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

Existing estimates of flight energetics in glossophagine flower bats, the heaviest hovering vertebrate taxon, suggest disproportionately high expenditure of mechanical power. We determined wingbeat kinematics and mechanical power expenditure for one of the largest flower bats (Leptonycteris curasoae Martinez and Villa) during hovering flight in normodense and hypodense gas mixtures. Additional experiments examined the effects of supplemental oxygen availability on maximum flight performance. Bats failed to sustain hovering flight at normoxic air densities averaging 63% that of normodense air. Kinematic responses to hypodense aerodynamic challenge involved increases in wing positional angles and in total stroke amplitude; wingbeat frequency was unchanged. At near-failure air densities, total power expenditure assuming perfect elastic energy storage was 17-42% greater than that for hovering in normodense air, depending on the assumed value for the profile drag coefficient. Assuming a flight muscle ratio of 26%, the associated muscle-mass-specific power output at the point of near-failure varied between 90.8 W kg(-1) (profile drag coefficient of 0.02) to 175.6 W kg(-1) (profile drag coefficient of 0.2). Hyperoxia did not enhance hovering performance in hypodense air, and, with the exception of a small increase (10%) in stroke plane angle, yielded no significant change in any of the kinematic parameters studied. Revised energetic estimates suggest that mechanical power expenditure of hovering glossophagines is comparable with that in slow forward flight.
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PMID:Hovering flight mechanics of neotropical flower bats (Phyllostomidae: Glossophaginae) in normodense and hypodense gas mixtures. 1240 93

We tested the hypothesis that integrated sympathetic and cardiovascular reflexes are modulated by systemic CO2 differently in hypoxia than in hyperoxia (n = 7). Subjects performed a CO2 rebreathe protocol that equilibrates CO2 partial pressures between arterial and venous blood and that elevates end tidal CO2 (PET(CO2)) from approximately 40 to approximately 58 mmHg. This test was repeated under conditions where end tidal oxygen levels were clamped at 50 (hypoxia) or 200 (hyperoxia) mmHg. Heart rate (HR; EKG), stroke volume (SV; Doppler ultrasound), blood pressure (MAP; finger plethysmograph), and muscle sympathetic nerve activity (MSNA) were measured continuously during the two protocols. MAP at 40 mmHg PET(CO2) (i.e., the first minute of the rebreathe) was greater during hypoxia versus hyperoxia (P < 0.05). However, the increase in MAP during the rebreathe (P < 0.05) was similar in hypoxia (16 +/- 3 mmHg) and hyperoxia (17 +/- 2 mmHg PET(CO2)). The increase in cardiac output (Q) at 55 mmHg PET(CO2) was greater in hypoxia (2.61 +/- 0.7 L/min) versus hyperoxia (1.09 +/- 0.44 L/min) (P < 0.05). In both conditions the increase in Q was due to elevations in both HR and SV (P < 0.05). Systemic vascular conductance (SVC) increased to similar absolute levels in both conditions but rose earlier during hypoxia (> 50 mmHg PET(CO2)) than hyperoxia (> 55 mmHg). MSNA increased earlier during hypoxic hypercapnia (> 45 mmHg) compared with hyperoxic hypercapnia (> 55 mmHg). Thus, in these conscious humans, the dose-response effect of PET(CO2) on the integrated cardiovascular responses was shifted to the left during hypoxic hypercapnia. The combined data indicate that peripheral chemoreceptors exert important influence over cardiovascular reflex responses to hypercapnia.
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PMID:Peripheral chemoreceptor contributions to sympathetic and cardiovascular responses during hypercapnia. 1256 39

In the present study, we observed the haemodynamic changes, using echocardiography and Doppler, in ten healthy volunteers during 6 h of compression in a hyperbaric chamber with a protocol designed to reproduce the conditions as near as possible to a real dive. Ambient pressure varied from 1.6 to 3 atm (1 atm=101.325 kPa) and partial pressure of inspired O2 from 1.2 to 2.8 atm. Subjects performed periods of exercise with breathing through a closed-circuit self-contained underwater breathing apparatus (SCUBA). Subjects did not eat or drink during the study. Examinations were performed after 15 min and 5 h. After 15 min, stroke volume (SV), left atrial (LA) diameter and left ventricular (LV) end-diastolic diameter (LVEDD) decreased. Heart rate (HR) and cardiac output (CO) did not vary, but indices of the LV systolic performance decreased by 10% and the LV meridional wall stress increased by 17%. After 5 h, although weight decreased, the serum protein concentration increased. Compared with values obtained after 15 min, SV and CO decreased, but LV systolic performance, LA diameter, LVEDD and LV meridional wall stress remained unchanged. Compared with the reference values obtained at sea level, total arterial compliance decreased, HR remained unchanged and CO decreased. In conclusion, hyperbaric hyperoxia results in significant haemodynamic changes. Initially, hyperoxia and the SCUBA system are responsible for reducing LV preload, increasing LV afterload and decreasing LV systolic performance, although CO did not change. Prolonged exposure resulted in a further decrease in LV preload, because of dehydration, and in a further increase in LV afterload, due to systemic vasoconstriction, with the consequence of decreasing CO.
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PMID:Haemodynamic effects of hyperbaric hyperoxia in healthy volunteers: an echocardiographic and Doppler study. 1464 Nov 6

Neurological complications such as stroke are known consequences of sickle cell disease (SCD). In order to improve methods for the evaluation of stroke risk in SCD, MRI was used to evaluate cerebrovascular function in transgenic mouse models of human SCD. It is hypothesized that oxygen-sensitive imaging in the brain will reveal areas of excess deoxygenation that are either at risk of or the result of vaso-occlusion. Arterial spin labeling (ASL) perfusion was performed in order to correlate BOLD results with microvascular cerebral blood flow. Upon comparison with control animals, there was a relative increase in BOLD hyperoxia response of 42-67% (P < 0.001) in the transgenic mice while cerebral blood flow during normoxia was reduced by 30-40% (P < 0.02). Hyperoxia caused cerebral blood flow to decrease in control mice, whereas blood flow increased in the sickle transgenic mice. These results indicate impairment in brain autoregulation in the sickle cell transgenic mice leading to increased cerebral deoxyhemoglobin. Increased deoxyhemoglobin coupled with reduced perfusion may further increase the risk of vaso-occlusion and stroke. This may reflect polymer reduction or reduced cell adhesion during hyperoxia. The MRI protocol is noninvasive and thus directly applicable to a clinical population.
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PMID:Decreased cerebral perfusion correlates with increased BOLD hyperoxia response in transgenic mouse models of sickle cell disease. 1500 94

Stroke causes heterogeneous changes in tissue oxygenation, with a region of decreased blood flow, the penumbra, surrounding a severely damaged ischemic core. Treatment of acute ischemic stroke aims to save this penumbra before its irreversible damage by continued ischemia. However, effective treatment remains elusive due to incomplete understanding of processes leading to penumbral death. While oxygenation is central in ischemic neuronal death, it is unclear exactly what actual changes occur in interstitial oxygen tension (pO2) in ischemic regions during stroke, particularly the penumbra. Using the unique capability of in vivo electron paramagnetic resonance (EPR) oximetry to measure localized interstitial pO2, we measured both absolute values, and temporal changes of pO2 in ischemic penumbra and core during ischemia and reperfusion in a rat model. Ischemia rapidly decreased interstitial pO2 to 32% +/- 7.6% and 4% +/- 0.6% of pre-ischemic values in penumbra and core, respectively 1 hour after ischemia. Importantly, whilst reperfusion restored core pO2 close to its pre-ischemic value, penumbral pO2 only partially recovered. Hyperoxic treatment significantly increased penumbral pO2 during ischemia, but not in the core, and also increased penumbral pO2 during reperfusion. These divergent, important changes in pO2 in penumbra and core were explained by combined differences in cellular oxygen consumption rates and microcirculation conditions. We therefore demonstrate that interstitial pO2 in penumbra and core is differentially affected during ischemia and reperfusion, providing new insights to the pathophysiology of stroke. The results support normobaric hyperoxia as a potential early intervention to save penumbral tissue in acute ischemic stroke.
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PMID:Interstitial pO2 in ischemic penumbra and core are differentially affected following transient focal cerebral ischemia in rats. 1509 Nov 15

A major limitation in thrombolysis for acute ischemic stroke is the restricted time window for safe and effective therapy. Any method that can extend the reperfusion time window would be important. In this study, we show that normobaric hyperoxia extends the time window for effective reperfusion from 1 to 3 hours in rats subjected to focal cerebral ischemia. Normobaric hyperoxia did not increase cellular markers of superoxide generation or brain levels of matrix metalloproteinase-9. Normobaric hyperoxia may be a clinically feasible adjunct method for significantly increasing the time window for effective thrombolytic therapy in acute ischemic stroke.
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PMID:Normobaric hyperoxia extends the reperfusion window in focal cerebral ischemia. 1578 65

The main goal in the treatment of acute ischemic stroke is prompt arterial recanalization. Thrombolysis with recombinant tissue plasminogen activator (rtPA) is efficient in humans, but shows significant problems including slow and incomplete recanalization and frequent bleeding complications. Limited therapeutic window (the first three hours after onset) is the major limitation resulting in reach too few patients. Therefore, adjunctive therapies extending the reperfusion time window, increasing efficacy and reducing side effects of rtPA are needed. Ultrasound augmentation of rtPA-mediated thrombolysis is suggested to overcome some of these problems, but low-frequency ultrasound (less than 1 MHz) is not safe and high frequency ultrasound (2 MHz) is not much effective. We suggest that normobaric hyperoxia (NBO) may increase the efficacy of ultrasound and rtPA combination in addition to its own efficacy in acute ischemic stroke. Briefly, NBO increases arterial partial oxygen pressure (pO(2)) significantly up to 6-fold. Increase of pO(2) results in an increase of dissolved oxygen in the blood according to Henry's law. Enhanced dissolved oxygen increases gas nuclei formation around and inside of the clot, and decreases the Blake threshold. Under ultrasound field, these small gas nuclei form nano bubbles which fuel inertial cavitation as substrates, and therefore increase the clot fragmentation and lysis. This hypothesis has not been tested so far. The combination of rtPA, therapeutic ultrasound and NBO may be more efficacious than rtPA alone or its combination with ultrasound as acute stroke treatment modality, because each has different and probably additive mechanism of action.
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PMID:Hyperoxia potentiated sonothrombolysis as a method of acute ischemic stroke therapy. 1614 45

Increased Apolipoprotein D (ApoD) expression has been reported in various neurological disorders, including Alzheimer's disease, schizophrenia, and stroke, and in the aging brain . However, whether ApoD is toxic or a defense is unknown. In a screen to identify genes that protect Drosophila against acute oxidative stress, we isolated a fly homolog of ApoD, Glial Lazarillo (GLaz). In independent transgenic lines, overexpression of GLaz resulted in increased resistance to hyperoxia (100% O(2)) as well as a 29% extension of lifespan under normoxia. These flies also displayed marked improvements in climbing and walking ability after sublethal exposure to hyperoxia. Overexpression of Glaz also increased resistance to starvation without altering lipid or protein content. To determine whether GLaz might be important in protection against reperfusion injury, we subjected the flies to hypoxia, followed by recovery under normoxia. Overexpression of GLaz was protective against behavioral deficits caused in normal flies by this ischemia/reperfusion paradigm. This and the accompanying paper by Sanchez et al. (in this issue of Current Biology) are the first to manipulate the levels of an ApoD homolog in a model organism. Our data suggest that human ApoD may play a protective role and thus may constitute a therapeutic target to counteract certain neurological diseases.
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PMID:Overexpression of a Drosophila homolog of apolipoprotein D leads to increased stress resistance and extended lifespan. 1658 12

Both hypoxia and hyperoxia have major effects on cardiovascular function. However, both states affect ventilation and many previous studies have not controlled CO(2) tension. We investigated whether hemodynamic effects previously attributed to modified O(2) tension were still apparent under isocapnic conditions. In eight healthy men, we studied blood pressure (BP), heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI) and arterial stiffness (augmentation index, AI) during 1 h of hyperoxia (mean end-tidal O(2) 79.6 +/- 2.0%) or hypoxia (pulse oximeter oxygen saturation 82.6 +/- 0.3%). Hyperoxia increased SVRI (18.9 +/- 1.9%; P < 0.001) and reduced HR (-10.3 +/- 1.0%; P < 0.001), CI (-10.3 +/- 1.7%; P < 0.001), and stroke index (SI) (-7.3 +/- 1.3%; P < 0.001) but had no effect on AI, whereas hypoxia reduced SVRI (-15.2 +/- 1.2%; P < 0.001) and AI (-10.7 +/- 1.1%; P < 0.001) and increased HR (18.2 +/- 1.2%; P < 0.001), CI (20.2 +/- 1.8%; P < 0.001), and pulse pressure (13.2 +/- 2.3%; P = 0.02). The effects of hyperoxia on CI and SVRI, but not the other hemodynamic effects, persisted for up to 1 h after restoration of air breathing. Although increased oxidative stress has been proposed as a cause of the cardiovascular response to altered oxygenation, we found no significant changes in venous antioxidant or 8-iso-prostaglandin F(2alpha) levels. We conclude that both hyperoxia and hypoxia, when present during isocapnia, cause similar changes in cardiovascular function to those described with poikilocapnic conditions.
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PMID:Effects of short-term isocapnic hyperoxia and hypoxia on cardiovascular function. 1690 69

This study was designed to compare the effect of intraoperative administration of 100% oxygen (F1O2 = 1.0) with 50% O2 (air-O2 mixture, F1O2 = 0.5) on cardiovascular and respiratory parameters in adults undergoing coronary artery surgery. Nineteen patients were assigned to receive either F,O2 = 1.0 (group A) or F1O2 = 0.5 (group B) in a randomized fashion. Anesthesia was induced with fentanyl (15 microg/kg) and diazepam (0.1 to 0.2 mg/kg) and maintained with fentanyl (total dose 50 microg/kg) and isoflurane. A bubble oxygenator (F1O2 = 1.0) was used during cardiopulmonary bypass (CPB) in both groups. Hemodynamic and respiratory profiles were determined at specific intervals prior to incision, following CPB, and postoperatively. Patients ventilated with F1O2 = 0.5 were well oxygenated at measured intraoperative intervals (PaO2 range 90 to 268 mmHg, saturation 95% to 99%), with adequate mixed venous O2 levels (PvO2 range 35 to 65 mmHg, saturation 63% to 89%). Compared with patients receiving F1O2 = 1.0, those receiving F1O2 = 0.5 had significantly greater increases in cardiac index (CI) (mean +/- SEM B: 87% +/- 18% v A: 26% +/- 12%) and stroke index (B: 10% +/- 5% increase vA: 14% +/- 7% decrease), and a larger decrease in peripheral resistance (B: 38% +/- 7% v A: 4% +/- 12%) at postoperative day 1 relative to preincision values (P < 0.05). At postoperative day 1, both groups had an elevated alveolar-to-arterial O2 gradient (A: 55% +/- 19% v B: 48% +/- 17% increase) and shunt fraction (A: 58% +/- 28% v B: 99% +/- 35% increase). Although O2 consumption increased similarly in both groups at postoperative day 1 relative to preincision values (A: 91% +/- 23% v B: 113% +/- 16%), O2 delivery was enhanced more in group B than in group A (67% +/- 17% v 20% +/- 13% increase, respectively, P < 0.05). The data suggest that significant hemodynamic derangements may occur with hyperoxia and that intraoperative administration of 50% O2 may be more appropriate during coronary artery surgery.
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PMID:Effects of inspired oxygen tension on hemodynamics and pulmonary gas exchange in patients undergoing coronary artery surgery. 1717 54


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