Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of breathing 21% O2, 21% O2 + 5% CO2, 10% O2 + 4% CO2 and 10% O2 on the sleep-waking rhythm, respiratory rate, diaphragmatic EMG, inspiratory (Ti) and expiratory (Te) times were studied in rats. They carried chronically implanted electrodes to permit polygraphic recordings of the ECoG, EOG and dorsal neck and integrated diaphragmatic EMG activity. Average respiratory rates, independent of state of consciousness varied depending on the gas mixture breathed. Sleep-waking times, expressed as percentages, were determined as a function of the gas mixture breathed. Oxygen deficiency caused PS deprivation which was partially alleviated by the addition of 4% CO2. Diaphragmatic EMG activity decreased during PS when rats breathed gas mixtures rich in CO2 but increased when they breathed 10% O2. In general, at a given frequency of breathing, Ti was shorter during PS than during SWS except when rats breathed 10% O2. It is concluded that: (1) regardless of the state of consciousness hypoxia is a more potent stimulus of respiratory rate than hypercapnia, (2) diaphragmatic effort is reduced when rats breathe CO2 enriched gas mixtures but is increased by hypoxia due to changes in upper airway resistance, and (3) low O2 content of an inspired gas disrupts the inspiratory and expiratory off-switch mechanisms, this disruption being prevented by the addition of CO2.
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PMID:An electrophysiological analysis of sleep and respiration of rats breathing different gas mixtures: diaphragmatic muscle function. 616 Sep 72

The relationships between brain blood flow (BBF) and ventilation (VI) were studied during sleep in 13 goats. Unilateral BBF was continuously measured with an electromagnetic flow probe; total and regional BBF were assessed by the radioactive microsphere technique in four animals. Interacting changes in VI and BBF occurred during both slow wave (SWS) and rapid eye movement (REM) sleep. During SWS, significant decreases in VI and increases in arterial PCO2 occurred compared to wakefulness. BBF during SWS correlated linearly with arterial CO2 tension (PaCO2); nd the relationship was similar to that for awake goats breathing CO2. During REM sleep, VI was significantly less than both the awake (W) and SWS states due principally to a decrease in tidal volume. BBF during REM sleep was significantly and substantially increased compared with both the W and SWS states; this increase was shared by all brain areas. The increase in BBF during REM sleep was greater than that predicted from changes in PaCO2. In five goats provided with chronic sagittal sinus fistulae, arteriovenous oxygen difference was measured in separate studies and found to be significantly lower during REM sleep compared with W; brain O2 consumption was similar in magnitude in the REM and W states. Thus, the high BBF of REM sleep was also unexplained by an increase of brain metabolic activity. We conclude that, during SWS, increases in BBF are explained by hypoventilation and hypercapnia. In contrast, during REM sleep, BBF is substantially in excess of that expected from PaCO2 or brain metabolism. It is postulated that this excess of BBF during REM sleep could reduce the central chemoreceptor pH relative to that present in SWS. The combination of reduction of sensitivity to CO2 and lower tissue PCO2 during REM sleep makes it likely that the output of the central chemoreceptors during this state is less than that during SWS and wakefulness. This may contribute to the low tidal volume and respiratory irregularities of this sleep period.
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PMID:Correlation between ventilation and brain blood flow during sleep. 642 78

We have previously described a canine model of obstructive sleep apnea (OSA) in which sleep-wake state is monitored continuously by a computer that produces tracheal occlusion when sleep occurs. Our aim was to assess the effects of long-term application of this model on resting ventilation and on the ventilatory and arousal responses to hypercapnia and hypoxia. Five dogs were maintained on the model for 15.5 +/- 1.7 (mean +/- SE) wk, with a mean apnea index of 57.5 +/- 4.5 occlusions/h of sleep. Resting ventilation and the ventilatory and arousal responses to progressive hypoxic and hypercapnic rebreathing were assessed during wakefulness (W) and both slow-wave (SWS) and rapid-eye-movement (REM) sleep at baseline prior to intervention, at the end of the OSA phase, and following a 1 to 3-mo recovery period. During the period of OSA there were small changes in respiratory timing at rest, but no significant changes in PCO2 or SaO2. As compared with baseline, the ventilatory response to hypoxia during OSA was strikingly reduced during W, and significantly although less markedly reduced during SWS and REM. The reduction was due to a decreased breathing frequency response to hypoxia. In addition, during OSA there was a significant decrease from baseline in SaO2 at arousal during hypoxic rebreathing in both SWS and REM. All responses returned to normal during recovery. In contrast to hypoxia, hypercapnic ventilatory responses during OSA were slightly increased over their baseline values both in W and SWS, owing to a leftward shift of the ventilation-versus-PCO2 relationship. During recovery, these responses reverted partly to baseline for W and reverted completely to baseline for SWS. There were no significant changes in arousal PCO2 during hypercapnic rebreathing in either SWS or REM across the pre-OSA baseline, OSA, and post-OSA recovery periods. We conclude that long-term application of the OSA model is associated with a selective, reversible decrease in ventilatory and arousal responses to hypoxia.
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PMID:Ventilatory and arousal responses to hypoxia and hypercapnia in a canine model of obstructive sleep apnea. 931 9

In this study, we examined the cardiorespiratory patterns of harbour seal pups under normoxic/normocarbic (air), hypoxic/normocarbic (15%, 12%, and 9% O2 in air), and normoxic/hypercarbic (2%, 4%, and 6% CO2 in air) conditions while awake and sleeping on land. Animals were chronically instrumented to record electroencephalogram (EEG), electromyogram (EMG), and electrocardiogram (EKG) signals, which, along with respiration (whole-body plethysmography) and oxygen consumption (VO2), were recorded from animals breathing each gas mixture for 2-4 h on separate days. Our results show that for animals breathing air, VO2 was not significantly lower during slow-wave sleep (SWS; 7.71 +/- 0.39 mL O2 min(-1) kg(-1); all measurements are mean +/- SEM) than during wakefulness (WAKE; 8.80 +/- 0.25 mL O2 min(-1) kg(-1)) and was unaffected by changes in respiratory drive. Although there was no significant fall in VO2 associated with a decrease in arousal state, breathing frequency (f(R)) did decrease (from 18.80 +/- 1.50 breaths min(-1) in WAKE to 10.40 +/- 0.49 breaths min(-1) in SWS), while the incidence of long apneas (>20 s) increased (12.76 +/- 4.06 apneas h(-1) in WAKE and 31.95 +/- 2.37 apneas h(-1) in SWS). Breathing was rarely seen during rapid eye movement (REM) sleep. Tachypnea was present at all levels of increased respiratory drive; however, hypoxia induced a dramatic bradycardia regardless of arousal state, while hypercarbia produced a tachycardia in SWS only. The hypoxic and hypercarbic chemosensitivities of harbour seal pups were similar to those of terrestrial mammals; however, unlike terrestrial mammals, where hypoxic and hypercarbic sensitivities are often reduced during SWS, the sensitivity of harbour seal pups to hypoxia and hypercarbia remained unchanged during the decrease in arousal state from WAKE to SWS.
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PMID:Respiratory chemosensitivity during wake and sleep in harbour seal pups (Phoca vitulina richardsii). 1554 2