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 creases in ventilation and similar levels of hypocapnia.

4 with postural orthostatic tachycardia and/or hypocapnia.

5 orm of either orthostatic tachycardia and/or hypocapnia.

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

7 h production insofar as speech often induces hypocapnia.

8 d speech-breathing insofar as speech induces hypocapnia.

9 ented NO decrease in endothelial cells under hypocapnia.

10 Elevated respiratory rate resulted in hypocapnia.

11 decreased CBF likely because hypoxia induced hypocapnia.

12 rebral flow was normal to increased, despite hypocapnia.

13 during hypercapnia and undershooting during hypocapnia.

14 ct cerebrovascular reactivity to hypoxia and hypocapnia.

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

16 in response to hypoxia and to decrease with hypocapnia.

17 l rates, despite supplemental CO2 to prevent hypocapnia.

18 f the cerebrovascular response to hyper- and hypocapnia.

19 ator of splanchnic perfusion during systemic hypocapnia.

20 ity during wakefulness and in the absence of hypocapnia.

21 o hypoxia stimulates ventilation and induces hypocapnia.

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

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

24 +/- 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-

25 were markedly slower with hypercapnia versus hypocapnia (24 5 vs. 7 5 s, respectively) likely indicat

26 were markedly slower with hypercapnia versus hypocapnia (24 5 vs. 7 5 s, respectively; stage effect:

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

28 m 0.167 +/- 0.036 Hz at the lowest values of hypocapnia (28.1 +/- 1.9 mmHg) to 0.094 +/- 0.040 Hz at

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

30 ched stepwise iso-oxic alterations in PaCO2 (hypocapnia: -5, -10 mmHg; hypercapnia: +5, +10 mmHg) pri

31 ched stepwise iso-oxic alterations in PaCO2 (hypocapnia: -5, -10 mmHg; hypercapnia: +5, +10 mmHg) pri

32 Hyperventilation-induced hypocapnia affects hemodynamic function and enhances col

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

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

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

36 (33%) had hypercapnia only, 18 (9%) had both hypocapnia and hypercapnia exposure, and 60 (31%) had no

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

38 Hypocapnia and hypercapnia were common after cardiac arr

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

40 Hypocapnia and hypercapnia were independently associated

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

42 Repeated DAC increased reactivity to hypocapnia and intravenous histamine.

43 selectively suppressed neuronal responses to hypocapnia and mild hypercapnia.

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

45 ugh ventilatory acclimatization, but elicits hypocapnia and respiratory alkalosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 reactivity to hypercapnia (CVR(HYPER) ) and hypocapnia (CVR(HYPO) ), respectively.

63 Hypocapnia decreases the drive to breathe and induces ap

64 Hypocapnia did not further inhibit respiratory motor out

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

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

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

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

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

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

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

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

73 n participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no chang

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

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

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

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

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

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

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

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

82 The hypocapnia-mediated decrease of alveolar fluid reabsorpt

83 During hypocapnia, NO levels in the endothelial cells decreased

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

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

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

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

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

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

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

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

92 (44 +/- 12 ml/s versus 81 +/- 7 ml/s during hypocapnia, p = 0.048), as was the decrease in Pcrit (-2

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

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

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

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

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

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

99 Hypocapnia reduces intracranial pressure and is used by

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

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

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

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

104 on of oxygenation and a comparable degree of hypocapnia, suggesting differential thresholds of O(2) a

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

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

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

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

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

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

111 MCAVm responses to hypocapnia were studied by voluntary hyperventilation wi

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

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