ライフサイエンスコーパス: respiratory acidosis

1 nate and base excess, indicating compensated respiratory acidosis.

2 g is limited to sheep akin to sheep maternal respiratory acidosis.

3 riation, or differences in the management of respiratory acidosis.

4 anges in cerebrovascular tone in response to respiratory acidosis.

5 unction and may blunt renal compensation for respiratory acidosis.

6 phragm force output, despite hypercapnia and respiratory acidosis.

7 e positioned, and 14 patients had refractory respiratory acidosis.

8 However, lowering Vts may result in respiratory acidosis.

9 In medullary raphe neurones, respiratory acidosis (5%--> 9% CO(2)) caused a rapid fal

10 Maternal respiratory acidosis, a common finding in sheep studies

11 Respiratory acidosis, a decrease in blood pH caused by a

12 tracellular pH levels such as those found in respiratory acidosis--a known risk factor for SIDS--prod

13 levels (mean +/- SEM) from term babies with respiratory acidosis (acute hypoxia), normal babies, and

14 ations in arterial [HCO(3)(-) ] during acute respiratory acidosis/alkalosis contribute to cerebrovasc

15 ive ventilation due to refractory hypoxia or respiratory acidosis and high plateau airway pressures.

16 Oxygen-breathing conscious mice sustained respiratory acidosis and, consequently, reduced cell pro

17 Episodes of hypoxia, respiratory acidosis, and bradycardia occurred more freq

18 resuscitation results in profound hypoxemia, respiratory acidosis, and significantly worse 24-hr neur

19 th groups had similar (mean +/- SD) baseline respiratory acidosis (arterial pH, 7.22 +/- 0.08; Pa(CO(

20 ~95% of RTN (Nmb) neurons causes compensated respiratory acidosis because of alveolar hypoventilation

21 All animals developed a metabolic and a respiratory acidosis during the infusion of oleic acid.

22 ore pH.Measurements and Main Results: During respiratory acidosis, electrodialysis reduced plasma chl

23 Heliox improves respiratory acidosis, encephalopathy, and the respirator

24 g-protective ventilation is often limited by respiratory acidosis, extracorporeal membrane oxygenatio

25 complete and slower compensatory response to respiratory acidosis (final pH = 7.29 +/- 0.03; P < 0.00

26 In the COPD exacerbation with respiratory acidosis group, the primary outcome occurred

27 increase in the arterial-alveolar gradient, respiratory acidosis, histological changes similar to th

28 nction in pulmonary disorders in relation to respiratory acidosis, impaired gas exchange, systemic co

29 an pCO2 above 1,000 muatm by 2100 - inducing respiratory acidosis in fish that must be corrected thro

30 t maintains arterial CO2 levels and prevents respiratory acidosis in the face of increased metabolism

31 channel, and suggests an important role for respiratory acidosis in triggering the fatal arrhythmia

32 Tactics to reduce respiratory acidosis include reductions in ventilation c

33 ity (n = 3), inadequate oxygenation (n = 3), respiratory acidosis (n = 3), and undocumented (n = 1).

34 nts with hypercapnic respiratory failure and respiratory acidosis nonresponsive to noninvasive ventil

35 ced either through reduction of ventilation (respiratory acidosis) or through lactic acid infusion (m

36 tuations associated with profound hypoxemia, respiratory acidosis, or hemodynamic compromise.

37 moderate bronchoconstriction; more profound respiratory acidosis (PaCO2 137+/-41 torr (18.2+/-5.5 kP

38 Blood gases (on 6 L/min oxygen) showed respiratory acidosis (pH, 7.15 [normal range, 7.38-7.42]

39 Blood gases (on 6 L/min oxygen) showed respiratory acidosis (pH, 7.15 [normal range, 7.38-7.42]

40 injection and after the PET scan implicated respiratory acidosis that was induced by oxygen breathin

41 Despite respiratory acidosis, there was no decrease in trandiaph

42 airing arterial oxygenation and facilitating respiratory acidosis throughout exercise.

43 In brainstem slices of wild-type mice, respiratory acidosis triggered robust elevations in [Ca(

44 Respiratory acidosis was never detected, although a mild

45 iratory failure (PaO2/FIO2 < 85 mm Hg and/or respiratory acidosis with pH < 7.25) who were successful

46 As risk factors for SIDS include apnea and respiratory acidosis, Y1103 and wild-type channels were