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

This study assessed the effects of experimentally elevated plasma catecholamine levels on gill ventilation in rainbow trout (Oncorhyncus mykiss) exposed to various external ventilatory stimulants. Trout were exposed to hypoxia (water PO2 (PwO2) = 90 Torr) or hypercapnia (water PCO2 (PwCO2) = 4.5 Torr) for 30 min. These conditions caused gill ventilation volume (Vw) to increase by 2.3- and 1.5-fold, respectively, but did not stimulate release of catecholamines into the blood. While the stimulus (hypoxia or hypercapnia) was maintained, fish were given a bolus injection (0.3 ml), followed by intra-arterial infusion (0.6 ml.h-1), of a catecholamine mixture (2 x 10(-5) mol.l-1 adrenaline + 5 x 10(-6) mol.l-1 noradrenaline) to mimic the physiological concentrations and ratios of these catecholamines observed under more severe hypoxic or hypercapnic conditions. In hypoxic fish, this treatment caused a significant, but transient (5 min) depression of ventilation while during hypercapnia, the administration of exogenous catecholamines caused a more prolonged hypoventilatory response. These hypoventilatory responses occurred despite a catecholamine-induced blood acidosis (a potential ventilatory stimulant). To assess the importance of initial Vw and/or blood respiratory status on catecholamine-mediated hypoventilation, these experiments were repeated under hyperoxic (PwO2 = 640 Torr) hyperoxic hypercapnic (PwO2 = 510 Torr, PwCO2 = 4.8 Torr) or normoxic (PwO2 = 151 Torr) conditions in which Vw was either depressed (3.9-fold during hyperoxia) or unaffected. Intra-arterial infusion of catecholamines did not affect Vw under either of these experimental conditions. These results demonstrate that during a respiratory challenge, such as hypoxia or hypercapnia, physiologically relevant levels of circulating catecholamines can depress Vw and therefore do not support a stimulatory role for circulating catecholamines in the control of ventilation in fish.
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PMID:The effects of catecholamines on ventilation in rainbow trout during hypoxia or hypercapnia. 190 29

1. The peripheral, arterial chemoreceptors in the carotid body are active and responsive in the fetus. At birth, when oxygenation increases, the chemoreceptors are silenced. Over the next few days the sensitivity is reset toward the adult level and the chemoreceptors influence breathing during normal conditions. In order to investigate the underlying mechanisms of this resetting we examined the strength of the chemoreflex in newborn rats and correlated this to the contents of dopamine and noradrenaline in the carotid bodies of the newborn pups and near-term fetuses. Furthermore, turnover rates of dopamine and noradrenaline were determined in newborn rats up to 1 week of age by analysis of catecholamine decreases after inhibition of synthesis with alpha-methyl-p-tyrosine. 2. Chemoreceptor influence was assessed by the method of 'physiological chemodenervation' with hyperoxia of 15-20 s duration in unanaesthetized rat pups. Relative changes in ventilation elicited by hyperoxia were determined by body plethysmography. We found no change in ventilation on the day of birth either in vaginally born rats or in near-term pups delivered by Caesarean section. After 1 day there was a significant decrease in ventilation of -19.4 +/- 2.3% (mean +/- S.E.M.) and at 7 days of age the decrease was -28.8 +/- 2.2%, suggesting an increasing influence from the peripheral chemoreceptors. 3. The contents of dopamine and noradrenaline were measured by high-performance liquid chromatography. Dopamine increased from 3.7 +/- 0.4 pmol (pair of carotid bodies)-1 in the fetus to a peak of 15.9 +/- 2.6, 6-12 h after birth followed by a decline to 7.1 +/- 0.7 at 7 days of age. Noradrenaline levels increased from 1.3 +/- 0.3 in the fetus to 9.6 +/- 1.1 pmol (pair of carotid bodies)-1 after 4 days. The turnover rate of dopamine decreased from 4.4 pmol (pair of carotid bodies)-1 h-1 0-6 h after birth to 1.0 at 6-12 h of age. The turnover rate of noradrenaline also decreased over the first hours following delivery. 4. Since dopamine is an inhibitory neuromodulator in this system, we suggest that the increase in sensitivity seen after the first day of life is, at least in part, due to a decrease in the release of dopamine and thus a removal of an inhibitory mechanism.
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PMID:Development of the arterial chemoreflex and turnover of carotid body catecholamines in the newborn rat. 221 78

1. Noradrenaline (NA;ED90) caused a contraction of the rat aorta which could be separated into two components, a rapid response mediated by release of intracellular Ca2+ and a more slowly developing contraction which relied principally upon Ca2+ influx. 2. Exposure to acute (30 min) hypoxia has been previously shown to reduce the NA-induced contraction (by 28.0 +/- 2.7%, n = 168) which recovered completely upon re-oxygenation (recovery response). In the present study, prolonged exposure to hypoxia (70 h) caused a more pronounced reduction (39.7 +/- 3.0%, n = 90) of the NA-induced contraction, but, re-oxygenation then produced incomplete recovery to 77.9 +/- 3.9% (n = 90) of the control response. 3. Prolonged exposure to 95% O2 caused a 36.5 +/- 3.1% (n = 42) reduction of NA-induced contractions, whereas prolonged exposure to 21% O2 only caused a small (12.6 +/- 3.4%, n = 6) depression of these responses. 4. The component of the NA-induced contraction mediated by release of intracellular Ca2+ is 39.8 +/- 1.3% (n = 83) of the NA contraction in Ca-containing Krebs solution and was previously found to be unaffected by acute hypoxia. However, following prolonged exposure to either hypoxia or 21% O2, this component only reached 30.7 +/- 2.2% (n = 32) or 28.3 +/- 0.9% (n = 6) of the control response, respectively. Prolonged exposure to 95% O2 caused a more pronounced reduction of this component of contraction which then reached 19.1 +/- 2.1% (n = 12) of the control response. 5. Verapamil (10nM-10 microM) produced similar concentration-dependent reductions of NA-induced contractions elicited during control conditions or acute hypoxia; under these conditions, 1 microM verapamil caused a 34.1 + 6.9% (n = 6) and a 41.8 + 2.9% (n = 18) reduction of these responses respectively. However, recovery responses caused by re-oxygenation of tissues exposed to acute hypoxia were more sensitive to verapamil which, at a concentration of 1 microM, caused a 59.2 + 2.7% (n = 18) reduction of these responses. Verapamil (10 nM-10 microM) also caused similar pronounced concentration-dependent reductions of contractions elicited during prolonged exposure to normoxia or hyperoxia and of recovery responses obtained following re-oxygenation of tissues exposed to prolonged hypoxia; 1 microM verapamil caused a 62.5 + 1.1% (n = 6), 77.2 + 3.8% (n = 12) and a 68.0 + 4.3% (n = 12) reduction of these responses respectively. In contrast, contractions elicited during prolonged hypoxia were less sensitive to verapamil which at a concentration of 1 microM only caused a 16.2 + 2.2% (n 12) reduction of these responses. 6. The present study indicates that prolonged exposure of the rat aorta to either hypoxic or oxygenated conditions causes attenuation of NA-induced contraction. However, these effects are also accompanied by changes in tissue Ca2+ handling which differ under each condition and might account for the observed modifications in tissue sensitivity to the calcium-entry blocker verapamil.
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PMID:The effects of verapamil upon noradrenaline-induced contraction of the rat isolated aorta following acute and prolonged alterations in PO2. 261 85

The effect of intravenous norepinephrine (NE) administration on three O2-dependent parameters of cerebral oxygenation was studied in the parietal cortex of skull intact anesthetized rats. Reflectance spectrophotometry was used to measure in vivo changes in cortical hemoglobin saturation (Hb/HbO2), blood volume (BV), and cytochrome c oxidase (cyt. a,a3) oxidation-reduction state. The influence of arterial pressure of oxygen (paO2) on norepinephrine-induced changes in cortical microcirculatory O2 delivery and cyt. a,a3 redox state was tested under conditions of normoxia, hypoxia, and hyperoxia. Norepinephrine produced cyt. a,a3 redox changes which were independent of compensatory alterations in cortical blood volume and changes in systemic blood pressure at the tested physiological extremes. During normoxia, NE caused dose-dependent systemic pressure-related increases in the oxidation level of cyt. a,a3. Conversely, in hypoxia NE caused a reduction. Microcirculatory and cyt. a,a3 redox responses to low doses of NE during hyperoxia were similar to those obtained at high doses during normoxia. The kinetic pattern of changes in hemoglobin saturation, cyt. a,a3 redox state, and cortical blood volume during normoxia and hypoxia was consistent with direct alteration in oxygen delivery to the respiratory chain and possible modification of cerebral oxidative metabolism. Blood-brain barrier alterations and vascular smooth muscle resistance changes to NE under tested conditions of oxygenation are postulated to be responsible for the observed results.
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PMID:In vivo modulation of norepinephrine-induced cerebral oxygenation states by hypoxia and hyperoxia. 299 87

For almost 10 years, numerous studies have shown that the pulmonary endothelium is endowed with a certain number of metabolic properties related to the uptake and hydrolysis of circulating vasoactive substances. Noradrenaline, serotonin, adenosine and possible certain prostaglandins are transported in the endothelial cells, according to processes which have now been clearly defined, and are there metabolised. Other compounds, including peptides (bradykinin, angiotensin I), or nucleotides (ATP, ADP, AMP) are hydrolysed in contact with the plasma membrane of the endothelium, without penetrating within the cell. For certain substrates (serotonin, angiotensin I), the properties of the pulmonary endothelial cell may be extended to systemic endothelial cells. For other substances, there would appear to be a specificity of endothelial function according to the site. It would appear that the lung, by virtue of its richness in endothelial cells, is capable of influencing concentrations of the circulating substances and, as a result, vascular tone. The existence of delicate processes of the uptake of substances has also been used to test the integrity of the cellular function of the pulmonary endothelium under experimental pathological condition, such as hyperoxia. However, before such a technique, based upon measurement os extraction of amines or other substances from various parts of the pulmonary circulation could be applied clinically, a critical consideration must be undertaken of the multiple factors involved in these processes. The major problem lies in the difficulty of distinguishing between dysfunction of the endothelial cells or a decrease in their number.
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PMID:[Measurement of pulmonary endothelial function; its potential clinical value]. 611 Dec 67

To determine the importance of dopamine and noradrenaline as neurotransmitters during chemoreception in the cat carotid body we investigated the contents of both compounds as well as the activity of dopamine-beta-hydroxylase (DBH) under different arterial PO2 and PCO2 conditions. The superior cervical ganglion was used as a control organ. In the carotid body and the ganglion an inverse relationship exists between the catecholamine content and the DBH activity. The carotid body has a high catecholamine content with a low DBH activity whereas the superior cervical ganglion has a low catecholamine content and high DBH activity. Hypercapnia did not produce any significant change in the catecholamine content or in the DBH content of the carotid body. However, in comparison with hyperoxia, hypoxia produced a significant change (p less than 0.05) in the noradrenaline content without changing the DBH activity. The dopamine content under these conditions did not change significantly. The results may indicate that the high catecholamine content of the carotid body is the result of a high retention and/or low rate of degradation rather than of a high rate of synthesis.
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PMID:Dopamine-beta-hydroxylase activity of the cat carotid body under different arterial O2 and CO2 conditions. 641 72

In Wistar rats exposed during one hour to mixtures of oxygen and carbon dioxide producing hypoxia, hypercapnia, hyperoxia and hypocapnia, and so on, adrenaline contents of the suprarenals is reduced by high concentration of carbon dioxide (30%), with or without hypoxia. Noradrenaline contents is increased by carbon dioxide (15 to 30%). Hypercapnia is more potent than hypoxia as a suprarenal stimulus.
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PMID:[CO2 and the catecholamine content of the adrenal medulla of the rat]. 644 72

The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical activity, which has been shown not to be a simple deprivation of aerobic processes. Strips of rat portal vein (RPV), rabbit ear artery (REA) and rabbit common carotid artery (RCC) were studied under isotonic conditions, contracted by 10(-6) noradrenaline (NA). Reduction of Po2 to less than 3KPa during NA constraction led to relaxation which was rapid and 90% complete in RPV, rapid and 60% in REA: the relaxation began when tissue Po2 was decreasing and was not lower than 5.5 K Pa. RCC responded slowly and only some strips relaxed. The rapidity and magnitude of relaxation for each type of vessel was comparable to that produced by removal of external calcium. Also for any one type of VSM the response to NA was abolished or diminished to a similar extent by preliminary exposure to hypoxia, or by preliminary removal of calcium. Preliminary hypoxia diminished 50 mmol.1(-1) K+ contractions as much as it diminished NA contractions. Preliminary 1-2 hour exposure to hyperoxia diminished the subsequent relaxant effect of hypoxia. Inhibition of glycolysis (iodoacetic acid) had no effect on normoxic NA contraction or on hypoxic relaxation, but prevented or diminished the subsequent recovery on reoxygenation. Low oxygen tension appears to act in VSM as though it interferes with net influx or utilisation of external calcium.
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PMID:Responses of systemic vascular smooth muscle to hypoxia. 690 37

The increase in ventilation caused by exercise is controlled by a combination of neural and chemical events, although the precise contribution and relative importance of these signals is still debated. It is generally agreed that the genesis of exercise hyperpnoea lies within the central nervous system and that peripheral reflexes, both chemical and neural, modulate central drive. Recently, attention has once again focused on the idea that circulating factors, in particular potassium, may play an important role in this modulation by stimulating known areas of peripheral chemoreception. Arterial chemoreceptors, muscle chemoreflex and slowly adapting pulmonary stretch receptors are all excited by hyperkalaemia. When potassium is raised to mimic exercise concentrations it increases ventilation in anaesthetised animals. This response is abolished by surgical denervation of the arterial chemoreceptors and is markedly reduced by chemical denervation with hyperoxia. Hypoxia enhances the ventilatory response to hyperkalaemia, and the stimulatory effects of potassium are further increased when combined with lactic acid or raised concentrations of noradrenaline. Hyperkalaemia can also increase the hypoxic sensitivity of the arterial chemoreflex in exercise. There is a close temporal relationship between potassium and ventilation during exercise, but changes in potassium are not proportionally related to changes in ventilation. When all data are taken together, there is good evidence that potassium has a supporting role in the control of exercise hyperpnoea, predominantly through modulation of the arterial chemoreflex.
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PMID:Potassium and breathing in exercise. 910 35

Six Welsh gelding ponies were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) prior to induction of anaesthesia with midazolam at 0.2 mg/kg and ketamine at 2 mg/kg i.v.. Anaesthesia was maintained for 2 h using 1.2% halothane concentration in oxygen. Heart rate, electrocardiograph (ECG), arterial blood pressure, respiratory rate, blood gases, temperature, haematocrit, plasma arginine vasopressin (AVP), dynorphin, beta-endorphin, adrenocorticotropic hormone (ACTH), cortisol, dopamine, noradrenaline, adrenaline, glucose and lactate concentrations were measured before and after premedication, immediately after induction, every 20 min during anaesthesia, and at 20 and 120 min after disconnection. Induction was rapid, excitement-free and good muscle relaxation was observed. There were no changes in heart and respiratory rates. Decrease in temperature, hyperoxia and respiratory acidosis developed during anaesthesia and slight hypotension was observed (minimum value 76 +/- 10 mm Hg at 40 mins). No changes were observed in dynorphin, beta-endorphin, ACTH, catecholamines and glucose. Plasma cortisol concentration increased from 220 +/- 17 basal to 354 +/- 22 nmol/L at 120 min during anaesthesia; plasma AVP concentration increased from 3 +/- 1 basal to 346 +/- 64 pmol/L at 100 min during anaesthesia and plasma lactate concentration increased from 1.22 +/- 0.08 basal to 1.76 +/- 0.13 mmol/L at 80 min during anaesthesia. Recovery was rapid and uneventful with ponies taking 46 +/- 6 min to stand. When midazolam/ketamine was compared with thiopentone or detomidine/ketamine for induction before halothane anaesthesia using an otherwise similar protocol in the same ponies, it caused slightly more respiratory depression, but less hypotension. Additionally, midazolam reduced the hormonal stress response commonly observed during halothane anaesthesia and appears to have a good potential for use in horses.
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PMID:Midazolam and ketamine induction before halothane anaesthesia in ponies: cardiorespiratory, endocrine and metabolic changes. 913 43


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