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

Aspirin administration, at a dosage producing plasma levels within the human therapeutic range, caused marked inhibition of production of both vascular prostacyclin (a vasodilator) and platelet thromboxane (a vasoconstrictor) in beagle puppies. In addition, aspirin-treated, oxygen-exposed puppies developed retinopathy of significantly greater severity than their unmedicated, oxygen-exposed littermates. Direct ophthalmoscopic observations indicated that whereas sustained oxygen breathing produced retinal vasoconstriction in unmedicated puppies, retinal vessels of aspirin-treated littermates became more dilated or remained unchanged. It is postulated that retinal vasoconstriction may be a normal physiologic mechanism to protect the immature retina from damaging effects of high blood oxygen levels; i.e., it may be a protective rather than a pathologic process in response to hyperoxia. Many vascular anomalies which characterize the human disease were present in the retinas of the puppies. Several of the most severely affected puppies treated with aspirin even displayed grade III cicatricial retinopathy (falciform retinal fold). Thus, a major criticism of the retrolental fibroplasia animal model has been addressed by producing cicatricial retrolental fibroplasia in puppies, and the confidence with which results from experimental animal studies might be extrapolated to the clinical situation is thereby strengthened.
Pediatr Res 1981 Sep
PMID:Retrolental fibroplasia: evidence for a role of the prostaglandin cascade in the pathogenesis of oxygen-induced retinopathy in the newborn beagle. 702 56

Halothane is known to inhibit the ventilatory responses to hypoxia and hypercapnia. In order to determine whether this inhibition was mediated by peripheral chemoreceptors, the authors measured the effect of halothane on the response of carotid body chemoreceptors to these stimuli. Cats were decerebrated under brief halothane anesthesia, paralyzed, and ventilated. Chemoreceptor activity was recorded from single- or few-fiber preparations of carotid sinus nerve, and the inspiratory drive was recorded from the whole phrenic nerve. Steady-state responses were measured at three levels of CO2 tension (19-92 mmHg) during hyperoxia, and at four levels of O2 tension (35-450 mmHg) at a fixed PaCO2. Both responses were measured before, during, and after 0.5-1.0 per cent halothane was inspired. The halothane inhalation was maintained for at least 30 min before the responses were obtained. Halothane reduced the slope of chemoreceptor response to hypercapnia to about 48 per cent of the control slope. The response to hypoxia was reduced to about 58 pr cent of the control response. The increase in firing after intravenous nicotine (100 micrograms), summed for 20 s, was reduced to 25 per cent of the prehalothane control values; that after NaCN (25 micrograms) was reduced to 17 per cent of the control value. The effect of halothane was prompt (half complete in 1-2 min) and reversible. This finding explains some of the inhibition of the ventilatory responses to hypoxia and hypercapnia caused by halothane.
Anesthesiology 1982 Sep
PMID:Halothane depresses the response of carotid body chemoreceptors to hypoxia and hypercapnia in the cat. 711 37

The development of bacterial infections is a common complication during treatment with high concentrations of oxygen. To study the effect of hyperoxia on phagocytes, the adherence, chemotaxis, ingestion rates, degranulation as well as the bactericidal activity were measured in alveolar macrophages (AMs) and polymorphonuclear leukocytes (PMNs) obtained from guinea pigs exposed to 85% oxygen. The animal exposure to a Fi O2 of 85% impaired the adherence to nylon-wool, the chemotactic activity and the phagocytic rate of paraffinoil-droplets of AMs and PMNs. In AMs the secretion of beta-glucuronidase upon stimulation with opsonized zymosan was also diminished. In addition, the bacterial activity of AMs and PMNs demonstrated a reduction of 50%. These phagocytic defects may be caused by cytoskeleton alteration, induced by the increase of oxygen derived metabolites, representing an additional sepsis promoting factor during hyperoxia.
Blut 1982 Sep
PMID:Effects of hyperoxia on phagocytosis. 711 85

Bacterial endotoxin has a marked protective effect against pulmonary O2 toxicity in rats placed directly in atmospheres of greater than 95% O2. To determine whether endotoxin treatment during exposure to relatively low levels of hyperoxia would protect rats from the accelerated O2 toxicity that normally occurs when these rats are transferred to greater than 95% O2, we gave endotoxin or saline 1) during exposure to 40% O2 (5 days), or 2) during exposure to 40%-60%-85% O2 (2 days at each level). Saline-treated rats showed significantly decreased tolerance on transfer to greater than 95% O2 [LT50 = 47.5 h (exposure 1) and 48.5 h (exposure 2)] compared with normal nonpreexposed rats (LT50 = 66 h). In contrast, endotoxin-treated rats showed a marked tolerance on transfer to greater than 95% O2 [% of rats surviving 72 h = 14/16 (88%) endotoxin-treated vs. 2/16 (13%) saline-treated]. The endotoxin-treated rats, unlike the saline-treated rats, showed significant elevations in lung superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase levels after the O2 preexposure periods; this may account for their significantly improved tolerance when challenged with greater than 95% O2 exposure.
J Appl Physiol Respir Environ Exerc Physiol 1981 Sep
PMID:Endotoxin reverses the decreased tolerance of rats to greater than 95% O2 after preexposure to lower O2. 732 58

The conventional Douglas bag calculation for estimating O2 uptake (VO2) during exercise in normoxia and hyperoxia, VO2 = VE . (FIO2 . FEN2/FIN2 - FEO2), was tested against two other valid calculations: the Fick equation, VO2 = VI . FIO2 - VE . FEO2, and the equation VO2 = VI - VE - VCO2 (VE and VI are expired and inspired ventilation, respectively; FEO2 and FIO2 are expired and inspired O2 contents, respectively; FEN2 and FIN2 are expired and inspired N2 contents, respectively; and VCO2 is CO2 production.). These calculations are based on different assumptions, in part, and are affected to a varying degree of errors in volume or gas fraction measurements. With the conventional Douglas bag technique, we found evidence of an overestimate of VO2 during hyperoxia. After the introduction of a mixing chamber for sampling expired air, the means of the three methods were not significantly different. The variability among the methods was least with the conventional calculation but increased with higher O2 fractions. The average VO2 for submaximal exercise in hyperoxia was not significantly different from that of normoxia. VO2 max was significantly higher in hyperoxia. The increased variability of the Douglas bag method in hyperoxia may lead to overestimates of VO2 max unless special precautions are taken.
J Appl Physiol Respir Environ Exerc Physiol 1981 Sep
PMID:Measurement of metabolic rate in hyperoxia. 732 74

Both distal (canine lung strips) and proximal (bovine trachealis strips) airway smooth muscle contract in isolated organ baths as the percentage of environmental oxygen is increased from 12% to 95%. This effect is blocked by prostaglandin synthetase inhibitors (indomethacin, 10(-4)M; meclofenamate, 10(-4)M). To determine whether this contractile response is due to molecular oxygen, or to other products of oxidative metabolism, we examined the effects of ozone, hydrogen peroxide, and superoxide radical generating systems (paraquat and xanthine-xanthine oxidase) on the smooth muscle preparations. Ozone (3 ppm), paraquat (2 mM), and xanthine (10(-3)M)-xanthine oxidase (1 unit) were without effect. Hydrogen peroxide (10(-5)-10(-3)M) produce consistent contractions in both preparations, an effect which was appreciably greater in an hypoxic environment and which was blocked by both indomethacin and meclofenamate. Contraction from both hyperoxia and hydrogen peroxide was partially reversed by various oxygen radical scavengers, including methional (10 mM), ascorbic acid (10 mM), nitroblue tetrazolium (0.3 mM), butylated hydroxyanisole (1 mM), and 2',7' naphthalonediol (1 mM). These results suggest that hyperoxic contraction in airway smooth muscle is mediated by active oxygen species, perhaps by their effects on prostaglandin metabolism.
Respir Physiol 1981 Sep
PMID:Hydrogen peroxide contracts airway smooth muscle: a possible endogenous mechanism. 733 Apr 88

Exposure of dark- or light-adapted mice to 1--3 ATA oxygen for times ranging from 15 min to 4 h caused a progressive increase in P-450, which peaked and then decayed. The rate of decay appears to be independent of PO2. A linear, inverse relationship was noted between the PO2 in the range of 1--4 ATA and the duration of exposure needed to obtain maximum P-450 levels. Cytochrome P-450 was induced by hyperoxia in vitro in a suspension of hepatocytes, and this induction was prevented by inhibitors of transcription and translation and by disulfiram. Cytochrome P-450 induction is not a general phenomenon of stress, albeit physical restraint may decrease the level of P-450 induced. Induction was a specific effect of increased oxygen tensions and was not due to pressure per se. Neither equivalent pressures of compressed air in the in vivo experiments nor equivalent pressures of nitrogen in the in vitro experiments induced P-450. Induction in vivo was inhibited by disulfiram and metyrapone. Hyperoxia is the most rapid inducer of P-450 yet found, and this response may represent a protective mechanism against hyperoxia.
Undersea Biomed Res 1980 Sep
PMID:In vivo and in vitro induction of cytochrome P-450 synthesis in hyperoxia. 742 54

We have previously found an age-dependent relaxing effect of furosemide in normal fetal, newborn, and adult guinea pig airways with fetal trachea exhibiting the greatest relaxation and adult tissue the least. This study was designed to expand upon this finding by determining if in vivo hyperoxic exposure would influence in vitro airway relaxation mediated by the loop diuretics, furosemide and ethacrynic acid, and the beta 2-adrenoceptor agonist, salbutamol. Newborn guinea pigs were raised in > 95% FiO2 until ill; controls in room air. Isometric relaxation to 3 x 10(-5) M furosemide, 3 x 10(-6) M ethacrynic acid, or 10(-8)-10(-6) M salbutamol was recorded in 3 x 10(-6) M histamine-constricted airway rings. Ethacrynic acid, like furosemide, relaxed newborn guinea pig airways. Hyperoxia did not alter the contractile effect of 3 x 10(-6) M histamine but did significantly decrease the relaxing effect of furosemide, ethacrynic acid, and salbutamol. Loop diuretic mediated airway relaxation was accentuated in HEPES buffer when compared with Krebs, whereas salbutamol-mediated relaxation was unaffected. These results suggest that hyperoxia nonspecifically decreases airway responsiveness to the relaxing agents studied.
Pediatr Res 1995 Sep
PMID:Acute hyperoxic injury attenuates the relaxing effects of "loop" diuretics and salbutamol on large airways of newborn guinea pigs. 749 47

In full-term newborn rats, propylthiouracil (PTU) treatment has been previously shown to decrease susceptibility to O2-induced lung damage and improve survival during hyperoxic exposure. However, no differences were found in lung antioxidant enzyme (AOE) activity responses to hyperoxia compared with O2-exposed untreated (control) term rats. To further explore possible pulmonary protective effects of PTU treatment in prematurely delivered animals, we administered PTU (0.015%) in drinking water to timed-pregnant rats for the final 10 d of gestation prior to delivery 1 d before term, and during lactation; control pregnant/nursing rats received untreated water. Both groups of 21-d premature rat pups were randomized to either > 95% O2 or room air exposure after birth for up to 14 d. The left lungs of 7-d exposure pups were used to quantitate the concentrations of AOE mRNA by solution hybridization; the right lungs of the same pups were assayed for AOE activities. PTU treatment resulted in survival rates of O2-exposed preterm rat pups that were consistently higher at all time periods in hyperoxia including 7 d [PTU, 67 of 82 (82%) versus control pups, 58 of 113 (51%); p < 0.001] and 14 d [PTU, 31 of 39 (79%) versus control, 15 of 66 (23%); p < 0.001]. Further evidence of increased tolerance to > 95% O2 in PTU pups included a significant decrease in the incidence of microscopic intraalveolar edema and a significant increase in lung tissue surfactant-related phospholipids compared with O2-exposed control pups.(ABSTRACT TRUNCATED AT 250 WORDS)
Pediatr Res 1995 Sep
PMID:Premature rats treated with propylthiouracil show enhanced pulmonary antioxidant enzyme gene expression and improved survival during prolonged exposure to hyperoxia. 749 49

1. Incubation of Escherichia coli with 0.7 mM doxorubicin in MBS-glucose medium resulted in complete growth inhibition, an inhibition that was blocked by placing specific amino acids (AA) in the medium. 2. The mechanism of protection by AA was similar to that reported previously for cells poisoned by hyperoxia and by paraquat, e.g. of 20 common AA, ten percent, ten do not and the branched-chair AA are among those required for inhibition. 3. Unlike hyperoxia and paraquot stringency which caused elevation of intracellular concentrations of guanosine tetraphosphate (ppGpp), doxorubicin inhibition did not elevate ppGpp. 4. Concentrations of ppGpp were increased by isoleucine starvation as expected, and the subsequent addition of doxorubicin did not abolish that increase; however, pretreatment with doxorubicin prevented the induction of stringency by isoleucine starvation. 5. This suggests that doxorubicin directly inhibits ppGpp synthesis or protein biosynthesis to leave tRNA loaded as is the case with chloramphenicol.
Gen Pharmacol 1995 Sep
PMID:Protection by selective amino acid solutions against doxorubicin induced growth inhibition of Escherichia coli. 755 72


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