睡眠ラットにおける間欠的低酸素暴露後の呼吸出力促進

抄録

Ventilatory long-term facilitation (vLTF) following acute intermittent hypoxia (AIH) has been reported to variable extent in unanesthetized rats. However, none of these studies reported sleep-state, a critical variable in many physiological functions. We hypothesized that vLTF would be preferentially expressed in sleeping vs. awake Lewis rats following AIH. The sleep-wake state of unrestrained rats was determined from implanted EEG and nuchal EMG electrodes. Tidal volume (VT), frequency (f), minute ventilation (VE) and CO2 production (VCO2) were determined in unanaesthetized male Lewis rats via plethysmography before, during and after AIH (five, 5-min exposures, 10.5% O2; 5-min normoxic intervals) or acute sustained hypoxia (25-min exposures, 10.5% O2, ASH). VE, VT and f in quiet wakefulness (QW) or NREM sleep were normalized to its own baseline value during the corresponding state during baseline, pre-hypoxia conditions. LTF was observed in VE after AIH, but not ASH. Following AIH in NREM, VE gradually increased and reached maximum level at 20 min post-hypoxia, remaining at that level for at least 60 min (26.6±5.2% baseline). The main contributor to vLTF was VT (13.5±2.3%), with a lesser increase in f (7.4±1.7%). The corresponding increase in VE/VCO2 was 35.5±2.4% baseline. In QW, significant vLTF was not observed. The duration, magnitude, and pattern in vLTF in NREM were similar to phrenic LTF in anesthetized rats. In conclusion, vLTF is highly state and pattern sensitive in unanesthetized rats. (Supported by NIH HL65383, HL07654, HL68255). [J Physiol Sci. 2006;56 Suppl:S75]