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

A review of anatomical and biochemical responses of the lung to high concentrations of oxygen leads us to postulate a biphasic adaptive response. The early phase entails a defense against life-threatening pulmonary edema engendered by destruction of oxygen susceptible cells forming most of the air-blood interface. This defense is brought about by type II alveolar cell replication to reform a continuous epithelial layer in the alveoli; its success would depend upon the rapidly with which this continuity can be reestablished. Factors favoring a successful defense would include an initial large population of type II cells or the ability of type II cells to divide fast enough to reestablish continuity before of oxygen-sensitive cells (type 1 alveolar epithelial and endothelial cells) proceeds to fatal pulmonary edema; both conditions probably exist in young animals, which are known to be more resistant to hyperoxia than old animals. The second phase of adaptation would require the development of increased tolerance of previously susceptible cells to continued exposure to high oxygen concentrations to prevent their total destruction. We postulate that here the development of new biochemical defenses or the augmentation of those previously present would play a major role.
Fed Proc 1978 Sep
PMID:Biochemical and anatomical adaptation of the lung to oxygen-induced injury. 2 61

Central respiratory drive responding to pH changes was eliminated by bilateral coagulation or cold block of area S (intermediate area) on the ventral medullary surface in 7 anaesthetized cats. Arterial pH, PCO2, and PO2 (4 cats) and the respiratory response to hypoxia and hypercapnia (6 cats) were observed before and after coagulation. After coagulation in hyperoxia the arterial pH dropped from 7.30 to 7.09, the arterial PCO2 was elevated from 4.80 kPa to 8.17 kPa (6 cats). Ventilation increased by 477 ml at a PCO2a of 6.58 kPa when PO2a was reduced from 39.5 kPa to 8.5 kPa before coagulation, after coagulation ventilation increased by 241 ml (4 cats). The peripheral chemoreceptors guaranteed spontaneous breathing even in hyperoxia. The data reveal that the loss of respiratory homeostasis by elimination of the S areas is due to the loss of central chemosensitive drive with concomitant reduction of peripheral chemoreceptor effect.
Pflugers Arch 1979 Sep
PMID:Respiratory response to hypoxia and hypercapnia after elimination of central chemosensitivity. 4 38

To study the ultrastructural effects of hyperoxia on the kidney, young adult Sprague Dawley rats were exposed to 3 atmospheres absolute (ATAs) of pure oxygen for 5 hours and were killed in a time sequence varying from immediately to 30 days after exposure. Their renal cortices were processed for electron microscopy. Selective mitochondrial changes were observed within sublethally and transiently altered proximal tubular epithelial cells. The most consistent finding was the accumulation of 0.08 mu to 0.5 mu round to ovoid homogeneous matrical inclusions which frequently formed larger confluent amorphous masses. The inclusions stained intensely with lead and uranium but appeared homogeneously electron-lucent in unstained sections. Energy-dispersive x-ray analysis revealed that they did not contain calcium or phosphorus. The inclusions were different from the innately electron-opaque flocculent densities commonly found in pathologically altered mitochondria. Since the mitochondria containing them were removed by autophagocytosis, it is suggested that the inclusions were associated with selective mitochondrial degeneration induced by hyperoxia. No glomerular lesions were found.
Am J Pathol 1979 Sep
PMID:Selective mitochondrial degeneration in renal tubules following hyperbaric oxygen exposure. 22 8

Secretion of alpha-amylase by the human parotid gland increased significantly during eight days of hyperbaric exposure. This hyperactivity of the parotid gland presumably resulted from increased autonomic nervous system (ANS) activity attributable to (1)psychological stress in the form of anticipation; (2) dive-related factors, i.e., hyperoxia, PN2, physical stress; or (3) a combination of both. The etiology of the effect must await additional studies, but a consistent and significant elevation in alpha-amylas secretion was found. This previously undescribed effect of hyperbaric exposure indicates that parotid alpha-amylase sampling holds promise as a noninvasive means of monitoring physical and psychological stress, and as an indirect measure of ANS tone.
Undersea Biomed Res 1979 Sep
PMID:Human parotid alpha-amylase secretion as a function of chronic hyperbaric exposure. 31 98

The present study is the first investigation to demonstrate, by employing the combined approach of immunologically and electron microscope methods, the presence of actin-like contractile proteins in the mammalian retina, the corneal epithelium and endothelium, the iris, and the ciliary body, and to confirm their presence in lens epithelium. This is also the first report to demonstrate by these methods the presence of microfilaments and intermediate filaments in retinal vascular endothelium. Since we have shown that actin filaments are especially abundant in immature retinal endothelial cells, the question of their function arises, and we have discussed their possible relevance to the closure of immature retinal vessels when exposed to hyperoxia.
Br J Ophthalmol 1978 Sep
PMID:Contractile proteins in retinal endothelium and other non-muscle tissues of the eye. 36 Oct 70

There is in vitro evidence to support the notion that directed migration (chemotaxis) is involved in the recruitment of alveolar macrophages in vivo. Because O2 is widely used in the treatment of pulmonary diseases, we examined the effect of hyperoxia on migration of guinea pig alveolar macrophages in vitro. Migration was measured in blind-well chambers incubated in either room air or hyperoxia. N-formyl-methionyl-phenylalanine was used to stimulate random migration and to produce directed migration. Migration was quantified by counting the number of mononuclear cells per oil immersion field that had migrated completely through a polycarbonate filter with 5-micrometer pores. The average PO2 in the cell suspensions incubated in room air was 100 mm Hg. In the hyperoxic environments, the average PO2 at 1 h was 260 mm Hg, whereas at 2 and 3 h, it was 410 and 425 mm Hg, respectively. In 6 separate experiments, there was no significant difference between the mean response to N-formyl-methionyl phenylalanine in hyperoxia and in room air after 1 h of incubation. After 2 and 3h of incubation, however, the response in hyperoxia was significantly (P less than 0.002) lower than that in room air. The decreased response in hyperoxia did not appear to result from loss of viability of responding cells, diminished adherence of cells to the filters, loss of activity of N-formyl-methionyl phenylalanine exposed to high PO2, or failure of the cells to exhibit directed migration. Instead, it appeared that hyperoxia decreased the response of alveolar macrophages primarily by impairing random migration.
Am Rev Respir Dis 1979 Sep
PMID:The effect of hyperoxia on migration of alveolar macrophages in vitro. 48 31

To study transvascular filtration of fluid and microvascular permeability to protein in the lung during prolonged hyperoxia, we measured lung lymph flow, protein transport, and simultaneous pulmonary vascular pressures of six lambs breathing 100 percent O2 for five days. Lymph flow doubled, protein flow increased by 131 percent, and radioactive tracer studies demonstrated a clearcut increase in pulmonary microvascular permeability to protein after five days of continuous O2 breathing.
Lymphology 1979 Sep
PMID:Pulmonary oxygen toxicity: increased microvascular permeability to protein in unanesthetized lambs. 54 18

The effect of exposure to oxygen on lung metabolism of prostaglandin E2 to 15-keto-prostaglandin E2 and 13-14-dihydro-15-keto-prostaglandin E2 was studied in the isolated, perfused rat lung. During a 30-sec period, lungs were infused with varying concentrations of prostaglandin E2 labeled with hydrogen-3 and the fraction metabolized during one passage was determined. At a prostaglandin E2 concentration of 5 nM, which approximates that in normal mixed venous blood, an average of 93 per cent of infused prostaglandin was metabolized by normal lungs. At prostaglandin E2 concentrations of 2 to 70 micrometer, the fraction metabolized decreased. The computed concentration of prostaglandin E2 for half-maximal rate of metabolism was 4.2 micrometer. Metabolism of prostaglandin E2 by isolated lungs was unaffected by exposure of rats to greater than 97 per cent oxygen at 1 atmosphere absolute for 24 hours, but was markedly depressed after both 36 and 48 hours of hyperoxia. These results indicate that exposure of the rat to oxygen for 36 and 48 hours is associated with decreased ability of the lung to metabolize prostaglandin E2 to its keto derivatives and may result in increased concentration of prostaglandin E2 in the systemic arterial blood.
Am Rev Respir Dis 1978 Sep
PMID:Effect of O2 exposure on pulmonary metabolism of prostaglandin E2. 70 83

Chronic hyperoxia produces pathological changes in lung which can be fatal. With an interest in delineating dietary factors which might affect the pulmonary response to hyperoxia, we fed rats a semi-synthetic diet containing polyunsaturated fatty acids (PUFA) as either 5% or 78% of the fat complement. The rats were exposed to pure oxygen at one atmosphere. Half the animals in each diet group were injected with aspirin during the hyperoxic exposure. Radioimmunoassay of lung prostaglandins (PG) F2alpha, E2 and E1 were performed at 0, 24, 48 and 72 hours. The major findings were: (1) Feeding the high PUFA diet elevated lung PG synthetic potential tenfold over that of low PUFA-fed animals. There was no effect of diet on mortality. (2) Hyperoxia significantly increased F2alpha-synthetic potential during the first 24 hours of hyperoxia and moderately increased the synthetic potential of E2 and E1. (3) Aspirin significantly depressed synthetic potential of all three PG prior to oxygen exposure but its effect was overcome during hyperoxia. Aspirin-injected rats showed 80% mortality in oxygen vs. 50% for saline controls.
Prostaglandins Med 1978 Sep
PMID:Dietary fat type and ambient oxygen tension influence pulmonary prostaglandin synthetic potential. 71 63

Impedance plethysmography was used to measure resting cardiac stroke volume (SV) and thoracic conductive volume (TCV) in four divers at intervals during a prolonged dry saturation dive (17 days at 18.6 ATA and 7 days' decompression). Resting heart rate (HR), blood pressure (BP), and pulmonary minute ventilation (VE) were measured 4 times per day for the duration of the 30-day experiment. The vital capacity (VC) and its subdivisions IC and ERV were measured by spirometry every 3 days. In nonsmokers, VC fell significantly with time (r = 0.64), while VC in smokers increased nearly 400 ml during the first week at pressure before tending to fall with time. Compared to predive, the mean ERV was increased 629 ml at pressure, while VE and respiratory rate were not changed. The increased ERV did not persist postdive and was probably the result of the increased work of breathing a dense gas (4.1 g/liters). Residual volume (RV) measured by nitrogen dilution before and after the dive increased 38% and remained significantly increased (22%) even after one year in 4 divers. It is suggested that hyperoxia (0.3 ATA PO2) combined with increased gas flow resistance caused the VC to fall and RV to increase. The major cardiovascular findings were a transient bradycardia associated with increased stroke volume leading to a significant increase in resting cardiac output associated with an increased rate of rapid ventricular filling, TCV, and BP at depth. Lowering the ambient temperature for 3 days did not re-establish the bradycardia, suggesting that hyperbaric bradycardia is not due to a subtle cold stress.
Undersea Biomed Res 1977 Sep
PMID:Hana Kai II: a 17-day dry saturation dive at 18.6 ATA. IV. Cardiopulmonary functions. 91 Mar 17


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