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

Experiments were performed to determine whether T2* and resonance frequency weighted MR images are sensitive to effects of hyperoxia on model tumors. Hyperoxia can increase tumor oxygen tension and thus affect T2* and/or the average resonance frequency within each image voxel due to the paramagnetism of oxygen itself or through modulation of the oxidation state of hemoglobin. Alternatively, changes in T2* during hyperoxia may reflect changes in tumor water content due to changes in systemic blood pressure. Mammary adenocarcinomas implanted in the flanks of rats were studied. Imaging sequences were preceded by two 90 degrees pulses separated by an evolution period of 50 or 75 ms and followed by a crusher gradient to eliminate transverse magnetization. This pulse sequence produced images which were sensitized to both T2* and the average resonance frequency of each voxel. Images were produced at 2 T using a gradient echo imaging method with a TR of 3 s. Images obtained during inhalation of air and 100% O2 were compared. Significant increases in image intensity were observed in most tumors during hyperoxia, particularly at the tumor center. The increase was accentuated when the evolution period was increased and greatly reduced when a 180 degrees refocusing pulse was placed at the center of the evolution period. These results suggest that hyperoxia reduces local magnetic susceptibility gradients leading to an increase in T2* or causes a shift in resonance frequency. The magnitude of this change may be a function of the rate at which oxygen is delivered to and metabolized by tumors and may also reflect tumor oxygen tension under normoxic conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hyperoxia on T2* and resonance frequency weighted magnetic resonance images of rodent tumours. 806 23

Near-infrared spectroscopy is a noninvasive bedside technique for monitoring hemoglobin saturation (HbO2%) in brain vasculature. The method linearly relates the optical signal detected from the surface of the head to HbO2%. To do so, the method relies on constant transcranial optical pathlength and light scattering as well as minimal interference by tissues overlying the brain. This study examined these premises. Optical signals from a dual-wavelength, near-infrared spectrometer were correlated with sagittal sinus HbO2% in 7 anesthetized piglets subjected to 7 different physiological conditions: normoxia, moderate and severe hypoxia, hyperoxia, hypocapnia, hypercapnic hyperoxia, and hypotension. These conditions were induced by varying the inspired O2 concentration (7-100%), ventilatory rate (5-35 breaths/min), and blood pressure (phlebotomy 20 ml/kg) to force HbO2% over a wide range (5-93%). To evaluate interference by tissues overlying the brain, correlations were repeated after the scalp and skull were rendered ischemic. Transcranial optical pathlength was measured by phase-modulated spectroscopy. Linear relationships between optical signals and sagittal sinus HbO2% were found with correlation coefficients ranging from -0.89 to -0.99 (p < 0.05) among animals; however, slope and intercept had coefficients of variability of approximately 15 and 333%, respectively. Almost identical linear expressions were observed whether scalp and skull were ischemic or perfused. Transcranial optical pathlength was constant in each animal, but ranged from 10 to 18 cm among animals. The data indicate that the assumptions underlying near infrared spectroscopy are reasonably accurate in a given animal, but that the constants for transcranial optical pathlength and light scattering are not the same in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Near-infrared monitoring of the cerebral circulation. 834 68

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3-7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4-5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32-95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15-20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.
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PMID:Arterial blood gas tensions during breath-hold diving in the Korean ama. 837 76

Lifelong high-altitude residents of North and South America acquire blunted hypoxic ventilatory responses and exhibit decreased ventilation compared with acclimatized newcomers. The ventilatory characteristics of Himalayan high-altitude residents are of interest in the light of their reportedly lower hemoglobin levels and legendary exercise performance. Until recently, Sherpas have been the only Himalayan population available for study. To determine whether Tibetans exhibited levels of ventilation and hypoxic ventilatory drives that were as great as acclimatized newcomers, we compared 27 lifelong Tibetan residents of Lhasa, Tibet, China (3,658 m) with 30 acclimatized Han ("Chinese") newcomers matched for age, body size, and extent of exercise training. During room air breathing, minute ventilation was greater in the Tibetan than in the Han young men because of an increased respiratory frequency, but arterial O2 saturation and end-tidal PCO2 did not differ, indicating similar levels of effective alveolar ventilation. The Tibetan subjects had higher hypoxic ventilatory response shape parameter A values and hypercapnic ventilatory responsiveness than the Han subjects. Among the Han subjects, duration of high-altitude residence correlated with the degree of blunting of the hypoxic ventilatory drive. Paradoxically, hyperoxia (inspired O2 fraction 0.70) increased minute ventilation and decreased end-tidal PCO2 in the Tibetan but not in the Han men. We concluded that lifelong Tibetan residents of high altitude neither hypoventilated nor exhibited blunted hypoxic ventilatory responses compared with acclimatized Han newcomers, suggesting that the effects of lifelong high-altitude residence on ventilation and ventilatory response to hypoxia differ in Tibetan compared with other high-altitude populations.
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PMID:Hypoxic ventilatory responsiveness in Tibetan compared with Han residents of 3,658 m. 844 7

Intravascular sickling, red cell-endothelium interaction, and altered microvascular responses have been suggested to contribute to the pathophysiology of human sickle cell disease, but have never been demonstrated under in vivo flow. To address this issue, we have examined a transgenic mouse line, alphaHbetaSbetaS-Antilles [betaMDD] which has a combined high (78%) expression of beta S and beta S-Antilles globins. In vivo microcirculatory studies using the cremaster muscle preparation showed adhesion of red cells, restricted to postcapillary venules, in transgenic mice but not in control mice. Electron microscopy revealed distinct contacts between the red cell membrane and the endothelium surface. Some red cells exhibiting sickling were regularly observed in the venular flow. Infusion of transgenic mouse red cells into the ex vivo mesocecum vasculature also showed adhesion of mouse red cells exclusively in venules. Under resting conditions (pO2, 15-20 mmHg), there were no differences in the cremaster microvascular diameters of control and transgenic mice; however, transgenic mice showed a drastic reduction in microvascular red cell velocities (Vrbc) with maximal Vrbc decrease (> 60%) occurring in venules, the sites of red cell adhesion and sickling. Local, transient hyperoxia (pO2, 150 mmHg) resulted in striking differences between control and transgenic mice. In controls, oxygen caused a 69% arteriolar constriction, accompanied by 75% reduction in Vrbc. In contrast, in transgenic mice, hyperoxia resulted in only 8% decrease in the arteriolar diameter and in 68% increase in VrBC; the latter is probably due to an improved flow behavior of red cells as a consequence of unsickling. In summary, the high expression of human sickle hemoglobin in the mouse results not only in intravascular sickling but also red cell-endothelium interaction. The altered microvascular response to oxygen could be secondary to blood rheological changes, although possible intrinsic differences in the endothelial cell/vascular smooth muscle function in the transgenic mouse may also contribute. These sickle transgenic mice could serve as a useful model to investigate vasoocclusive mechanisms, as well as to test potential therapies.
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PMID:In vivo demonstration of red cell-endothelial interaction, sickling and altered microvascular response to oxygen in the sickle transgenic mouse. 867 55

To study whether nitric oxide (NO) affects surfactant function, 36 young rats inhaled one of the following humidified environments for 24 h: 1) air; 2) 95% O2; 3) air and 100 parts/million (ppm) NO; and 4) 95% O2 and 100 ppm NO. The treatments did not change the recovery of phospholipid from bronchoalveolar lavage (BAL). Exposure to NO of animals that breathed either air or 95% O2 increased the minimum surface tension of surfactant from BAL at low (1.5 mumol/ml), but not at high (4 mumol/ml), phosphatidylcholine concentration. After inhaled NO, the nonsedimentable protein of BAL decreased the surface activity of surfactant (1 mumol phosphatidylcholine/ml) more than the protein from the controls. NO treatment of animals that breathed either air or 95% O2 affected neither the quantity nor the molecular weight distribution of nonsedimentable protein. Hyperoxia increased the amount of the nonsedimentable protein, whereas NO increased the iron saturation of transferrin. The surfactant fraction and the nonsedimentable protein from BAL were separately exposed to 80 ppm NO in vitro. NO exposure had no effect on the surface activity of surfactant fraction. NO exposure of nonsedimentable protein from the control animals (no NO) increased the inhibition of the surface activity and changed the adsorption spectrum of the protein, suggesting conversion of hemoglobin to methemoglobin. Nonsedimentable protein from NO-exposed animals contained methemoglobin. We propose that surfactant dysfunction caused by inhaled NO is in part due to alteration of protein(s) in epithelial lining fluid that in turn inactivates surfactant.
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PMID:Surfactant dysfunction after inhalation of nitric oxide. 880 10

It is now possible to detect quantitative changes in cytochrome aa3 by means of near-infrared spectrophotometry. This technique is also suitable for determining oxidised hemoglobin (HbO2), reduced hemoglobin (Hb), cerebral blood volume, and the redox state of cytochrome aa3 (cyt aa3) in the tissues. The significance of elevated cyt aa3, measured by near-infrared spectrophotometry, is still unclear, so we investigated this question using both near-infrared spectrophotometry and oxygen saturation meters in endotoxemic dogs. Ten anaesthetised mongrel dogs were injected with endotoxin (E. coli 0111: B4 Difco 2 mg/kg i.v.) and the redox state of Hb and cyt aa3 was determined in real time by near-infrared spectrophotometry. The levels of arterial and cisternal venous oxygen saturation were recorded simultaneously by two Oximetrix 3 saturation meters to calculate the cerebral arterial and venous oxygen saturation difference (Sata-vO2D) in real time. HbO2 decreased along with the fall in mean arterial pressure and remained at a low level, while Hb increased and remained at a high level. The cerebral blood volume decreased in the endotoxic early stage and then returned gradually towards baseline. Cyt aa3 showed an increase following endotoxin injection and maintained an oxidised form. The cerebral Sata-vO2D rose to about three times the control level. From these observations, an increase of oxidised cytochrome aa3 after endotoxin administration seems to be a compensatory protective effect in response to the cerebral oxygen demand rather than over-oxygenation or hyperoxia.
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PMID:Significance of elevated cytochrome aa3 in a state of endotoxemia in dogs. 895 75

Recent studies have shown a considerable extent of diffusive O2 transfer from precapillary vessels, but the occurrence of O2 influx into postcapillary vessels (diffusive shunting) is still controversial. In this study, we investigated diffusive shunting between pre- and postcapillary vessels in muscle tissue and pH changes in the microvessels in an attempt to determine the physiological significance of the parallel arrangement of arterial and venous vessels in tissue oxygenation. We used rat cremaster muscles and controlled the breathing of anesthetized rats using urethane with FIO2 set at 0.3 and 0.12. We employed a noninvasive spectrophotometric method of measuring pH, using a pH-sensitive dye (1-hydroxypyrene-3,6,8-trisulfonic acid) and the O2 saturation level of hemoglobin (SO2) in microvessels from small arteries down to arterioles and from venules up to small veins. At FIO2 0.30, pH significantly decreased from 7.39 +/- 0.02 to 7.26 +/- 0.05 (SD) in precapillary vessels and remained close to constant during passage through postcapillary vessels. At FIO2 0.12, pH decreased from 7.36 +/- 0.03 to 7.01 +/- 0.06 in precapillary vessels and then increased in postcapillary vessels from 6.75 +/- 0.19 to 7.27 +/- 0.08. At FIO2 0.30, SO2 decreased from 98.6 +/- 5.4 to 64.2 +/- 4.5% in precapillary vessels and increased from 62.5 +/- 6.5 to 89.4 +/- 4.1% in postcapillary vessels. At FIO2 0.12, SO2 decreased from 47.0 +/- 5.5 to 25.1 +/- 3.8% in precapillary vessels and remained close to constant in postcapillary vessels. In conclusion, during hyperoxia, diffusive shunting of O2 was enhanced, and during hypoxia, acid was accumulated in peripheral vessels. It is speculated that acid accumulated due to back-diffusion of CO2 from venous to arterial microvessels, liberating O2 bound to hemoglobin via the Bohr effect. The diffusive shunting of O2 and counterdiffusion and accumulation of CO2 may contribute to the homeostasis of tissue oxygenation levels.
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PMID:Oxygen saturation and pH changes in cremaster microvessels of the rat. 896 89

A new index, termed 'useful ratio' of the blood oxygen binding curve, was derived on the basis of the characteristic features of hemoglobin oxygen (transported, reserve and practically non-usable hemoglobin oxygen). The index gives the ratio of the useful to the predicted total hemoglobin oxygen of patients. It is functionally related to the fraction of the measured transpulmonary shunt (FShunt), shows high correlation with the blood gases (pO2 and pCO2), correlates moderately with the hydrogen exponent, poorly with the oxygen affinity (P50) and the metabolic acid-base parameters (cHCO3), and does not show to be essentially related to the total oxygen concentration (cO2) and PO2(x), the new index proposed in the Oxygen Status Algorithm. Diagnostically, this index has much the same value as that of the calculated shunt (FShunt); it can be used only in diagnosing the conditions of hyperoxia, normoxia, and hypoxia and excludes detecting those of hyperoxemia, normoxemia, and hypoxemia. Simultaneous assessment of this index together with pO2(x) enhances further the diagnostics of respiratory insufficiency providing the necessary information about the mechanism of respiratory decompensation that is of importance for an efficacious treatment.
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PMID:A new index for assessing arterial oxygen profile in patients with respiratory failure. 897 54

Currently, hyperoxia is being investigated as a method for producing contrast in magnetic resonance images of the brain, solid tumors, and the eye. However, the underlying physiological mechanisms involved in this type of contrast are still not completely understood. For example, under what conditions would dissolved plasma oxygen contribute to the hyperoxia-induced contrast? Using the eye as a model system, we varied the level of dissolved plasma oxygen and observed different patterns of contrast in the vitreous. The observed contrast changes were consistent with tissue oxygen buffering by hemoglobin at an arterial PO2 of 200 mm Hg and dissolved oxygen offloading at arterial PO2's > 350 mm Hg. These data demonstrate that dissolved plasma oxygen does not become an important contrast mechanism until the arterial oxygen tension exceeds approximately 350 mm Hg. The implication of this result to studies in other organs is discussed.
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PMID:Role of dissolved plasma oxygen in hyperoxia-induced contrast. 908 33


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