ライフサイエンスコーパス: O2 saturation

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

7 kidneys were able to extract oxygen from VB (O2 saturation, 31 +/- 7% to 16 +/- 4%; p =.01).

8 30%) and then 7 minutes of airway occlusion (O2 saturation, 5%), producing cardiac arrest, followed b

9 - 3 %; 80 % O2 saturation, -62 +/- 1 %; 75 % O2 saturation, -61 +/- 3 %; P = 0.37).

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 +/-

12 versus 38+/-3 grams/dL; P=0.004), and lower O2 saturations (84+/-4% versus 98+/-2%; (P<0.001).

13 nity of HbS and found that its effect on HbS O2 saturation and cell sickling correlated with that on

14 Arterial O2 saturation and maximal work capacity increased in bot

15 Among all fetuses, blood O2 saturation and plasma glucose, insulin and insulin-li

16 Body weight, arterial O2 saturation, and heart rate were monitored daily.

17 d hypoxic responses secondary to anemia, low O2 saturation, and microvascular obstruction.

18 moxia (NormEx) and isocapnic hypoxia (HypEx; O2 saturation approximately 85%) before and after local

19 rmoxic and normocapnic hypoxic (80% arterial O2 saturation) conditions.

20 Soil moisture, through changes in soil %O2 saturation, determined predominance of methanotrophy

21 We measured ventilation, arterial O2 saturation, end-tidal CO2 (PET,CO2), blood pressure (

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

24 te >22/min, abnormal chest imaging findings, O2 saturation lower than 90%, and aspartate aminotransfe

25 inuous measures of mixed (or central) venous O2 saturation may provide the answer.

26 nspired O2 of 300 or less, and/or a ratio of O2 saturation measured with pulse oximeter to fraction o

27 usate gases and electrolytes (pH, pCO2, pO2, O2 saturation, Na(+), K(+), Cl(-), Ca(2+), HCO3(-), gluc

28 Neither ventilation, arterial O2 saturation nor mild anemia could account for the decr

29 etermine the effect of endurance training on O2 saturation of Mb (SmbO2) and PmbO2 kinetics during mu

30 parameters, including sample weight and the O2 saturation of the Cu-reduction reactor.

31 intermittent hypoxia (IH), simulating blood O2 saturation profiles during obstructive sleep apnoea (

32 intermittent hypoxia (IH), simulating blood O2 saturation profiles during obstructive sleep apnoea (

33 ing normoxia and mild systemic hypoxia (85 % O2 saturation; pulse oximetry of the earlobe).

34 Blood O2 saturation (r(2) = 0.80, P < 0.0001) and plasma gluco

35 .5 +/- 0.9 mmHg; range, 67-88 mmHg; arterial O2 saturation (Sa,O2), 92.3 +/- 0.2%; range, 87-94%).

36 fied a key hypoxia threshold at a 30% buffer O2 saturation that induces a stable and potentially surv

37 e increased O2 delivery; at S2 onset, venous O2 saturation was 21 +/- 4% and 65 +/- 5% in SPON and PU

38 was 16 (95% CI, 13-19), and the mean minimum O2 saturation was 83% (95% CI, 81%-85%).

39 ation, arterial pO2 (mm Hg) and mixed venous O2 saturation (%) were significantly higher in the posit