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1 acute lung injury have been shown to improve arterial oxygen tension.
2 ged as a potential strategy to rapidly raise arterial oxygen tensions.
3 -expiratory lung volume, but did not improve arterial oxygen tension and caused a reduction in cardia
4 onsistent with the hypothesis that increased arterial oxygen tension and consequently increased CSF P
7 An inverse relationship was observed between arterial oxygen tension and the magnitude of hyperleukoc
8 iratory volume in 1 second (FEV1), of 20% in arterial oxygen tension, and of 20% in the 6-minute walk
10 0.7), PaO2 (35+/-3.1 mm Hg), and alveolar to arterial oxygen tension difference (AaDO2) (26+/-3 mm Hg
11 ped respiratory distress; PaO2, the alveolar-arterial oxygen tension difference (AaPO2) and venous ad
12 f carbon monoxide (DL(CO)), and the alveolar-arterial oxygen tension difference P(A-a)O(2) were measu
14 ignificantly, slowing blood flow velocity at arterial oxygen tension even without additional contribu
15 expected to broaden the permissible range of arterial oxygen tensions for pulmonary/tissue oxygen tra
16 eased inspiratory time, and widened alveolar-arterial oxygen tension gradient (all p < or = 0.001); t
18 d neutrophils, PaO2/FIO2 ratio, and alveolar-arterial oxygen tension gradient in acid-induced lung in
20 ratio, followed by shunt fraction, alveolar-arterial oxygen tension gradient, FIO2, PaO2, respirator
21 ur after the instillation of perflubron, the arterial oxygen tension increased by 138 percent and the
22 007) and inversely correlated with wake-time arterial oxygen tension (P = 0.0007) and oxygen saturati
24 essentially proportional to the decrease in arterial oxygen tension (PaO2) below the normoxic level.
25 delines instructing for explicit targets for arterial oxygen tension (PaO2, 55-86 mm Hg) and oxyhemog
27 canning, and a marked improvement in resting arterial oxygen tension while breathing air to 10.3 kPa
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