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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To determine the role of hypoxic pulmonary vasoconstriction in pneumococcal pneumonia, hemodynamic measurements were made in 16 dogs before, and within 36 hours after, intrapulmonary administration of type III pneumococcus. Ten dogs with one lobe or more of pneumonia increased their pulmonary vascular resistances and slightly decreased their arterial O2 tensions. Hypoxia increased and
hyperoxia
decreased their pulmonary vascular resistances. During O2 breathing, arterial PO2 was less during than before the pneumonia and increased when pulmonary perfusion was diverted away from the diseased lung. In 2 dogs breathing air, forcing the cardiac output through the diseased lung caused an increase in vascular resistance that could clearly be reduced by O2 breathing. In 5 dogs, lung mast cell counts showed no decrease in the lobes with pneumonia. In pneumococcal pneumonia, the hypoxic pulmonary pressor mechanism serves to decrease blood flow to the diseased lobes and, thus, to maintain the arterial PO2. Lung mast cells could participate in this response.
Am Rev Respir Dis 1975
Dec
PMID:Preservation of hypoxic pulmonary pressor response in canine pneumococcal pneumonia. 0 Sep 35
10 Blood acid-base changes were studied at 17 degrees C in immersed crabs (Carcinus maenas) exposed to hypoxic and hyperoxic conditions, by measuring the pH and the CO2 partial pressure, PbCO2, and by calculating the bicarbonate concentration. 20
Hyperoxia
first induces a marked respiratory acidosis with a rise of PbCO2. This acidosis is compensated thereafter by a non-ventilatory increase of the blood buffer base concentration. These results are discussed in relation to the general problems concerning the control of the blood acid-base balance in aquatic animals.
J Physiol (Paris) 1975
Dec
PMID:[Blood acid-base changes produced by variations of water oxygenation in the crab Carcinus maenas (author's transl)]. 0 15
To investigate the influence of variations in arterial oxygen tensions (PaO2), arterial carbon dioxide tensions (PaCO2), and arterial pH on long bone medullary pressures, seven anaesthetized dogs were investigated. Comparing the control medullary pressures, i.e. the mean medullary pressures obtained at the normal range of PaO2 (75--110 mmHg) with the mean medullary pressures corresponding to the range of PaO2 of less than 75 mmHg, statistically significant (P less than 0.05) decreases were seen in both epiphyseal, metaphyseal and diaphyseal medullary pressures, from 27.6 +/- 5.0 to 15.5 +/- 3.6 mmHg, from 23.5 +/- 2.9 to 13.9 +/- 2.3 mmHg and from 27.7 +/- 3.9 to 18.3 +/- 2.5 mmHg (all mean values +/- s.e. mean), respectively.
Hyperoxia
, hypocapnia, hypercapnia or metabolic acidosis had no effect on medullary pressures in any of the regions studied.
Acta Orthop Scand 1979
Dec
PMID:Observations on long bone medullary pressures in relation to arterial PO2, PCO2 and pH in the anaesthetized dog. 4 59
The reactivity of subpleural strips of lung parenchyma reflects primarily the tone of the smooth muscle in the peripheral airways. Lung strips taken from ten dogs relaxed when the oxygen level in the gas bubbling through the bath was reduced from 95% to 18%. Subsequent hypocapnia (carbon dioxide reduced from 5% to 0%) induced contraction of all strips. These changes were reversed when the oxygen or carbon dioxide tensions were restored to control levels. Addition of either indomethacin or meclofenamate, two chemically dissimilar inhibitors of prostaglandin synthetase, reduced the resting tone in each of six strips and prevented the hyperoxic constriction which was observed in paired, control strips (oxygen increased from 18% to 95%). Blockers of histamine and catecholamines had no effect. The reactivity of the distal airways to changes in gas tension provides a mechanism by which ventilation and perfusion can be matched. The action of indomethacin and meclofenamate indicates that a prostaglandin-like substance may be involved in the maintenance of distal airway tone and in the constriction produced by
hyperoxia
. The addition of prostaglandin F2 alpha or E1, after meclofenamate, in a further nine pairs of strips did not restore the hyperoxic constriction. This suggests that prostaglandins may mediate, rather than merely facilitate, the response.
Respir Physiol 1979
Dec
PMID:Distal airway responses to changes in oxygen and carbon dioxide tensions. 52 47
The effects of
hyperoxia
at ambient pressure on thyroid function and thyroid hormone metabolism have been assessed. Thyroidal activity was depressed in mice and rats by exposure to
hyperoxia
, due at least in part to a decrease in the rate of secretion of pituitary thyrotropin. The effects of
hyperoxia
on the peripheral deiodination of thyroxine (T4) were dependent on the concentration of oxygen employed and/or the duration of exposure; exposure to 40--80% oxygen for 96 h resulted in decreases in the rate of deiodination and in the deiodinative clearance of [125I]T4.
Hyperoxia
also resulted in a marked fall in the serum concentration of endogenous T4 and a decrease in T4-binding activity in serum. Many of these effects of
hyperoxia
were prevented by the concomitanat administration of large amounts of vitamin E (alpha-tocopherol acetate). These decreases in thyroid function and T4 metabolism were associated with a decrease in the rate of whole body oxygen consumption. Thus, the deleterious effects of oxygen in the rat were not due, even in part, to an oxygen-induced hyperthyroid state in the peripheral tissues.
Am J Physiol 1978
Dec
PMID:Role of thyroid gland in oxygen toxicity. 73 22
Two hundred suckling mice from 20 litters were used for determining their functional development of the hyperoxic convulsion mechanism. It was found that 1 to 12-day-old mice did not develop convulsion when they were subjected to oxygen under high pressure. The hyperoxic convulsion was observed in 1 of 10 13-day-old (10%), 3 of 10 14-day-old (30%), 16 of 20 15-day-old (80%) and all of 16-day-old mice (100%). This finding indicates that the hyperoxic convulsion mechanism of the young mice takes 13-16 days for functional maturation. Besides, it was shown that
hyperoxia
could cause pulmonary damage, the incidence of which also increased with age of suckling mice.
Chin J Physiol 1975
Dec
31
PMID:High oxygen pressure-induced convulsions in suckling mice. 123 37
To evaluate the regulation of endothelial cell Cu,Zn-SOD, we have exposed bovine pulmonary artery endothelial cells in culture to
hyperoxia
and hypoxia, second messengers or related agonists, hormones, free radical generating systems, endotoxin, and cytokines and have measured Cu,Zn-SOD protein of these cells by an ELISA developed in our laboratory. Control preconfluent and confluent cells in room air contained 196 +/- 18 ng Cu,Zn-SOD/10(6) cells. A23187 (0.33 microM), forskolin (10 microM), isobutylmethylxanthine (0.1 mM), dexamethasone (1 microM), triiodothyronine (1 microM) and retinoic acid (1 microM) failed to alter this level of Cu,Zn-SOD. Exposure to anoxia and
hyperoxia
both elevated the level approximately 1.5-2.0-fold over 20% oxygen-exposed controls at 48-72 hr. Similarly, exposures to glucose oxidase (0.0075 units/ml), menadione (12.5 microM), xanthine-xanthine oxidase (10 microM, 0.03 units/ml) and H2O2 (0.0005%) increased the level up to two-threefold over controls at 24-48 hr. Lipopolysaccharide, TGF beta 1, TNF alpha, and Il-1 also increased levels of cellular Cu,Zn-SOD, but only in proliferating cells. Il-2, Il-4, interferon-gamma, and GM-CSF had no effect on Cu,Zn-SOD. All treatments that elevated SOD resulted in inhibition of cellular growth, but decreased growth of cells at confluence alone was not associated with increased Cu,Zn-SOD. We propose from these studies that Cu,Zn-SOD of endothelial cells is not under conventional second messenger or hormonal regulation, but that up-regulation of the enzyme is associated with (and perhaps stimulated by) free-radical or oxidant production that also may be influenced by availability of certain cytokines under replicating conditions.
J Cell Physiol 1992
Dec
PMID:Regulation of Cu,Zn-superoxide dismutase in bovine pulmonary artery endothelial cells. 133 80
The current study traces the development of contractile cells in the nonmuscular segments of rat lung microvessels in hyperoxic pulmonary hypertension. New intimal cells first develop into a well-defined layer beneath the endothelium and internal to an elastic lamina. Ultrastructurally, these cells are found to be 1) fibroblasts recruited to the vessel wall from the interstitium and 2) intermediate cells, a population of preexisting vascular cells (structurally between a smooth muscle cell and a pericyte). Early in
hyperoxia
(days 3 through 7), interstitial fibroblasts migrate and align around the smallest vessels in which an elastic lamina is either absent or fragmentary. These cells then are incorporated into the vessel wall by tropoelastin secretion and the formation of an elastic lamina along their abluminal margin. After day 7, the new mural fibroblasts acquire the features of contractile cells, namely a basal lamina, extensive microfilaments, and dense bodies. In other vessels, as early as day 3 of
hyperoxia
, intermediate cells within the vessel intima begin to acquire the additional filaments and dense bodies of contractile cells. As
hyperoxia
continues, each cell pathway gives rise to vessels with distinct intimal or medial layers of contractile cells. In this way, thick-walled 'newly muscularized' vessel segments form adjacent to the capillary bed.
Am J Pathol 1992
Dec
PMID:Ultrastructural analysis of contractile cell development in lung microvessels in hyperoxic pulmonary hypertension. Fibroblasts and intermediate cells selectively reorganize nonmuscular segments. 146 6
Rat brain mitochondria were isolated and their respiration was polarographically measured without contact with air oxygen. Gas-saturated experimental mixtures close to the in vivo partial oxygen pressure (normoxic) were compared with the air-saturated, i.e. hyperoxic, mixtures. The rate of phosphorylating oxidation of added succinate under normoxic conditions was found to be 70-100% higher compared with hyperoxic ones. The addition of succinate dehydrogenase activators results in a more than two-fold stronger stimulation of succinate oxidation under normoxia than under
hyperoxia
. Thiol group donors are shown to stimulate respiration under
hyperoxia
and not under normoxia. Hyperoxic conditions prevented oxidation of the low succinate concentrations corresponding to the physiological ones.
FEBS Lett 1992
Dec
21
PMID:Air saturation of the medium reduces the rate of phosphorylating oxidation of succinate in isolated mitochondria. 146 56
Prolonged apnea and cardiovascular changes have been elicited in infant animals by the application of water to the laryngeal mucosa. Previous reports have produced conflicting evidence in regard to the possible role of arterial chemoreceptors in modulating this reflex. The present study was designed to determine the effect of carotid body stimulation or suppression on the duration of apnea and severity of cardiovascular changes in response to water in the larynx of piglets. The role of swallowing in terminating the apnea was also investigated. Hypoxia and isoproterenol, both carotid body stimuli, caused decreased apnea duration.
Hyperoxia
was associated with prolonged apnea duration; however, dopamine, which inhibits carotid body chemoreceptors, produced no significant change. Hypotension and bradycardia were only observed after prolonged apnea or chemoreceptor stimulation, supporting the concept that the cardiovascular component of the laryngeal chemoreflex is a result of changes in blood gas concentration rather than a direct response to laryngeal chemostimulation. The interval between water application and initiation of swallowing was not significantly affected by hypoxia or carotid body stimulation and swallowing did not always occur before resumption of breathing.
Otolaryngol Head Neck Surg 1992
Dec
PMID:Arterial chemoreceptor influences on the laryngeal chemoreflex. 147 Apr 57
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