P <0.05) for both groups and types of test: for normoxia: NG 27.3-30.41*min(-1) and HG 30.3-32.31*min(-1) and for hyperoxia: NG 24.7-25.6 and HG 27.9-31.21*min(-1). Although working at the same intensity relative to HR(max), HG showed significantly lower [La] following a single training session, yet maximal values were unchanged after training. Both groups showed a significant increase in the percentage of type IIA fibers post-training but HG retained a larger percentage of IIB fibers. Mitochondrial enzymes; citrate kinase, 3-hydroxyacyl CoA dehydrogenase, and cytochrome c-oxidase were increased in the normoxic trained subjects (P <0.05). In summary, training induced adaptive responses in maximal aerobic power, HR, SV, Q(c), [La], and muscle fiber type composition, independent of inspired PO(2). Intramuscular data suggested there may be some differences between hyperoxic and normoxic training and these were substantiated by mitochondrial enzyme and lactate findings. Our data would suggest that transport mechanisms may limit the ability to increase aerobic power.
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PMID:Cardiorespiratory and metabolic adaptations to hyperoxic training. 886 67

Owing to their small size and hovering locomotion, hummingbirds are the most aerobically active vertebrate endotherms. Can hyperoxia enhance the flight performance of this highly oxygen-dependent group? Hovering performance of ruby-throated hummingbirds (Archilochus colubris) was manipulated non-invasively using hyperoxic but hypodense gas mixtures of sea-level air combined with heliox containing 35% O2. This manipulation sheds light on the interplay among metabolic power input, mechanical power output and aerodynamic force production in limiting flight performance. No significant differences in flight mechanics and oxygen consumption were identified between hyperoxic and normoxic conditions. Thus, at least in the present experimental context, hyperoxia did not change the major metabolic and mechanical parameters; O2 diffusive capacities of the respiratory system were probably not limiting to a significant extent. Compared with hummingbirds in our previous studies, the present experimental birds were heavier, had resultant shorter hover-feeding durations and experienced aerodynamic failure at higher air densities. Because hummingbirds have relatively stable wingbeat frequencies, modulation of power output was attained primarily through variation in stroke amplitude up to near 180 degrees. This result indicates that maximum hovering performance was constrained geometrically and that heavier birds with greater fat loads had less margin for enhancement of power production. Sexual dimorphism in flight adaptation also played a role, with males showing more limited hovering capacities, presumably as a trade-off for increased maneuverability.
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PMID:Hummingbird hovering performance in hyperoxic heliox: effects of body mass and sex. 911 Sep 57

To determine the influence of a saturation dive on cardiac function, Doppler-echocardiographic measurements were compared at sea level and during a 36 atm (3,650 kPa) He-O2 dive (gas density: 7 g/liter) in four healthy men. Left ventricular systolic function was studied from time motion measurements. Transmitral flow (E:A ratio) and isovolumetric relaxation time were used to assess left ventricular diastolic function. Cardiac output was derived from systolic pulmonary and aortic valvular flows. Cardiac output decreased 4.4 +/- 0.8 vs. 5.9 +/- 1.2 liter/min at sea level) whereas stroke volume, left ventricular ejection fraction, atria and ventricular diameters remained unchanged. Thus, the decrease in cardiac output was attributed to bradycardia (56 +/- 8 vs. 73 +/- 9 beats/min at sea level) which probably resulted from the slight hyperoxia (PI(O2), 0.4 atm). We found no evidence of left ventricular diastolic dysfunction. nor did we find valvular regurgitation or pulmonary hypertension. We conclude that Doppler-echocardiography can be used safely to investigate cardiac function during human saturation dives. Our results suggest that a 36 atm He-O2 dive does not modify cardiac or systolic and diastolic function except for a slight decrease in cardiac output correlated to bradycardia.
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PMID:Doppler-echocardiography study of cardiac function during a 36 atm (3,650 kPa) human dive. 917 65

Six male rowers rowed maximally for 2500 m in ergometer tests during normoxia (fractional concentration of oxygen in inspired air, F(I)O2 0.209), in hyperoxia (F(I)O2 0.622) and in hypoxia (F(I)O2 0.158) in a randomized single-blind fashion. Oxygen consumption (VO2), force production of strokes as well as integrated electromyographs (iEMG) and mean power frequency (MPF) from seven muscles were measured in 500-m intervals. The iEMG signals from individual muscles were summed to represent overall electrical activity of these muscles (sum-iEMG). Maximal force of a stroke (Fmax) decreased from the 100% pre-exercise maximal value to 67 (SD 12)%, 63 (SD 15)% and 76 (SD 13)% (P < 0.05 to normoxia, ANOVA) and impulse to 78 (SD 4)%, 75 (SD 14)% and 84 (SD 7)% (P < 0.05) in normoxia, hypoxia and hyperoxia, respectively. A strong correlation between Fmax and VO2 was found in normoxia but not in hypoxia and hyperoxia. The mean sum-iEMG tended to be lower (P < 0.05) in hypoxia than in normoxia but hyperoxia had no significant effect on it. In general, F(I)O2 did not affect MPF of individual muscles. In conclusion, it was found that force output during ergometer rowing was impaired during hypoxia and improved during hyperoxia when compared with normoxia. Moreover, the changes in force output were only partly accompanied by changes in muscle electrical activity as sum-iEMG was affected by hypoxic but not by hyperoxic gas. The lack of a significant correlation between Fmax and VO2 during hypoxia and hyperoxia may suggest a partial uncoupling of these processes and the existence of other limiting factors in addition to VO2.
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PMID:Effects of oxygen fraction in inspired air on force production and electromyogram activity during ergometer rowing. 940 60

The importance of diffusion and perfusion in terms of oxygen transport was evaluated by chronically altering environmental O2 availability (hypoxia or hyperoxia) and blood O2 content (carbon monoxide) through development in Xenopus laevis. Oxygen consumption (MO2), individual wet mass, heart rate (fH), and stroke volume (SV) were measured in animals raised from eggs to pre-metamorphic climax while maintained at 11, 21 and 35 kPa O2, combined with and without 2 kPa carbon monoxide. Additionally, cardiac output (Q), and a recently defined O2 consumption/transport quotient (MO2 x QO2(-1)) were calculated. Wet mass, MO2, and fH, were not significantly different between controls and experimental treatments at any developmental stage. However, with hemoglobin oxygen transport blocked by carbon monoxide, the exposed larvae showed an increased SV, Q and MO2 x QO2(-1). Combined, these data suggest that in spite of impaired blood O2 convection, normal aerobic metabolism was maintained, indicating that direct diffusion of O2 plays an important role in supplying oxygen during early development.
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PMID:The ontogeny of cardio-respiratory function under chronically altered gas compositions in Xenopus laevis. 962 36

The objective of our study was: (1) to compare the influence of moderate exercise on circulatory after-response in mildly hypertensive (n = 8) and normotensive male subjects (n = 9); (2) to examine the circulatory response to 3-min hyperoxic inactivation of arterial chemoreceptors at rest and during postexercise period in both groups. Hypertensive men (HTS) with a systolic blood pressure (SBP) 148 +/- 5 mm Hg, diastolic blood pressure (DBP) 92.4 +/- 4 mm Hg; and normotensive men (NTS), with a SBP 126 +/- 3 mm Hg, DBP 75.6 +/- 1.3 mm Hg, were submitted to 20-min of moderate exercise on a cycloergometer (up to the level of 55% of each subject's resting heart rate reserve). Finger arterial BP was recorded continuously with Finapres, impedance reography was used for recording stroke volume, cardiac output and arm blood flow. In HTS a significant decrease in SBP by 14.5 +/- 3.4 mm Hg, DBP by 8.9 +/- 1.9 mm Hg, total peripheral resistance (TPR) by 0.45 +/- 0.05 TPR u. (33.7 +/- 2.7%), and in arm vascular resistance (AVR) by 11.0 +/- 2.7 PRU u. (35.6 +/- 7%), was observed over a 60-min postexercise period. NTS exhibited insignificant changes in SBP, DBP, AVR except a significant decrease in TPR limited only to 20-min postexercise period. Hyperoxia decreased SBP, DBP and TPR in HTS. This effect was significantly attenuated during the postexercise period. Long-lasting antihypertensive effect of a single dynamic exercise in HTS suggests that moderate exercise may be applied as an effective physiological procedure to reduce elevated arterial BP in mild hypertension. We suggest also that the attenuation of the sympathoexcitatory arterial chemoreceptor reflex may contribute to a postexercise decrease in arterial BP and in TPR in mildly hypertensive subjects.
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PMID:Postexercise decrease in arterial blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in subjects with mild essential hypertension. 988 9

The mutual potentiation of the hepatotoxic effects of ethanol and hypoxia raised the question of whether such an interaction also occurs in the cardiovascular system. Therefore, anaesthetized rats were infused intravenously with ethanol (25 mg/kg x min.) over 90 min. to reach blood ethanol concentrations between 2.2 and 2.6 g/l and were ventilated artificially either with room air, 10% O2/90% N2 or 100% O2. Under normoxic conditions, ethanol produced a slow decrease of mean arterial blood pressure from 130 to 100 mmHg due to the decline in cardiac output and stroke volume (-20%) while heart rate and peripheral resistance remained unchanged. Hypoxia (arterial oxygen tension 35-38 mmHg) without ethanol produced immediate hypotension (-60 mmHg) without decreasing the cardiac output, i.e. by reducing peripheral resistance. In combination with ethanol, hypoxia produced an even stronger hypotension (-90 mmHg) due to reduction in both cardiac output and peripheral resistance. On the other hand, respiration with 100% O2 (arterial oxygen tension about 500 mmHg) elevated peripheral resistance, attenuated ethanol-induced cardiodepression and prevented ethanol-induced hypotension. The lethal doses of ethanol evaluated by infusing 75 mg/kg x min. ethanol until death amounted to 4.1 g/kg with 10% O2, to 5.5 g/kg with 20% O2 (room air) and to 6.9 g/kg with 100% O2. Thus decrease in vascular contractility induced by hypoxia combined with ethanol-induced cardiodepression may result in lethal cardiovascular failure. Hyperoxia, on the other hand, counteracts ethanol-induced cardiodepression and its acute toxicity by raising the vascular contractility.
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PMID:Influence of hypoxia and hyperoxia on the cardiovascular and lethal effects of ethanol. 1019 68

Obstructive sleep apnea (OSA) acutely increases systemic (Psa) and pulmonary (Ppa) arterial pressures and decreases ventricular stroke volume (SV). In this study, we used a canine model of OSA (n = 6) to examine the role of hypoxia and the autonomic nervous system (ANS) in mediating these cardiovascular responses. Hyperoxia (40% oxygen) completely blocked any increase in Ppa in response to obstructive apnea but only attenuated the increase in Psa. In contrast, after blockade of the ANS (20 mg/kg iv hexamethonium), obstructive apnea produced a decrease in Psa (-5.9 mmHg; P < 0.05) but no change in Ppa, and the fall in SV was abolished. Both the fall in Psa and the rise in Ppa that persisted after ANS blockade were abolished when apneas were induced during hyperoxia. We conclude that 1) hypoxia can account for all of the Ppa and the majority of the Psa response to obstructive apnea, 2) the ANS increases Psa but not Ppa in obstructive apnea, 3) the local effects of hypoxia associated with obstructive apnea cause vasodilation in the systemic vasculature and vasoconstriction in the pulmonary vasculature, and 4) a rise in Psa acts as an afterload to the heart and decreases SV over the course of the apnea.
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PMID:Neural and local effects of hypoxia on cardiovascular responses to obstructive apnea. 1071 Apr 8

Recent studies suggest that normobaric hyperoxia can be beneficial, if administered during transient stroke. However, increased oxygenation theoretically may increase oxygen free-radical injury, particularly during reperfusion. In the present study, the authors assessed the benefit and risks of hyperoxia during focal cerebral ischemia and reperfusion. Rats were subjected to hyperoxia (Fio2 100%) or normoxia (Fio2 30%) during 2-hour filament occlusion and 1-hour reperfusion of the middle cerebral artery. At 24 hours, the hyperoxia group showed 70% (total) and 92% (cortical) reduction in infarct volumes as compared to the normoxia group. Levels of oxidative stress were evaluated using three indirect methods. First, since oxygen free radicals increase blood-brain barrier (BBB) damage, Evan's blue dye extravasation was quantified to assess BBB damage. Second, the expression of heme oxygenase-1 (HO-1), a heat shock protein inducible by oxidative stress, was assessed using Western blot techniques. Third, an immunoblot technique ("OxyBlot") was used to assess levels of protein carbonyl formation as a marker of oxidative stress-induced protein denaturation. At 24 hours, Evan's blue dye extravasation per average lesion volume was similar between groups. There were no significant differences in HO-1 induction and protein carbonyl formation between groups, in the ipsilateral or contralateral hemispheres, at 6 hours and at 24 hours. These results indicate that hyperoxia treatment during focal cerebral ischemia-reperfusion is neuroprotective, and does not increase oxidative stress.
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PMID:Effects of normobaric hyperoxia in a rat model of focal cerebral ischemia-reperfusion. 1214 71

We explore three questions concerning arterial hyperoxygenation and focal ischemia. (1) Does greater benefit accrue with higher levels of arterial hyperoxemia? (2) Is the net effect of continuous (intraischemic plus postischemic) oxygen therapy toxic, or beneficial to middle cerebral artery infarction? (3) In view of free radical theories of reperfusion injury, does hyperoxia isolated to the reperfusion period damage tissue? Rats subjected to transient, focal, normothermic, normoglycemic ischemia were assessed at 2 weeks' survival. Arterial hyperoxygenation from 98.9 +/- 4.0 to 312.2 +/- 48.4mm Hg during ischemia improved (p < 0.05) neurological function, as did isolated reperfusion hyperoxemia, but treatment with continuous hyperoxemia both during and after ischemia yielded greatest benefit (p < 0.001). Cortical infarcts constituted 6.5 +/- 1.8% of the hemisphere at normoxia, but 2.3 +/- 0.9% at hyperoxic levels (p < 0.01). Hyperoxia isolated to the reperfusion period also reduced cortical necrosis, from 6.5% to 2.7 +/- 1.2%. However, continuous intraischemic and reperfusion hyperoxemia led to only 0.2 +/- 0.1% cortical necrosis (p = 0.0005). Increasing the degree of hyperoxemia did not augment the benefit. We conclude that (1) eubaric hyperoxemia improves neurological and neuropathological outcome, (2) continuous oxygen therapy offers the greatest benefit, and (3) reperfusion hyperoxemia is beneficial. The findings should allay clinical concerns regarding oxygen-induced reperfusion injury, and, by obviating hyperbaric chambers, encourage clinical trials studying arterial hyperoxemia in treating stroke.
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PMID:Eubaric hyperoxemia and experimental cerebral infarction. 1240 53

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