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

The results of the studies on the gas composition and acid-base equilibrium of the blood in patients operated upon under epidural anesthesia have proved the rise of venous hyperoxia and the drop of the gas utilization percentage both in anesthetized and non-anesthetized regions. At the level of the whole organism, however, no essential changes of oxygen metabolism are noted.
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PMID:[Gas composition and acid-base equilibrium of blood of patients operated on under conditions of epidural anesthesia]. 64 85

The influence of the method of anesthesia on the degree of changes of homeostasis after reconstructive operations on the abdominal aorta was studied in 95 patients. Under conditions of artificial ventilation of lungs fluothane narcosis was used in 9 patients, either narcosis--in 15 patients, combined neuroleptanalgesia--in 35 patients, epidural anesthesia with spontaneous respiration with atmospheric air--in 36 patients. It was shown that fluothane narcosis and neuroleptanalgesia brought about considerable changes of homeostasis and was followed by reliably greater amount of complications and lethal issues. A conclusion was made that general anesthetics, hyperoxia and artificial ventilation of lungs aggravate postischemic tissue alterations, inhibit hemopoiesis and functions of parenchymatous organs and provoke severe postoperative complications and lethal issues.
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PMID:[Changes in various indicators of homeostasis after operation on the abdominal aorta in relation to the method of anesthesia]. 165 58

Methemoglobin (MtHb) formation was studied during reconstructive operations on the abdominal aorta and its branches. It was established that the appearance of pain at rest and trophic tissue disorders in the lower extremities causes intensification of MtHb formation. The intensity of MtHb formation increases sharply during the operation and is determined by the injurious character of the intervention, level of arterial blood oxygenation, and the efficacy of nociceptive pulsation block. Arterial blood hyperoxia proved to be among the most important factors of increased MtHb formation and decreased blood oxygen capacity. Nociceptive pulsation block is less effective in general anesthesia than in epidural anesthesia and also increases the content of MtHb in the blood and the severity of the stress and reperfusion damages of the tissues and organs. On the basis of the results of the study it is concluded that normoxia of arterial blood and denervation of the operative zone reduce the risk of ischemic and hypoxic complications in patients with generalized atherosclerosis.
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PMID:[The effect of the methods of anesthesiological assistance and blood oxygenation on the oxygen-transport properties of the blood in reconstructive interventions on the abdominal aorta and vessels of the lower extremities]. 176 6

The effects of intravenous almitrine under normoxic, hyperoxic, and hypoxic conditions were studied in 5 male beagle dogs (mean weight 15.2 +/- 5 kg) anaesthetized with thiopentone. Plasma concentrations of thiopentone were maintained constant at 27-29 mg.1(-1). Each animal underwent twice the three different experiments, with a lapse of a fortnight between each experiment: a) breathing room air, with intravenous administration of 1 mg.kg-1 almitrine over 30 s, b) breathing room air, then pure oxygen for 15 min, followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing pure oxygen, and c) breathing room air, then progressively less oxygen (FIO2 0.18, 0.16, 0.14, 0.12 for 5 min each), followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing a mixture with 12% oxygen. Tidal volume, respiratory rate, minute ventilation, inspiratory and expiratory duration, arterial pH, PaO2 and PaCO2 were measured respectively in room air, after 100% oxygen, in hypoxia (FIO2 = 0.12), before, 5 and 10 min after the injection of almitrine. Hyperoxia depressed ventilation (-21%), whilst hypoxia stimulated it (+126%), although significantly less than in the awake animal. Almitrine restored the respiratory response to hypoxia, but hyperoxia did not suppress respiratory stimulation due to the drug. It would therefore seem likely that almitrine acts on peripheral arterial chemoreceptors, but also on other structures. The results of this study suggest that almitrine may be useful in restoring the respiratory response to hypoxia during recovery from anaesthesia.
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PMID:[Respiratory effects of almitrine on various levels of the fraction of inspired oxygen. A study in the anesthetized dog]. 210 57

Three groups of 50-day-old (i.e., postpuberty) rats have been studied: controls, rats exposed to 6 days of hypoxia [inspired fraction of O2 (FIo2) = 10% O2] when newborn (Nb-Hypox), and rats exposed to the same level and duration of hypoxia after weaning (Ad-Hypox). Ventilation during normoxic breathing was higher in Nb-Hypox than in controls or Ad-Hypox. The ventilatory response to acute hypoxia (10 min of 10% O2) was about one-half in Nb-Hypox than in the other two groups. Additional measurements performed on Nb-Hypox and controls showed minimal or no differences between the two groups in the ventilatory responses to hyperoxia and hypercapnia, heart rate and blood pressure at various FIO2, and blood biochemistry. Analysis of the Hering-Breuer reflexes, during barbiturate anesthesia, suggested a decreased central inhibition on inspiratory activity in Nb-Hypox, which with a lower sensitivity to inputs from the peripheral chemoreceptors may contribute to the normoxic hyperventilation and the blunted response to acute hypoxia. The ventilatory patterns of Nb-Hypox rats bear numerous similarities with those of high-altitude natives and could suggest that the highlander's ventilatory responses are not genetic characteristics but relate to chronic hypoxia early in life.
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PMID:Control of ventilation in adult rats hypoxic in the neonatal period. 222 Nov 51

Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia. All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) greater than 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 +/- 4.5 SD for D and 24.3 +/- 4.4 for C) to hypoxia (28.5 +/- 4.7 for D and 28.4 +/- 3.7 for C), and decreased during hyperoxia (16.9 +/- 3.0 for D and 17.4 +/- 3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 +/- 11.7 mm of Hg for D and 69.4 +/- 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postadulticide pulmonary hypertension of canine heartworm disease: successful treatment with oxygen and failure of antihistamines. 224 Jul 78

The ventilatory and hemodynamic responses to hypoxia, hyperoxia, and hypercapnia before and during sufentanil infusion were studied in 16 chronically tracheostomized dogs anesthetized with two concentrations, 1 and 0.5 minimal alveolar concentration (MAC) of isoflurane. Sufentanil was infused at a rate to obtain a constant end-tidal carbon dioxide (PETCO2) of approximately 50 mm Hg for each isoflurane level. Before the sufentanil infusion, the PETCO2 was increased to 50 mm Hg by adding CO2 to the inspired gas, to allow comparisons at isocapnic conditions. Sufentanil caused only minor hemodynamic changes but significantly reduced ventilation during both levels of isoflurane. The ventilatory response to hypercapnia decreased substantially, but there were no significant alterations in the ventilatory response to hypoxia. After sufentanil infusion, hyperoxia caused a larger decrease in minute ventilation and caused apnea in four dogs. These results suggest that administering sufentanil during isoflurane anesthesia causes a reduction in the contribution of the central chemoreflexes to ventilatory drive and, consequently, a relative increase in the contribution from the peripheral chemoreflexes.
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PMID:Ventilatory and cardiovascular responses to sufentanil infusion in dogs anesthetized with isoflurane. 252 4

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

In conscious intact cats, oxygen breathing for up to 1 h does not modify ventilation, and the ventilatory response to CO2 in hyperoxia is not consistently decreased. However, oxygen breathing induces sustained hyperventilation in conscious cats after carotid body denervation. In anesthetized cats, oxygen breathing provokes a hypoventilation which is transient under light anesthesia but more sustained under deeper levels of anesthesia. At all levels of anesthesia, the ventilatory response to CO2 is decreased in hyperoxia as compared with normoxia. These results suggest that: the effects of hyperoxia include a central stimulating component, seen only in conscious animals, which offsets the decreased ventilatory drive from peripheral chemoreceptors; this central component is sensitive to anesthesia, thus allowing an explanation for the permanent decrease in ventilation and decrease in ventilatory response to CO2 observed when oxygen is given during deep anesthesia; and anesthesia may help to purposefully unmask factors involved in the control of breathing, but it markedly alters the normal functioning of the respiratory network.
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PMID:Ventilatory response of the conscious or anesthetized cat to oxygen breathing. 309 10

Ventilatory effects of propofol, used as a sole agent for the induction and maintenance of general anaesthesia, were studied in 14 healthy unpremedicated patients. Subarachnoid anaesthesia was established before induction of general anaesthesia. Induction was with propofol 2.5 mg kg-1 given while the patients breathed 100% oxygen. We intended to start an infusion of propofol 100 micrograms kg-1 min-1; maintain it for at least 25 min; make a first set of quasi-steady-state observations; double the infusion; and repeat observations after 25 min. The single induction bolus plus single rate infusion was not totally satisfactory: further boluses were usually needed. At induction there was apnoea in all but three patients, sometimes lasting more than 3 min; hyperventilation before induction, combined with hyperoxia, probably exaggerated this. Established ventilatory rates were generally 30% higher than awake. One patient became bradypnoeic. Tidal volume and minute ventilation, and the Tl:Ttot ratio, were reduced. Doubling the infusion rate had no clear effect on frequency or tidal volume, but it further reduced the Tl:Ttot ratio and caused an increase in PE'CO2 of 1 kPa. The ventilatory response to carbon dioxide was 58% of baseline awake control (95% confidence limits +/- 26%) at the lower infusion rate, with further slight depression when the infusion rate was doubled. Doubling the rate of infusion of propofol did not give twice the effect on ventilation, and probably is not giving twice the "depth" of anaesthesia. We cannot say if this is for pharmacokinetic or pharmacodynamic reasons.
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PMID:Some ventilatory effects of propofol as sole anaesthetic agent. 312 6


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