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

To examine the interrelationship between the duration of apnea and changes in oxygen saturation, blood pressure, electroencephalogram (EEG), and heart rate, reflex apnea of 10, 20, 40, and 60 s duration was induced by stimulating the superior laryngeal nerves. Piglets (n = 11, age 5-14 days) were chronically instrumented for continuous monitoring of SaO2 and blood pressure and for sampling arterial blood. Ventilation was recorded using whole body plethysmography and EEG and electrocardiogram were measured by acutely placed subcutaneous electrodes. Central apnea produced an immediate rise in blood pressure and a decrease in SaO2 by 20 s. By 30 s into the apnea, EEG amplitude had already decreased. Major cardiac slowing did not occur until 80 s after the start of apnea. Hyperoxia delayed the start of desaturation, hypertension, and EEG attenuation. These data suggest that during superior laryngeal nerve-induced apnea in young piglets: 1) desaturation can reach profound levels rapidly, 2) EEG amplitude decreases substantially and becomes nearly isoelectric within 1 min, and 3) bradycardia is a late manifestation when compared to changes in oxygen saturation, blood pressure, and EEG.
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PMID:Cardiovascular and neurophysiologic changes during graded duration of apnea in piglets. 337 94

We wished to determine if mild hypocapnia above the "apneic threshold" would result in apnea or hypopnea during NREM sleep. Hypocapnia was induced by nasal mechanical hyperventilation for 1 min either under normoxia (51 trials, n = 7) or hyperoxia (43 trials, n = 5). Cessation of mechanical ventilation resulted in hypopnea due to reduced VT without a change in f. Central apnea occurred mostly under hyperoxic conditions (9/43 versus 2/51 trials under normoxic conditions), and only when complete inhibition of ventilatory motor output occurred during mechanical ventilation. Significant correlation between the magnitude of hypocapnia and nadir VE was noted under both normoxic and hyperoxic conditions. However, nadir VE was variable when hypocapnia was modest (-2 mmHg); further hypocapnia (-4 mmHg) was associated with consistent reduction in nadir VE below 30% of control under normoxic conditions, and central apnea under hyperoxic conditions. We conclude that: (1) Brief hyperventilation during NREM sleep is followed by hypocapnic hypopnea due to reduced VT and not breathing frequency; (2) Hypocapnia due to brief mild hyperventilation does not cause central apnea unless peripheral chemoreceptors are also inhibited; (3) Sustained hyperventilation or more severe hypocapnia may be required for the development of hypocapnic central apnea during NREM sleep.
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PMID:Post-hyperventilation hypopnea in humans during NREM sleep. 883 45