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

Friedreich's Ataxia (F.A.) is a degenerative disease which commonly leads to premature death of cardiorespiratory origin. To explain the early death of these patients, previous investigations have established the existence of 1) a cardiomyopathy in nearly 100% of cases, 2) a restrictive pulmonary syndrome of scoliotic origin and 3) a mild hypoxemia associated with slight respiratory alkalosis and a normal oxyhemoglobin dissociation curve. To further assess the cause of early death in patients with such neuromyopathy, we evaluated, in eleven F.A. patients, the sensitivity of the respiratory centers to hypercapnia, hypoxia, and hyperoxia. Ventilatory (VE, VT, F, VT/Ti) and occlusion pressure (P0.1) responses were taken as indices of the respiratory centers output during progressive hypercapnia (Read's method) and isocarbic hypoxia (Weil's method). We studied 11 Friedreich's Ataxia patients and 11 age, sex, and armspan matched controls. The responses of patients to hypercapnia were significantly greater than controls but their responses to hypoxia were similar to controls. Our study establishes that the respiratory centers are functioning adequately in early Friedreich's Ataxia and do not contribute to cardio-respiratory insufficiency in such neuromyopathy.
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PMID:Regulation of respiration in Friedreich's ataxia. 48 4

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
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PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.
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PMID:Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs. 230 2

The purpose of this study is to examine effects of hyperoxic gas mixtures on changes of blood indices during bicycle exercise of human. Oxygen-enriched gases (30% O2) were inspired during the ramp load exercise of 25 watt/min. Changes of blood indices were analyzed with Sequential Multiple Analyzer with the computer (SMAC). The improvement of exercise performance were discussed about relationship between function of hyperoxic gas and physiological mechanism. Three experimental conditions were set as follows (I) 30% O2 +N2 gases balance, (II) air (21% O2), and (III) 30% O2 +2% CO2 +N2 gases balance. Arterial blood were sampled from the radial artery of the forearm in order to analyze following items; 1) pH level, PaO2, PaCO2, and HCO3 of these blood gases, 2) Blood sugar, TG, and F-CH of the blood contents, 3) red blood corpuscle, white blood corpuscle, Hb, and Ht values, 4) LDH, CK, GOT, and GPT of the blood enzymes, 5) TP, ALB, Na, K, Ca and Cl of the electric ions. In the case of inspiring hyperoxic gases, the recovery rate of blood indices increased after this ramp load exercise remarkably, and the whole exercise metabolism were removed from acidosis tendency to alkalosis value of the resting condition significantly. At hyperoxic experimental conditions, the blood sugar and oxygen consumption were much more decreased than these at normal oxygen content one during both states of exercise and recovery times. These data of the blood indices would support strongly to the hypothesis that improvement of oxygen delivery should be depended upon the enhanced performance with the hyperoxic gases. There might be effects of the hyperoxia on the cellular metabolism and on function of the vascular muscle during those aerobic exercise.
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PMID:[Effects of breathing high concentrations of oxygen on changes in blood indices during bicycle exercise]. 238 13

In anaesthetised, mechanically ventilated Beagle dogs a moderate metabolic acidosis increased the pulmonary vascular resistance to a greater extent than moderate hypoxia. Alkalosis and hyperoxia did not alter the pulmonary vascular tone.
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PMID:The influence of hypoxia and hyperoxia during metabolic acidosis and alkalosis on pulmonary haemodynamics. 273 Jun 20

1. The effect of varying artificial respiratory volume (at a fixed rate of 54 min-1) on cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in control pithed rats or during pressor responses to either the alpha 1-adrenoceptor agonist phenylephrine or the alpha 2-agonist xylazine. Phenylephrine was investigated in the presence of propranolol (3 mg kg-1). The rats were pithed under halothane anaesthesia. 2. A respiratory volume of 15 ml kg-1 produced modest hypercapnia (PaCO2 = 47 mmHg), hypoxia (PaO2 = 60 mmHg) and acidosis (pH = 7.35) relative to control animals respired at 20 ml kg-1 (PaCO2 = 32 mmHg; PaO2 = 77 mmHg; pH = 7.47). In rats respired at 15 ml kg-1, total peripheral resistance was lower, and cardiac output greater (due to increased stroke volume), than in the controls. Lowering respiratory volume reduced distribution of cardiac output to the kidneys, increased it to the large intestine and also increased blood flow through the gastrointestinal tract, skin and spleen. A respiratory volume of 30 ml kg-1 gave mild hypocapnia (PaCO2 = 19 mmHg), hyperoxia (PaO2 = 101 mmHg) and alkalosis (pH = 7.59) compared to 20 ml kg-1 but had no effect on cardiac output distribution or organ blood flow although heart rate was 29% greater at 30 ml kg-1. 3. Xylazine (500 micrograms bolus followed by 100 micrograms min-1 infusion) at all three respiratory volumes gave well-sustained mean pressor responses of 62-64 mmHg by increasing both total peripheral resistance and cardiac output (resulting from increased stroke volume). It increased the proportion of cardiac output passing to the liver, reduced that going to the spleen and gastrointestinal tract and increased cardiac, renal and hepatosplanchnic blood flows. 4. The secondary, relatively sustained, pressor effect of phenylephrine (5 micrograms bolus followed by 0.4 micrograms min-1 infusion, i.v.) varied at the 3 respiratory volumes with mean values from 32 to 53 mmHg. This response was due to both increased total peripheral resistance and cardiac output (resulting from greater stroke volumes and/or heart rates). Phenylephrine increased the proportion of cardiac output passing to the gastrointestinal tract, heart, kidneys and hepatosplanchnic bed and increased cardiac, hepatosplanchnic, renal and gastrointestinal blood flows. 5. Respiratory volume had no effect on the cardiovascular effects of xylazine. However, respiratory volume modified the effects of phenylephrine on heart rate and changed the relative contributions of stroke volume and heart rate to the increased cardiac output. It also influenced the effects of phenylephrine on cardiac output distribution to the liver, epididimides and hepatosplanchnic bed and on blood flow through skeletal muscle and the large intestine. 6. Changes in respiratory volume of air ventilated pithed rats thus influence cardiac output, its distribution and regional blood flows. Such changes can also differently influence the responses of various vascular beds to phenylephrine whilst having no effect on their responses to xylazine.
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PMID:Effect of artificial respiratory volume on the cardiovascular responses to an alpha 1- and an alpha 2-adrenoceptor agonist in the air-ventilated pithed rat. 289 57

1. The ventilatory sensitivity to CO2 obtained from a non-steady-state step-ramp CO2 challenge (analogous to the Read rebreathing method) was compared with the one of the steady-state method. 2. Experiments were performed during normoxia on twenty cats anaesthetized with chloralose-urethane. In eight of these cats additional measurements were carried out during metabolic acidosis and alkalosis. 3. The slope of the non-steady-state ventilatory response curve to CO2 was not significantly different from the steady-state one only if the ratio of the step-wise increase in end-tidal PCO2 (PET,CO2) (A) above its resting value and the subsequent rate of rise of the PET,CO2 (R) was equal to the time constant of the central chemoreflex pathway (tau c). This also held true during metabolic acidosis and alkalosis. 4. It is predicted that in human beings during hyperoxia the ventilatory response line obtained with Read's rebreathing method is to a fair approximation shifted to the right by a value of A with respect to the steady-state response line, provided A/R = tau c. 5. We argue that Read's prescription that a PET,CO2 equilibrium should be established between mixed venous blood, arterial blood and end-tidal gas has to be regarded as an experimental condition leading to stable-experiments rather than dictated by physiological mechanisms.
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PMID:A pseudo-rebreathing technique for assessing the ventilatory response to carbon dioxide in cats. 311 73

Infants at risk for the development of persistent pulmonary hypertension of the newborn (PPHN) may require hyperventilation and muscle relaxation to improve lung compliance and oxygenation. During a 16-month period from June 1983 to October 1984, the author identified a separate population of infants who presented initially with symptoms indistinguishable from those of infants who develop severe PPHN, but who responded to hyperoxia (FiO2 = 1.00) and were successfully managed with supplemental oxygen without the need for intubation, hyperventilation, or muscle relaxation to achieve hypocarbic alkalosis and adequate oxygenation. We studied 20 infants, 15 with evidence of perinatal aspiration syndromes, and compared their initial responses to supplemental oxygen with those of 16 infants whose pulmonary hypertension was severe enough to require intubation, hyperventilation, and muscle relaxation for adequate control of oxygenation. No significant differences were noted in PaO2 response in FiO2 = 0.21 or 0.40. A significant rise in PaO2 was observed among infants with transient pulmonary vascular lability (TPVL), a milder form of pulmonary hypertension of the newborn, but not among infants with persistent pulmonary hypertension of the newborn, when exposed to FiO2 = 1.00 (250.7 torr versus 86.0 torr; P less than 0.0001). No significant differences in pH or PCO2 were observed. TPVL appears to present among term or post-term large-for-gestational age (LGA) infants, frequently delivered by cesarean section, who have experienced perinatal factors known to be associated with an increased risk of PPHN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transient pulmonary vascular lability: a form of mild pulmonary hypertension of the newborn not requiring mechanical ventilation. 323 88

Steady state breathing patterns, alveolar gases, and arterial blood gases and pH were measured during air, acute hypoxia, and acute hyperoxia in four awake cats 5 years after combined carotid body resection (CBR) and aortic depressor nerve section. Steady state breathing patterns and alveolar gases were also measured in these animals following 3 days of hypoxia (PIO2 = 110 Torr). The results show that the awake cat without carotid bodies and aortic depressor nerves hypoventilates during normoxia in relation to intact cats. Acute hypoxia resulted in respiratory acidosis, decreased tidal volume (VT), and decreased breath duration (TTOT). Exposure to hypoxia for three days resulted in no hyperventilation (isocapnia) but increased VT and TTOT from their levels during acute hypoxia. Acute hyperoxia resulted in respiratory alkalosis and increased VT. Moderate degrees of acute inspiratory hypoxia (FIO2 less than 0.12) induced a behavioral 'arousal' in these cats; this is in direct contrast to the lack of response seen shortly after CBR. Presumably, the recrudescence of chemosensitivity via unsectioned aortic chemoreceptor afferents played a key role in the arousal responses. However, there is no evidence in the cat for recrudescent chemoreceptor input to the respiratory control system with measurable steady state effect. We conclude that the peripheral chemoreceptors are essential for normal resting ventilatory control and for acclimation to chronic hypoxia.
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PMID:Hypoxic ventilatory control in the awake cat five years after carotid body resection. 362 10

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
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PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76


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