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

Death in normobaric hyperoxia was related in the past to pulmonary insufficiency of the edematous lung. However, high arterial O2 tension on final collapse led to the suggestion that the heart and not the lung is the first organ that fails. We measured aortic flow, coronary flow, left ventricular pressure, affluent and effluent PO2, PCO2, and pH in the working heart excised from control and normobaric O2-exposed rats (51-63 h). The oxygen consumption (VO2) of experimental hearts was not different from control, but mechanical power output (PVAP) (calculated from pressure-volume area) was reduced as a function of O2 exposure time. Myocardial contractility indexes, maximal elastance and maximal time derivative of pressure, increased as a function of O2 exposure time, being below control values after 50 h and above control values after 60 h. The individual slopes for the regression of VO2 vs. PVAP rose as a function of exposure time from values below control after 50 h exposure to values above control after 60 h. Energetic efficiency (PVAP/VO2) decreased as a function of O2 exposure time and points to possible heart failure in the intact animal. After 50 h O2 exposure the heart was energetically more efficient than the control. Possible changes in the heart are discussed.
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PMID:Heart energetic efficiency in O2-exposed rats studied in isolated working heart. 149 Sep 35

In patients with obstructive apnea, it was hypothesized that stimulation of the ventilatory system by hypercapnia during sleep would increase pharyngeal inspiratory muscle activity and thereby increase upper airway caliber. We predicted that this increase in caliber would decrease the number of apneas and sleep time spent apneic. In contrast, suppression of the ventilatory system activity with hyperoxia was predicted to decrease both inspiratory muscle activity and pharyngeal caliber and thereby increase the number of apneas and apnea time. In all 7 patients with symptomatic obstructive sleep apnea studied, 3 with upper airway narrowing obvious during wakefulness, inhalation of 3 to 6% CO2 preferentially stimulated upper airway inspiratory muscle tonic electrical activity relative to the activity of chest wall inspiratory muscles and diminished periodic breathing. Apnea time decreased from 60 +/- 2% (mean +/- SEM) of sleep time during ambient air inhalation to 12 +/- 3% during CO2 inhalation; 50% O2 had the reverse effect on inspiratory muscle tonic electrical activity and increased apnea time to 75 +/- 5% of sleep time. We conclude that manipulation of inspiratory muscle tonic activity and alteration of the pattern of breathing by CO2 and O2 inhalation lead to significant changes in the pattern of upper airway inspiratory collapse during sleep. We speculate that physiologic variables related to the control of upper airway inspiratory muscle function are instrumental in the pathophysiology of obstructive sleep apnea.
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PMID:Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations. 314 3

Since the effect of prolonged exposure to high concentrations of oxygen on regional ventilation and perfusion has not been previously, a reproducible primate model of oxygen toxicity was developed to investigate the pathophysiologic changes that occur. Regional ventilation and perfusion were measured by 133Xe techniques in 10 baboons before and after 108 hours of continuous exposure to an inspired oxygen concentration of more than 90%. Arterial blood gases, shunt fraction (QS/QT), cardiac output, physiologic dead space (VD/VT), and pulmonary vascular resistance were also measured. Light and electron microscopic histology confirmed early pathologic changes of oxygen toxicity in every animal after exposure. PaO2 in room air decreased markedly after exposure from 90 +/- 4 to 46 +/- 5 mm Hg, and QS/QT rose to 30 +/- 2%. VD/VT, PaCO2, and pH were not altered by exposure to hyperoxia. Similarly, cardiac output and pulmonary vascular resistance remained unchanged. The distribution of regional ventilation and perfusion remained normal during and after prolonged high-oxygen exposure. Early oxygen toxicity was characterized by profound hypoxemia without regional ventilation-perfusion mismatch. Although impaired diffusion through a thickened alveolar membrane may be partially responsible for this hypoxemia, the markedly increased alveolar-arterial oxygen gradient when FIO2 = 1.0 indicates that shunting at the alveolar level (secondary to absorptive collapse or pulmonary edema) is a major cause of the hypoxemia.
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PMID:Effects of oxygen toxicity on regional ventilation and perfusion in the primate lung. 722 86

It seems clear that the abundance of potential treatment options reflects the dearth of proved, effective options. Thus, although we appear to be on the brink of many potentially major breakthroughs in treatment, there currently remains a multitude of unanswered questions and the need for further study. At this point clinical recommendations must be limited to supportive care with moderation: oxygenation without hyperoxia; ventilation without hypocarbia; avoiding extremes of blood pressure, hematocrit, blood glucose, and body temperature. Unfortunately, data from human trials are extremely limited and often poorly controlled. Furthermore, even those few existing human studies have rarely--if ever--dealt with newborns infants (Table 2). In addition, many of the existing studies do not relate to generalized asphyxia but rather to single-organ reperfusion insults. Finally, there is the critical issue of timing. Unfortunately, much of the existing experimental data relate to prophylaxis rather than treatment, severely limiting their potential for clinical applicability. Interventions may have quite different effects when administered at different phases of this most intricate process. Hyperglycemia, for example, may be neuroprotective before an insult but detrimental if induced after an asphyxial episode. Conversely, the NMDA blocker MK-801 can adversely affect outcome when given before a global asphyxial insult but can reduce seizure-related damage when given during the hyperexcitability phase. Insulin-like growth factor is also neuroprotective only when given after an insult, but it is not helpful if given before. An intimate understanding of the pathophysiologic processes involved is essential before any attempts at applying the diverse data derived from numerous animal studies to the human situation in an intelligent manner. Future studies may focus on cocktails of different mixtures of the compounds discussed or on single multipotential drugs, which would make possible a multipronged approach. However, it is essential to investigate fully the potential for toxic drug interactions, as some combinations may be produce serious consequences. For example, Gluckman and Williams evaluated the potential of combining calcium channel blockers with NMDA receptor antagonists in hypoxic-ischemic rats and found that this combination led to rapid cardiovascular collapse. Other enticing approaches for future investigations will probably include some genetic-engineering-related studies in attempt to enhance endogenous antioxidant defenses with regulon stimulation or the administration of neurotrophic growth factors. Unavoidably, the trip from the laboratory to the bedside must of necessity be an arduous and rigorous one.
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PMID:Ischemia and reperfusion injury. The ultimate pathophysiologic paradox. 977 46

Immaturity and oxygen toxicity have been implicated in the pathogenesis of the neonatal disease bronchopulmonary dysplasia. The present study aimed to investigate the use of magnetic resonance imaging (MRI) to assess hyperoxia-mediated lung injury in the term and premature neonate. Term (gestation, 22 d) and premature (21 d) rat pups were exposed to hyperoxia (>95%) or air for a 6-d period (n = 7) and assessed for lung damage by MRI. Pulmonary signal intensities of T1-weighted images were significantly increased in both hyperoxia-exposed term and premature neonates, relative to air-breathing controls (p < 0.01). T2-weighted MRI signal intensities were also greater in premature and term rat pups exposed to hyperoxia, but failed to reach significance (p > 0.05). Elevated MRI pulmonary signal intensities may have represented an increase in magnetic resonance-detectable free water, possibly indicating an increase in edema. Corresponding histologic evidence of lung injury was detected in both term and premature rat pups exposed to hyperoxia. Histologic samples indicated focal regions of alveolar hemorrhage, immune cell infiltration, edema, and collapse in both term and premature rat neonates exposed to hyperoxia. Alveolar air space was assessed (n = 5) by light microscopy within a 0.5 mm2 region of the superior left and inferior right pulmonary lobes of each treatment group. Alveolar area of the superior left lung lobe of the premature hyperoxia treatment group was significantly smaller than other treatment groups (p < 0.05). Reduced area for respiratory exchange was probably a result of observed focal areas of edema and collapse. MRI-detectable increases in lung signal intensity may have represented an increase in hyperoxia-induced pulmonary edema in the 6-d-old rat neonate. Increases in signal intensity correlated with the appearance of edema in pulmonary histologic samples. Premature delivery had a less defined effect on lung injury but possibly exacerbated hyperoxia-mediated pulmonary damage.
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PMID:Magnetic resonance imaging of pulmonary damage in the term and premature rat neonate exposed to hyperoxia. 1156 94

In this Review, we focus on the functional properties of the respiratory system of pinnipeds and cetaceans, and briefly summarize the underlying anatomy; in doing so, we provide an overview of what is currently known about their respiratory physiology and mechanics. While exposure to high pressure is a common challenge among breath-hold divers, there is a large variation in respiratory anatomy, function and capacity between species - how are these traits adapted to allow the animals to withstand the physiological challenges faced during dives? The ultra-deep diving feats of some marine mammals defy our current understanding of respiratory physiology and lung mechanics. These animals cope daily with lung compression, alveolar collapse, transient hyperoxia and extreme hypoxia. By improving our understanding of respiratory physiology under these conditions, we will be better able to define the physiological constraints imposed on these animals, and how these limitations may affect the survival of marine mammals in a changing environment. Many of the respiratory traits to survive exposure to an extreme environment may inspire novel treatments for a variety of respiratory problems in humans.
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PMID:Respiratory function and mechanics in pinnipeds and cetaceans. 2851 70

Following return of spontaneous circulation (ROSC) after cardiac arrest, the challenge is to institute measures that ensure a higher likelihood of neurologically intact survival. Regardless of the cause of collapse, multiple organ systems may be affected secondary to post-cardiac arrest syndrome. Interventions required for post-ROSC care are bundled into a care regimen: prompt identification and treatment of the cause of cardiac arrest; and treatment of electrolyte abnormalities. It is also essential to establish definitive airway management to maintain normocapnic ventilation, prevent hyperoxia, and optimise haemodynamic management via judicious intravenous fluids and vasoactive drugs. Targeted temperature management after ROSC confers neuroprotection and leads to improved neurological outcomes. Glycaemic control of blood glucose levels at 6-10 mmol/L, adequate seizure management and measures to optimise neurological functions should be integrated into the care bundle. The interventions outlined can potentially lead to more patients being discharged from hospital alive with good neurological function.
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PMID:Post-resuscitation care. 2874 Oct 14

Mechanical ventilation during surgery is a highly complex procedure, particularly in cardiothoracic surgery, where patients need to undergo substantial hemodynamic management, involving large fluid exchanges and pharmacological manipulation of vascular resistance, as well as direct manipulation of the lungs themselves. Cardiothoracic surgery is burdened by a high rate of postoperative pulmonary complication (PPC), comorbidity, and mortality. Recent trials have examined various techniques to preserve lung function, although consensus on best practice has yet to be reached. This might be due to the close relationship between the circulatory and pulmonary systems. The use of a technique designed to prevent pulmonary complication might negatively impact the hemodynamics of an already critical patient. Stress-induced lung injury can occur during surgery for various reasons, some of which have yet to be fully investigated. In cardiac surgery, this damage is mainly ascribed to two events: cardiopulmonary bypass (CPB) and sternotomy. In thoracic surgery, on the other hand, overdistention and permissive hyperoxia, both routinely used on one lung to compensate for the collapse of the other, are generally to blame for lung injury. In recent years "protective" ventilation strategies have been proposed to spare lung parenchyma from stress-induced damage. Despite the growing interest in protective ventilation techniques, there are still no clear international guidelines for mechanical ventilation in cardiothoracic surgery. However, some recent progress has been made, with positive clinical outcomes.
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PMID:Mechanical ventilation management during cardiothoracic surgery: an open challenge. 3046 Feb 54