Journal of applied physiology
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We recently reported that glottic closure was present throughout central apneas in awake lambs. The present study tested whether glottic closure was also observed during periodic breathing (PB). We attempted to induce PB in 21 nonsedated lambs on return from hypocapnic hypoxia to room air. ⋯ Phasic inspiratory cricothyroid muscle EMG and phasic expiratory abdominal EMG disappeared at the nadir of PB. Active glottic closure at the nadir of PB, without abdominal muscle contraction, could be a beneficial mechanism, preserving alveolar gas stores for continuing gas exchange during the apneic/hypopneic phase of PB. However, consequences of active glottic closure on ventilatory instability, either enhancing or reducing, are unknown.
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We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (VT) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in VT because Pmus would be downregulated substantially as a result of small decreases in PCO2. ⋯ There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.
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Clinical Trial
Hypoxic ventilatory sensitivity in men is not reduced by prolonged hyperoxia (Predictive Studies V and VI).
Potential adverse effects on the O2-sensing function of the carotid body when its cells are exposed to toxic O2 pressures were assessed during investigations of human organ tolerance to prolonged continuous and intermittent hyperoxia (Predictive Studies V and VI). Isocapnic hypoxic ventilatory responses (HVR) were determined at 1.0 ATA before and after severe hyperoxic exposures: 1) continuous O2 breathing at 1.5, 2.0, and 2.5 ATA for 17.7, 9.0, and 5.7 h and 2) intermittent O2 breathing at 2.0 ATA (30 min O2-30 min normoxia) for 14.3 O2 h within 30-h total time. ⋯ In humans, prolonged hyperoxia does not attenuate the hypoxia-sensing function of the peripheral chemoreceptors, even after exposures that approach limits of human pulmonary and central nervous system O2 tolerance. Current applications of hyperoxia in hyperbaric O2 therapy and in subsea- and aerospace-related operations are guided by and are well within these exposure limits.
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Comparative Study Clinical Trial Controlled Clinical Trial
Efficacy of forced-air and inhalation rewarming by using a human model for severe hypothermia.
We recently developed a nonshivering human model for severe hypothermia by using meperidine to inhibit shivering in mildly hypothermic subjects. This thermal model was used to evaluate warming techniques. On three occasions, eight subjects were immersed for approximately 25 min in 9 degrees C water. ⋯ The core temperature afterdrop was 30-40% less during forced-air warming (0.9 degree C) than during control (1.4 degrees C) and inhalation rewarming (1.2 degrees C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-air warming (2.40 degrees C/h) than during control (0.41 degree C/h) and inhalation rewarming (0.23 degree C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.
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Clinical Trial Controlled Clinical Trial
Inhibition of shivering increases core temperature afterdrop and attenuates rewarming in hypothermic humans.
During severe hypothermia, shivering is absent. To simulate severe hypothermia, shivering in eight mildly hypothermic subjects was inhibited with meperidine (1.5 mg/kg). Subjects were cooled twice (meperidine and control trials) in 8 degrees C water to a core temperature of 35.9 +/- 0.5 (SD) degrees C, dried, and then placed in sleeping bags. ⋯ This was likely due to the increased thermoregulatory drive with the greater afterdrop and the short half-life of meperidine. These results demonstrate the effectiveness of shivering heat production in attenuating the postcooling afterdrop of core temperature and potentiating core rewarming. The meperidine protocol may be valuable for comparing the efficacy of various hypothermia rewarming methods in the absence of shivering.