ライフサイエンスコーパス: hypocapnia

1 ercise PcCO2 less than or equal to 35 mm Hg (hypocapnia).

2 to the inspirate, or it was allowed to fall (hypocapnia).

3 h production insofar as speech often induces hypocapnia.

4 d speech-breathing insofar as speech induces hypocapnia.

5 ented NO decrease in endothelial cells under hypocapnia.

6 Elevated respiratory rate resulted in hypocapnia.

7 decreased CBF likely because hypoxia induced hypocapnia.

8 rebral flow was normal to increased, despite hypocapnia.

9 during hypercapnia and undershooting during hypocapnia.

10 ct cerebrovascular reactivity to hypoxia and hypocapnia.

11 scular response to PET(CO(2)), especially to hypocapnia.

12 in response to hypoxia and to decrease with hypocapnia.

13 l rates, despite supplemental CO2 to prevent hypocapnia.

14 f the cerebrovascular response to hyper- and hypocapnia.

15 ator of splanchnic perfusion during systemic hypocapnia.

16 ity during wakefulness and in the absence of hypocapnia.

17 o hypoxia stimulates ventilation and induces hypocapnia.

18 (voluntary hyperventilation, n = 9) profound hypocapnia.

19 RP was increased by either hypocapnia (0% CO2 through the bronchoscope for 3 min) o

20 t reduction of cerebrovascular reactivity to hypocapnia (1.2 +/- 0.3 vs. 2.2 +/- 0.1%/mm Hg, p < 0.05

21 +/- 0.24 vs. 2.96 +/- 0.26 cm s-1 mmHg-1) or hypocapnia (1.31 +/- 0.18 vs. 1.32 +/- 0.19 cm s-1 mmHg-

22 demonstrated hyperventilation at rest, with hypocapnia (28 +/- 3.8 mm Hg), a normal (slightly alkali

23 The brain extracted more oxygen in face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% t

24 Hyperventilation-induced hypocapnia affects hemodynamic function and enhances col

25 These hyperadditive effects of CB hyper-/hypocapnia agree with previous findings using CB hyper-/

26 s a poorly understood condition of sustained hypocapnia and controversial etiology.

27 determined whether patients had exposure to hypocapnia and hypercapnia (defined as Paco(2) </=30 mm

28 (33%) had hypercapnia only, 18 (9%) had both hypocapnia and hypercapnia exposure, and 60 (31%) had no

29 However, the effect of hypocapnia and hypercapnia on blood cytokine production

30 Hypocapnia and hypercapnia were common after cardiac arr

31 ether post-return of spontaneous circulation hypocapnia and hypercapnia were independent predictors o

32 Hypocapnia and hypercapnia were independently associated

33 non-HCO3 buffers are also titrated in acute hypocapnia and hypercapnia, these disorders were induced

34 Repeated DAC increased reactivity to hypocapnia and intravenous histamine.

35 selectively suppressed neuronal responses to hypocapnia and mild hypercapnia.

36 ome an increased "wasted" ventilation led to hypocapnia and poor exercise ventilatory efficiency in c

37 d be prolonged when hyperventilatory-induced hypocapnia (and hence cerebral hypoperfusion) was preven

38 tary sniff maneuvers, normocapnic breathing, hypocapnia, and after return to normocapnia.

39 Perioperative factors including hypoxia, hypocapnia, and certain anesthetics have been suggested

40 rculatory responses to hypoxia, hypotension, hypocapnia, and hypercapnia after dhCPB and DHCA.

41 scular and oxygenation responses to hypoxia, hypocapnia, and hypotension were preserved after dhCPB a

42 ted the ability of nitric oxide to attenuate hypocapnia- and acetylcholine-induced constriction in th

43 c stimulation) and 62% expressed c-Fos under hypocapnia (approximately 3% end-tidal CO(2)) after PeF

44 Arrival hypercapnia and hypocapnia are common and associated with worse outcomes

45 delay time (rather than hyperventilation or hypocapnia) as causes of PB.

46 poxia and larger vasoconstriction to hypoxic hypocapnia at high altitude suggest that cerebrovascular

47 l hypoperfusion either at rest or induced by hypocapnia at pre-syncope does not impact OT, probably d

48 o effect on the slope of the CFV response to hypocapnia but it reduced the CFV response to hypercapni

49 The presence of prior hypocapnia, but not prior hyperventilation, caused a red

50 de (14.5 to 250 ppm) attenuated responses to hypocapnia by 38 +/- 0 to 74 +/- 0% (n = 6) and to acety

51 the degree to which the hyperventilation and hypocapnia can induce the changes known as ventilatory a

52 nce of prior hyperventilation, but not prior hypocapnia, caused an increase in the ventilatory sensit

53 Hypocapnia decreases the drive to breathe and induces ap

54 Hypocapnia did not further inhibit respiratory motor out

55 onomic responses to hypoxia, hypoxia-induced hypocapnia dominated CBF changes, tissues in awake condi

56 CFV were computed separately for hyper- and hypocapnia during the LBNP and no-LBNP conditions.

57 ventricular ejection fraction, patients with hypocapnia had lower resting PaCO2 and lung diffusing ca

58 lation on vascular barrier function, whereas hypocapnia had the opposite effect.

59 The group with hypocapnia, however, had worse mechanical inspiratory co

60 ood gas derangement (hypoxemia, hyperoxemia, hypocapnia, hypercapnia, and acidosis) was associated wi

61 ed in 15 rats during periods of normocapnia, hypocapnia, hypercapnia, and anoxia.

62 cerebrovascular responsiveness to hyper- and hypocapnia in healthy humans.

63 The responses to normoxic hypocapnia in the altitude subjects were also similar at

64 ased during hypercapnia and decreased during hypocapnia independent of pH.

65 fects of changing ventilatory stimuli on the hypocapnia-induced apneic and hypopneic thresholds in sl

66 Hyperventilation induced a longer hypocapnia-induced apneic period (51.5 +/- 9.9 versus 11

67 Sleep unmasks a highly sensitive hypocapnia-induced apnoeic threshold, whereby apnoea is

68 culature to increase oxygen unloading during hypocapnia-induced hypoperfusion.

69 vity persists, during wakefulness, even when hypocapnia makes it unnecessary.

70 Therapeutic measures preventing hypoxia/hypocapnia may correct cardiovascular accidents in patie

71 The hypocapnia-mediated decrease of alveolar fluid reabsorpt

72 During hypocapnia, NO levels in the endothelial cells decreased

73 The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body PC

74 ersus 0.51 +/- 0.19 versus 0.43 +/- 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively).

75 t hypoxia, reoxygenation, and hypercapnia or hypocapnia occur in both adults and children during untr

76 may result from direct metabolic effects of hypocapnia on colonic muscle or from changes in central

77 Of 193 patients, 52 (27%) had hypocapnia only, 63 (33%) had hypercapnia only, 18 (9%)

78 btained to examine the independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on

79 In the presence of either hypocapnia or sleep, hypoxia has been shown to induce pe

80 ry efficiency compared with patients without hypocapnia (P < 0.05).

81 (44 +/- 12 ml/s versus 81 +/- 7 ml/s during hypocapnia, p = 0.048), as was the decrease in Pcrit (-2

82 o2 and pial arteriolar diameter decreased to hypocapnia (Paco2, 25 torr) similarly in all groups.

83 Hypoxia (PO(2)=10-15 Torr) increased and hypocapnia (PCO(2)=7-9 Torr) decreased the cytoplasmic c

84 In hypocapnia (PCO2 approximately 18 Torr) with high PCO, a

85 Thus, hyperventilation and hypocapnia, per se, widened the DeltaPET(CO2) thereby pr

86 (2) hypercapnia (PET(CO(2)) = 45 mm Hg); (3) hypocapnia (PET(CO(2)) = 35 mm Hg, induced via hypervent

87 o changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor inp

88 Hypocapnia reduces intracranial pressure and is used by

89 d EEG activity was observed in subjects with hypocapnia-related apneas.

90 During NREM sleep, hypocapnia resulted in wasted ventilator trigger efforts

91 cerebral blood flow responses to hypoxia and hypocapnia, separately and together, in Andean high-alti

92 Compared with baseline, hypercapnia and hypocapnia significantly increased and decreased CBF, re

93 oth high-altitude groups showed responses to hypocapnia that were significantly smaller at Lima than

94 hypercapnia (inspired CO(2), 3 and 5%), and hypocapnia (voluntary hyperventilation).

95 After passive hyperventilation, hypocapnia was associated with apnea in 3 cases and vent

96 During NREM sleep, hypocapnia was induced via nasal mechanical ventilation.

97 ebrovascular reactivity to CO(2) (hyper- and hypocapnia) was lower in patients with apnea than in the

98 solized histamine, intravenous histamine, or hypocapnia were measured daily.

99 MCAVm responses to hypocapnia were studied by voluntary hyperventilation wi

100 tory assistance from pressure support causes hypocapnia, which combined with the lack of a backup rat

101 h CEU at baseline and during hypercapnia and hypocapnia while normoxia was maintained.