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

Intraretinal oxygen tension (pO2) and local electroretinogram (ERG) were simultaneously measured in miniature pigs using double-barreled recess type microelectrodes. Transretinal pO2 profiles were recorded during normoxia and hyperoxia in areas close to (juxta-arteriolar) or far from (intervascular) retinal arterioles. In normoxia, in both areas, the pO2 decreased from the inner retina and the choroid towards the middle of the retina. In the inner retina the gradient of the juxta-arteriolar pO2 profile was steeper than that of the intervascular profile. This characteristic persisted during the breathing of 100% O2. Analysis of the pO2 profiles shows that, even in hyperoxia, the choroid cannot supply O2 to the whole retina. The results also support the conclusions of previous work (Riva, Pournaras and Tsacopoulos, 1986) indicating that in the normal retina it is not the O2 diffusing from the choroid to the retinal arterioles the induces vasoconstriction of these vessels. In the miniature pig this constriction appears to maintain inner retina tissue pO2 at a constant level during hyperoxia. From the pO2 transretinal profiles and previously published choroidal O2 fluxes and pO2 values near retinal vessels an explanatory working hypothesis is formulated according to which O2 consumption (qO2) of the outer retina increases during hyperoxia in the miniature pig.
Exp Eye Res 1989 Sep
PMID:Diffusion of O2 in the retina of anesthetized miniature pigs in normoxia and hyperoxia. 279 32

Neonatal lung injury from hyperoxia and mechanical hyperventilation was studied in newborn piglets hyperventilated (arterial PCO2 15-20 Torr) for 24-48 h with 100% O2 and compared with unventilated controls. Pulmonary function testing was performed, and biochemical indicators of lung injury were analyzed from tracheobronchial aspirates at 0, 24, and 48 h. Lung sections were obtained for light and electron microscopy, and bronchoalveolar lavage fluid was analyzed for surfactant composition and activity. At 24 h significant changes in tracheobronchial aspirate albumin concentrations (up 78%) and percent of polymorphonuclear cells (up 16%) were demonstrated. At 48 h a 35% decrease in dynamic lung compliance (P less than 0.05) and a 36% increase in pulmonary resistance (P less than 0.05) were noted. Further biochemical abnormalities occurred with total cell counts increased by 271% (P less than 0.02), albumin 163% (P less than 0.05), total protein 217% (P less than 0.01), and elastase 108% (P less than 0.02). Pathological analyses revealed mild lung injury at 24 h and marked inflammation, abnormal inflation patterns, flattening of Clara cells, fibrinous exudate and edema, early collagen formation, and cell necrosis observed at 48 h. Bronchoalveolar lavage surfactant had normal biophysical activity. Results demonstrate that exposure of neonatal piglets to O2 and mechanical hyperventilation for 48 h cause severe progressive lung injury.
J Appl Physiol (1985) 1989 Sep
PMID:Lung injury in the neonatal piglet caused by hyperoxia and mechanical ventilation. 279 94

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of hyperoxia significantly increased inspiratory minute ventilation (VI) from the normoxic base line. In control experiments, with hypoxia, VI initially increased and then declined to levels that were slightly above the normoxic base line. Pretreatment with aminophylline significantly attenuated the hypoxic ventilatory decline. During transitions to pure O2 (cessation of carotid bodies' output), VI and breathing patterns were analyzed breath by breath with a moving-average technique, searching for nadirs before and after hyperoxia. On placebo days, at the end of hypoxia, hyperoxia produced nadirs that were significantly lower than those observed with room-air breathing and also significantly lower than when hyperoxia followed normoxia, averaging, respectively, 6.41 +/- 0.52, 8.07 +/- 0.32, and 8.04 +/- 0.39 (SE) l/min. This hypoxic depression was due to significant decrease in tidal volume and prolongation of expiratory time. Aminophylline partly prevented these alterations in breathing pattern; significant posthypoxic ventilatory depression was not observed. We conclude that aminophylline attenuated hypoxic central depression of ventilation, although it does not affect hyperoxic steady-state hyperventilation. Adenosine may play a modulatory role in hypoxic but not in hyperoxic ventilation.
J Appl Physiol (1985) 1989 Sep
PMID:Aminophylline effects on ventilatory response to hypoxia and hyperoxia in normal adults. 279 6

Pulmonary insults caused by transfusion, radiation, and hyperoxia share many clinical features with insults caused by serious pulmonary infections. The major objective in evaluating these patients is to establish the diagnosis with as much certainty as possible. Unfortunately, there are no clinical aspects or laboratory tests that are pathognomonic for these diseases; therefore, it is often necessary to rely on a knowledge of those features which help to distinguish these disorders from infectious etiologies. For example, patients suffering from transfusion-related acute lung injury (TRALI) experience onset of insult within 6 hours of a transfusion and have the presence of leukoagglutinins in their serum. Patients with radiation injuries frequently have roentgenographic infiltrates that conform to the ports of radiation. Despite extensive animal and human studies, factors distinguishing hyperoxic injury from infectious disorders remain poorly defined. These clinical features and others are reviewed to identify the essential components in the diagnosis of TRALI, acute radiation pneumonitis, and hyperoxic pneumonitis.
Semin Respir Infect 1988 Sep
PMID:Pulmonary insults due to transfusions, radiation, and hyperoxia. 305 15

The effects of inhalation of different gases were studied in neonatal rabbits with the following results: In neonates with normal heart rate (HR), hyperoxia induced by O2 inhalation did not appreciably affect HR, but it increased cerebral tissue PO2, while decreasing cerebral blood flow (CBF). In many of those which fell into a state of marked bradycardia, not only HR and CBF but also cerebral tissue PO2 levels were recovered as a result of O2 inhalation. CBF was increased even when HR was hardly changed (at least when the HR decrease was 10% or less) by hypercarbia due to inhalation of CO2 mixed air. Severe hyperoxia induced by N2O inhalation caused bradycardia and reduced CBF.
Nihon Sanka Fujinka Gakkai Zasshi 1986 Sep
PMID:Experimental study on the hemodynamics of the neonatal brain. 309 67

We have examined the effect of steady-state hyperoxia on the ventilation of sea level (SL) cats and cats acclimatized to simulated high altitude (HA) at 5500 m for three weeks. Three groups of cats were studied. In group I, the ventilatory responses to 10%, 21% and 100% O2 were studied at SL, and after acclimatization to HA, the ventilatory responses to 10% and 100% O2 were measured. In group II the ventilatory responses and femoral artery and superior sagittal sinus blood gases were measured in two sets of cats, one at SL and one at HA, during exposure to the gases outlined in group I. In group III, we examined the effect of chronic vagotomy on the ventilatory responses to the gas mixtures outlined in group I. Breathing 100% O2 at SL had no significant effect on ventilation, tidal volume, respiratory frequency, or cerebral blood flow (inferred from the cerebral veno-arterial CO2 difference). Ventilation was constant in the HA acclimatized cats while breathing 10% and 100% O2, but the ventilatory pattern changed dramatically during hyperoxia: respiratory frequency increased and tidal volume fell. Breathing 100% O2 was associated with changes in CBF, and venous PCO2 that might be expected to stimulate ventilation, but the change in ventilatory pattern suggests to us that hyperoxic disinhibition of central respiratory processes (which were modified by HA acclimatization) is the mechanism whereby ventilation is sustained during hyperoxia at HA. After vagotomy at HA, ventilation remained constant while breathing 100% O2, but the changes in respiratory pattern were no longer apparent. Therefore, vagal afferents seems to have a role in determining the pattern, but not necessarily the absolute level, of ventilation during hyperoxia. Cats vagotomized at SL prior to HA exposure did not show any evidence of HA ventilatory acclimatization; thus, the vagi may also play a heretofore unrecognized role in the process of acclimatization.
Respir Physiol 1986 Sep
PMID:Hyperoxic ventilatory responses of high altitude acclimatized cats. 309 74

We investigated the effects of nitroprusside and isoflurane on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia (fraction of inspired O2, FIO2, 0.4) and hypoxia (FIO2 0.1). Over the entire range of Q studied, 2-5 l.min-1.m-2, hypoxia increased PAP in 16 dogs ("responders") and did not affect PAP in 16 other dogs ("nonresponders"). A hypoxic pulmonary vasoconstriction (HPV) was restored in the nonresponders by intravenous administration of 1 g of acetylsalicylic acid (ASA). Nitroprusside (5 micrograms.kg-1.min-1) inhibited HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). End-tidal 1.41% isoflurane (a minimal alveolar concentration equal to one for dogs) did not affect HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). In the latter group isoflurane increased PAP at the highest Q studied (3-5 l.min-1.m-2) in hyperoxia and hypoxia. In a final group of eight dogs with Q kept constant, PAP remained unchanged during two consecutive sequences of alternated 30-min periods (maximum time to generate a PAP/Q plot) successively at FIO2 0.4 and 0.1, and the hypoxia-induced increase in PAP was reproducible. Thus the present experimental model appeared suitable for the study of the effects of hypoxia and drugs on pulmonary vascular tone of intact dogs. At the given doses HPV was inhibited by nitroprusside and not affected by isoflurane. Products of arachidonic acid metabolism possibly could be implicated in the pulmonary vascular effects of isoflurane.
J Appl Physiol (1985) 1987 Sep
PMID:Pulmonary arterial pressure-flow plots in dogs: effects of isoflurane and nitroprusside. 311 56

The acute phase of oxygen-induced retinopathy is associated with vasoconstriction and occlusion of the retinal vessels. Because this acute vasoobliterative phase could be due to the inhibition in retinal vessels of the production of the potent vasodilator and antithrombotic metabolite prostacyclin, animal experiments were performed to assess this possibility. Eight litters of 27 kittens (four to six days of age) were used. Control kittens were left in room air; hyperoxic kittens were placed in 80% oxygen for 48 hours; recovery kittens were returned to room air for 24 hours following hyperoxic exposure. Following treatments, the animals were killed, retinas isolated, and prostaglandin formation assessed. Retinal tissues produced 6-keto-prostaglandin F1 alpha, prostaglandin F2 alpha, prostaglandin E2, and thromboxane B2 from exogenous arachidonate. A significant (approximately 33%) reduction in retinal 6-keto-prostaglandin F1 alpha (the end product of prostacyclin) was observed both in the hyperoxic and recovery litter mates when compared with controls. Both of the experimental groups also demonstrated a reduction in total retinal prostanoids that paralleled the changes observed in prostacyclin, suggesting that the biochemical effect of hyperoxia on retinal vascular arachidonic acid metabolism occurred at the level of cyclooxygenase. A decrease in the local production of prostacyclin during hyperoxia is consistent with the histologic retinal changes observed during the acute phase of oxygen-induced retinopathy.
Pediatrics 1988 Sep
PMID:Changes in oxygen tension and effects on cyclooxygenase metabolites: III. Decrease of retinal prostacyclin in kittens exposed to hyperoxia. 313 33

We studied the interaction of O2 and CO2 at the peripheral chemoreceptors in 6 two-week-old awake lambs. The method used, which selectively tested the peripheral chemoreceptors, measured the immediate ventilatory (VE) response to pure O2 and then to O2 + CO2. From room air, the animal was switched abruptly to either pure O2 or O2 + 5% CO2, O2 + 7.5% CO2, or O2 + 10% CO2. VE was measured before and 8-10 sec after a step change in the inspired gas. In response to pure O2, VE/kg dropped 131 +/- 30 ml/min.kg (38%). Repeat O2 tests performed with the addition of CO2 showed that CO2 interacted to blunt the response to pure O2; the VE change from pre-test baseline to 8-10 sec being -77 +/- 42, -18 +/- 25, and +8.5 +/- 60 for 5%, 7.5%, and 10% added CO2 respectively. Carotid body denervation eliminated the immediate VE responses to O2 and CO2. We conclude that in the 2-week-old awake lamb, (1) hyperoxia suppresses the O2 drive output of the peripheral chemoreceptors, (2) during hyperoxia O2 and CO2 still interact at the chemoreceptor level, and (3) despite hyperoxia, the peripheral chemoreceptors retain a substantial graded response to incremental transient CO2 challenge.
Respir Physiol 1988 Sep
PMID:Peripheral chemoreceptor CO2 response during hyperoxia in the 14-day-old awake lamb. 314 Mar 31

Changes in pulmonary capillary filtration induced by hyperoxia were investigated in 15 dogs. After 12 h of normobaric hyperoxic exposure, animals were anesthetized and artificially ventilated with 100% O2. A pulmonary lymphatic vessel was cannulated, and lymph flow and protein content were measured together with pulmonary and systemic hemodynamics. An increase in pulmonary capillary filtration was found when compared with reference data (normoxic dogs in similar conditions) gathered from available literature: lymph flow increased from 21.8 +/- 13.4 to 125.2 +/- 131.6 microliter/min, and the lymph-to-plasma protein concentration ratio increased from 0.67 +/- 0.08 to 0.78 +/- 0.08. To characterize the mechanisms involved, left atrial pressure was increased in two stages (approximately 10 and approximately 25 mmHg). The results clearly indicated an increase in pulmonary capillary permeability as evidenced by a decrease of the minimal estimate of the protein reflection coefficient from 0.62 +/- 0.05 to 0.42 +/- 0.05.
J Appl Physiol (1985) 1988 Sep
PMID:Increase in pulmonary capillary permeability in dogs exposed to 100% O2. 318 83


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