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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The total Mg2+-ATPase and
Na+
, K+-ATPase activity was studied in the fractions of "400 g X for 20 min" and "900 g X for 30 min" conditionally called the fraction of the external cellular membranes and total fraction of mitochondria. The subcellular fractions were isolated from great hemispheres and stem part of the rat brain. The brain of control animals and those during a severe spasmodic attact induced by the oxygen action at a pressure of 6 ati was studied. The total ATPase activity is established to be practically the same in the studied brain areas and unchanged with
hyperoxia
.
Hyperoxia
accompanying by convulsions results in an increase in the activity of Mg2+-ATPase and in a decrease in that of
Na+
, K+-ATPase both in the cerebral cortex and the stem part. The authors suppose that the decrease in the enzyme activity may occur due to an inhibitory effect on it of the lipids reoxidation products formed in the brain with
hyperoxia
.
...
PMID:[ATPase activity of subcellular rat brain fractions following hyperoxia]. 13 79
Right and left gastrocnemius-plantaris muscle preparations in 20 dogs anesthetized with pentobarbital
sodium
were used to investigate the effect of
hyperoxia
on tension maintenance. Muscles were stimulated via the sciatic nerve for 20 min at 60 200-ms tetanic contractions/min (10 impulses/contraction). Direct muscle stimulation after the experimental period resulted in no significant change in tension. In control experiments the tension developed by the right or left muscles over the 20 min was not different. The tension developed by muscles perfused with hyperoxic blood decreased 14% after 20 min, whereas tension in the normoxic muscles decreased 35%. Blood flow in the hyperoxic muscles was significantly higher at 20 min (P less than 0.05). Pump perfusion of one of a pair of normoxic muscles resulted in a tension decrease of 13% in the pump-perfused muscles, whereas tension in the control muscles decreased 34%. Tension maintenance was flow dependent. The effect of
hyperoxia
could be mediated through the involvement of oxygen in the long-term control of muscle blood flow.
...
PMID:Interaction of hyperoxia and blood flow during fatigue of canine skeletal muscle in situ. 57 3
1. The influence of some drugs which affect the dopaminergic system was studied on chemosensory responses to dopamine (DA), acetylcholine (ACh),
sodium
cyanide NaCN) and hypoxia during experiments on pentobarbitone anaesthetized cats in which chemoreceptor activity was recorded from the peripheral end of a sectioned sinus nerve. 2. Spontaneous chemosensory activity was inhibited in a dose-dependent manner by DA (0.5-5 microgram, I.A.). Higher doses (10-50 microgram) caused a delayed increase in discharge and were associated with inconsistent inhibitory responses. 3. The DA antagonist alpha-flupenthixol (0.2 mg/kg, I.A.) blocked the inhibitory response to DA without affecting either the spontaneous discharge frequency or the response to ACh. The effect of NaCN was potentiated, and during hypoxia chemoreceptor activity increased more rapidly, although the maximum frequency attained was not appreciably different from control values. Similar results were obtained with haloperidol (0.5 and 1.0 mg/kg, I.V.). 4. Higher doses of alpha-flupenthixol (0.5-1.0 mg/kg, I.A.) increased spontaneous chemoreceptor activity, but this was regarded as a non-specific effect of the drug since at these doses the inhibitory effect of 5-hydroxytryptamine (5-HT) was also abolished. 5. The animals were exposed to alternate periods of hypoxia and
hyperoxia
following administration of the tyrosine hydroxylase inhibitor alpha-methyl p-tyrosine (AMPT, 0.2-10 mg/kg, I.A.). The inhibitory response previously evoked by amphetamine was abolished, and electron microscopic studies showed a great reduction in the number of dense-cored granules, both of which suggested that DA levels in the carotid body had been substantially reduced. Responses to NaCN and hypoxia were slightly potentiated following AMPT, but neither spontaneous activity nor the response to ACh was affected. 6. Apomorphine (0.05-0.2 mg/kg, I.A.) inhibited the chemoreceptor discharge for up to 45 min, an effect which was antagonized by alpha-flupenthixol (0.2 mg/kg, I.A.), implying it resulted from DA receptor stimulation. Although responses to NaCN, hypoxia and higher doses of ACh were reduced following administration of apomorphine, the reduction was not very marked. 7. These results are not compatible with the theory of Osborne & Butler (1975), that in normoxia DA is tonically released in the carotid body and suppresses spontaneous chemosensory activity. 8. It is concluded that DA modulates chemosensory activity by influencing the rate of increase in discharge, without affecting maximum discharge frequency. The mechanism whereby DA is released in response to increased chemosensory activity remains to be established.
...
PMID:Inhibitory action of dopamine on cat carotid chemoreceptors. 67 58
Exposure of rainbow trout to environmental
hyperoxia
(PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [
Na+
]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
...
PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56
Microscopic fluorometry was used to examine the effects of anoxia and cyanide (CN-) on cytosolic calcium [Ca2+]i of cultured carotid body (CB) glomus cells from newborn rabbits. Applications of high K+ and veratridine (VRT), a sodium channel activator, induced rapid and marked increases in [Ca2+]i. These effects were inhibited by D600 a calcium channel blocker. [Ca2+]i changes induced by VRT were also blocked by tetrodotoxin (TTX). Glomus cells exhibited a slow increase in [Ca2+]i in response to anoxia and CN-, and a slight decrease during
hyperoxia
. The effects of anoxia and CN- were blocked by D600 but not by TTX. We conclude that these stimuli induce calcium entry into glomus cells via voltage-dependent Ca2+ channels. Voltage-dependent
Na+
channels were not involved.
...
PMID:Response of cytosolic calcium to anoxia and cyanide in cultured glomus cells of newborn rabbit carotid body. 191 62
Exposure of adult rats to 85% ambient oxygen increased the content of surfactant proteins SP-A, SP-B, and SP-C recovered from alveolar lavage. The surfactant proteins increased during 1 to 7 d of oxygen exposure. The increased surfactant protein was associated with increased relative abundance of mRNA encoding each of the proteins in lung tissue. Exposure to
hyperoxia
progressively increased the amounts of the surfactant proteins in alveolar lavage fluid as estimated by immunoblot analysis after
sodium
dodecyl sulfate-polyacrylamide gel electrophoresis. The mRNAs encoding SP-A (1.7 and 1.0 kb), SP-B (1.6 kb), and SP-C (0.9 kb) increased significantly after oxygen exposure for 5 d. The present findings support the concept that oxygen exposure mediates surfactant protein expression at a pretranslational level.
...
PMID:Increased expression of pulmonary surfactant proteins in oxygen-exposed rats. 199 Oct 71
The effects of HCl infusion on multipoint mean pulmonary arterial pressure (PAP)/cardiac index (CI) plots in pentobarbital-anesthetized dogs whose lungs were ventilated alternately in
hyperoxia
(fraction of inspired O2 [FIO2], 0.4) and hypoxia (FIO2, 0.1) were investigated. Over the range of CI studied (1 to 5 l.min-1.m-2), hypoxia increased PAP in 22 dogs (responders) and did not affect PAP in 16 other dogs (nonresponders). In eight nonresponders, two repetitions of alternated 0.4 and 0.1 FIO2 exposures did not restore hypoxic pulmonary vasoconstriction (HPV), defined as a hypoxia-induced increase in PAP at a given flow. Intravenous infusion of 2 M HCl (2 mmol.kg-1.h-1) decreased arterial pH from normal to around 7.20 in eight responders and eight nonresponders. This metabolic acidosis increased PAP at all levels of CI in
hyperoxia
and in hypoxia in all the dogs, enhanced HPV in the responders, and restored HPV in the nonresponders. In eight responders, 2 M HCl infusion (2 mmol.kg-1.h-1) together with a 7%
sodium
bicarbonate infusion (adjusted to maintain arterial pH unchanged) did not affect hyperoxic or hypoxic PAP/CI plots. Pretreatment with 1 g acetylsalicylic acid iv (6 dogs) did not affect the pulmonary vasoreactivity to HCl-induced (2 M HCl, 2 mmol.kg-1.h-1) metabolic acidosis. It was concluded that in intact dogs: 1) metabolic acidosis enhances HPV; 2) at the given dose, HCl does not produce pulmonary vascular effects unrelated to the circulating blood pH; and 3) it is unlikely that the pulmonary vasoreactivity to metabolic acidosis is mediated by products of the cyclooxygenase pathway.
...
PMID:Enhancement of hypoxic pulmonary vasoconstriction by metabolic acidosis in dogs. 216 53
Resistance of mice to altitude, gas, hemic, tissue, mixed or hyperoxis hypoxia, to oxidative phosphorylation uncoupling agents and to X-ray irradiation during 2 days after exposure to severe acute hypobaric hypoxia was investigated. No significant changes were found in animal resistance to hemic and tissue hypoxia and to oxidative phosphorylation uncoupling agents. Resistance to hypoxic hypoxia was 2.5 times higher at the 2nd hour of the posthypoxic period and returned to the baseline by the 24 th hour. Resistance to
sodium
nitrite and potassium persulphate that cause hypoxia of mixed type, to
hyperoxia
and X-raying increased significantly by the 24th hour and returned to the baseline by the 48th hour of the posthypoxic period. The potential role of the antioxidative system in the induction of resistance to oxidative agents and X-ray irradiation during the posthypoxic period is discussed.
...
PMID:[Resistance of mice to hypoxia of various types and to X-ray radiation in the post-hypoxic period]. 232 67
To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital
sodium
-anesthetized dogs ventilated alternately in
hyperoxia
[fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In
hyperoxia
, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.
...
PMID:Inhibition of hypoxic pulmonary vasoconstriction by increased left atrial pressure in dogs. 237 17
Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction (HPV). This has been explained by a reflex vagal (Chapleau et al., 1988) or sympathetic (Naeije et al., 1989) pulmonary vasodilation. We therefore investigated the effects of bilateral cervical vagotomy and of muscarinic block (atropine sulfate 0.1 mg.kg-1 i.v.) on multipoint pulmonary arterial pressure (Ppa)-cardiac index (Q) plots in 16
sodium
pentobarbital-anesthetized dogs ventilated alternately in
hyperoxia
(fraction of inspired O2, FIO2, 0.4) and in hypoxia (FIO2 0.1). Over the range of Q studied, 2 to 5 L.min-1.m-2, hypoxia increased Ppa and did not change pulmonary capillary wedge pressure (Ppw). After bilateral cervical vagotomy or after atropine, Ppa and Ppw at all levels of Q were not modified either during
hyperoxia
or during hypoxia. These results show that the parasympathetic system does not affect the global hypoxia-induced pulmonary vasopressor response and thus suggest that the depressor effect of chemoreceptor stimulation on HPV is not vagally mediated.
...
PMID:Absence of parasympathetic control of pulmonary vascular pressure-flow plots in hyperoxic and hypoxic dogs. 260 23
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