ライフサイエンスコーパス: normocapnia

1 L/min/%, p < 0.05] with acute restoration to normocapnia).

2 her contribution from RAP in comparison with normocapnia.

3 al mortality than compensated hypercapnia or normocapnia.

4 c breathing, hypocapnia, and after return to normocapnia.

5 epithelial injury and cell death compared to normocapnia.

6 nclusion of the study, a total of 90 mins of normocapnia.

7 going hypercapnia for 6 hrs with a return to normocapnia.

8 change during hypercapnia or with return to normocapnia.

9 was returned to the baseline value, that is, normocapnia.

10 97% total CO2 production) while maintaining normocapnia.

11 duced the respiratory rate while maintaining normocapnia.

12 arteriovenous CO2 removal while maintaining normocapnia.

13 argeted mild hypercapnia and 853 to targeted normocapnia.

14 eurologic outcomes at 6 months than targeted normocapnia.

15 ting reductions of 5 and 10 mmHg compared to normocapnia.

16 ificant decrease in respiratory rate (RR) at normocapnia, an elevated RR during hypoxia, and an atten

17 entilating the piglets with 100% O(2) during normocapnia and concomitantly topically applying artific

18 The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body PCO2 approxima

19 atory response indices were found between CB normocapnia and hypercapnia.

20 1.10-1.26) when compared with patients with normocapnia and normal pH (p < 0.001).

21 A total of 252,812 patients (normocapnia and normal pH, 110,104; compensated hypercap

22 combination of pH and carbon dioxide levels (normocapnia and normal pH, compensated hypercapnia [norm

23 , with the lowest mortality in patients with normocapnia and normal pH.

24 roup, arterial blood pH was 7.42 +/- 0.02 at normocapnia and was maintained at 7.37 +/- 0.01 while Pa

25 graphy) were performed during 5 min at rest (normocapnia) and during four breathing manoeuvres: 5% an

26 rate (ECG) were performed for 5 min at rest (normocapnia) and during hypercapnia induced by breathing

27 /- 0.19 versus 0.43 +/- 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively).

28 at normocapnia to 7.14 +/- 0.01 (p < .01 vs. normocapnia) as blood PCO2 increased to 81.2 +/- 1.8 tor

29 V(T) = 8 mL/kg, respiratory rate adjusted to normocapnia) at low (n = 2, positive end-expiratory pres

30 During normocapnia, both RAP and CrCP make a significant contri

31 At 30 mins of normocapnia, CBF had returned to baseline and remained a

32 omy, Sprague-Dawley rats were randomized to (normocapnia; FICO2 0.00) or (hypercapnic acidosis; FICO2

33 Guidelines recommend normocapnia for adults with coma who are resuscitated af

34 apnia group and in 350 of 784 (44.6%) in the normocapnia group (relative risk, 0.98; 95% confidence i

35 apnia group and in 382 of 832 (45.9%) in the normocapnia group (relative risk, 1.05; 95% CI, 0.94 to

36 tory-related sympathetic activity in rats in normocapnia, hypercapnia or after CIH.

37 e were compared in 15 rats during periods of normocapnia, hypocapnia, hypercapnia, and anoxia.

38 ous arterial spin labeling to measure CBF at normocapnia (ie, breathing room air) and hypercapnia.

39 To maintain normocapnia, minute ventilation was reduced from 3.8 +/-

40 repair was measured in AEC type 1 exposed to normocapnia (NC, 40 Torr) or HC (80 Torr), +/- trometham

41 went 4 hours of mechanical ventilation under normocapnia or hypercapnic acidosis, and nuclear factor-

42 ade a highly significant contribution during normocapnia (P < 0.0001) and was the sole determinant of

43 ng injury under the following conditions: a) normocapnia (Paco2 35 to 45 torr [4.7 to 6.0 kPa]) and n

44 In the dark, normocapnia (PCO2 approximately 30 Torr) with high PCO p

45 rr) in normoxic (pO2 approximately 100 Torr) normocapnia (pCO2 approximately 30 Torr, pH approximatel

46 on to ameliorate hypoventilation and restore normocapnia regardless of the cause of respiratory dysfu

47 o baseline of CBF and cerebral metabolism at normocapnia seen in our study with lambs may explain why

48 ities were significantly lower than those of normocapnia, showing stimulus interaction.

49 carbon dioxide [Paco(2)], 50 to 55 mm Hg) or normocapnia (target Paco(2), 35 to 45 mm Hg).

50 However, compared with normocapnia the probability of wound repair was signific

51 When preceded by nitrous oxide, midazolam or normocapnia, the risk of inducing epileptiform activity

52 ial blood pH decreased from 7.41 +/- 0.03 at normocapnia to 7.14 +/- 0.01 (p < .01 vs. normocapnia) a

53 the pH-corrected group (8.5 +/- 1.6 mm Hg at normocapnia to 7.7 +/- 4.2 at 1 hr).

54 the autoregulation index from 5.70 +/- 1.58 (normocapnia) to 4.14 +/- 2.05 (hypercapnia; P < 0.0001).

55 e pH-uncorrected group (9.0 +/- 1.5 mm Hg at normocapnia vs. 26.8 +/- 5.1 at 1 hr, p < .05), and rema

56 p < .05]; pH-corrected group: 4.1 +/- 0.4 at normocapnia vs. 5.7 +/- 0.4 L/min at 1 hr [p < .05]).

57 (pH-uncorrected group: 4.3 +/- 0.6 L/min at normocapnia vs. 6.8 +/- 1.0 L/min at 1 hr [p < .05]; pH-

58 Normocapnia was achieved using significantly higher PIP

59 ere intubated and mechanically ventilated to normocapnia with room air.