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1 ypoxemia index (percentage of time below 90% O2 saturation).
2 levels of systemic hypoxia (85, 80 and 75 % O2 saturation).
3 rpnoea, and isocapnic hypoxia (85 % arterial O2 saturation).
4 KE (p < 0.05) but had no effect on arterial O2 saturation.
5 not enhanced with dopamine despite the lower O2 saturation.
6 subjected to 30 minutes of hypoxia (arterial O2 saturation, 30%) and then 7 minutes of airway occlusi
8 30%) and then 7 minutes of airway occlusion (O2 saturation, 5%), producing cardiac arrest, followed b
10 poxia (85 % O2 saturation, -64 +/- 3 %; 80 % O2 saturation, -62 +/- 1 %; 75 % O2 saturation, -61 +/-
11 - 2 %) and the three levels of hypoxia (85 % O2 saturation, -64 +/- 3 %; 80 % O2 saturation, -62 +/-
13 nity of HbS and found that its effect on HbS O2 saturation and cell sickling correlated with that on
18 moxia (NormEx) and isocapnic hypoxia (HypEx; O2 saturation approximately 85%) before and after local
22 ite gradients correlated with the hemoglobin O2 saturation gradient (P<0.05) and inversely with cardi
23 WT mice resulted in reduced carotid arterial O2 saturation (hypoxemia), lung pathology, pulmonary ede
25 usate gases and electrolytes (pH, pCO2, pO2, O2 saturation, Na(+), K(+), Cl(-), Ca(2+), HCO3(-), gluc
27 etermine the effect of endurance training on O2 saturation of Mb (SmbO2) and PmbO2 kinetics during mu
29 intermittent hypoxia (IH), simulating blood O2 saturation profiles during obstructive sleep apnoea (
30 intermittent hypoxia (IH), simulating blood O2 saturation profiles during obstructive sleep apnoea (
33 .5 +/- 0.9 mmHg; range, 67-88 mmHg; arterial O2 saturation (Sa,O2), 92.3 +/- 0.2%; range, 87-94%).
34 fied a key hypoxia threshold at a 30% buffer O2 saturation that induces a stable and potentially surv
35 e increased O2 delivery; at S2 onset, venous O2 saturation was 21 +/- 4% and 65 +/- 5% in SPON and PU
36 ation, arterial pO2 (mm Hg) and mixed venous O2 saturation (%) were significantly higher in the posit
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