ライフサイエンスコーパス: isocapnic

1 Isocapnic acidosis (5 % CO(2), 7 mM HCO(3)(-), pH(o) 6.8

2 hypercapnic acidosis also had no response to isocapnic acidosis (n = 12).

3 Isocapnic acidosis (pH(o) 7.16; [NaHCO(3)](o) 15 mM) ind

4 ones tested (n = 15) were also stimulated by isocapnic acidosis, and all CO2-inhibited neurones teste

5 d neurones tested (n = 19) were inhibited by isocapnic acidosis.

6 Neurones were also exposed to isocapnic acidosis.

7 quencies than during NREM sleep (p < 0.001); isocapnic and hypercapnic conditions did not differ (p =

8 machine rates during wakefulness and during isocapnic and hypercapnic NREM sleep.

9 rved during wakefulness and sleep, and under isocapnic as well as hypocapnic conditions.

10 ied out by three different levels of hypoxic isocapnic blood (PO2 approximately 58, 40 and 22 mmHg) o

11 Single-unit chemoreceptor responses to isocapnic changes in oxygenation within the arterial oxy

12 The larger the VT applied during the isocapnic CMV (120-200% of eupnea) and the longer the du

13 Isocapnic cold air hyperventilation (ISH) is believed to

14 hty volunteers individually underwent an 8-h isocapnic exposure to hypoxia (end-tidal P(O2)=55 Torr)

15 measured while breathing room air and during isocapnic hyperoxia (100% O2 breathing) and isoxic hyper

16 le pump alone), during unloaded cycling with isocapnic hyperpnea (muscle and ventilatory pump), durin

17 d that this resetting would not occur during isocapnic hyperpnoea at the same breathing rate and dept

18 While isocapnic hyperpnoea did not alter heart rate, arterial

19 e modified Oxford technique during normoxia, isocapnic hyperpnoea, and isocapnic hypoxia (85 % arteri

20 atory tract by having eight subjects perform isocapnic hyperventilation for 1, 2, 4, and 8 min at a c

21 Isocapnic hyperventilation is a promising therapy for CO

22 aluations including bronchoprovocations with isocapnic hyperventilation of frigid air, methacholine a

23 easured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49

24 We studied the effects of isocapnic hyperventilation on five adult mechanically ve

25 Isocapnic hyperventilation utilizing mechanical ventilat

26 0 normal and 13 asthmatic subjects performed isocapnic hyperventilation with frigid air while the fra

27 Isocapnic hyperventilation, in our animal model, did not

28 At 130 +/- 4 days, a 1 h episode of acute, isocapnic hypoxaemia (9 % O(2) in N(2), to reduce caroti

29 station) we investigated the effect of acute isocapnic hypoxaemia (arterial Po2, 12.5 +/- 0.6 mmHg) o

30 Seven animals were given repeated acute isocapnic hypoxaemia (Pa,O2 reduced to ca. 13 mmHg) for

31 At 130 +/- 2 days, a 1 h episode of acute, isocapnic hypoxaemia (to reduce carotid P(O(2)) to 12 +/

32 the mechanism producing a fall in RO during isocapnic hypoxaemia in the neonate.

33 e during normoxia, isocapnic hyperpnoea, and isocapnic hypoxia (85 % arterial O2 saturation).

34 ity frequently induced by acute intermittent isocapnic hypoxia (AIH, three 5 min isocapnic hypoxic ep

35 hrenic nerve amplitude (integral Phr) during isocapnic hypoxia (arterial partial pressures of O2, 60,

36 rm blood flow responses (plethysmography) to isocapnic hypoxia (arterial saturation approximately 85%

37 esented with two or three, 5 min episodes of isocapnic hypoxia (FIO2 approximately 0.11), separated b

38 de of the ventilatory sensitivities to acute isocapnic hypoxia (G(pO2)) and hyperoxic hypercapnia, th

39 luntary contraction in normoxia (NormEx) and isocapnic hypoxia (HypEx; O2 saturation approximately 85

40 The respiratory response to isocapnic hypoxia (inspired O2 fraction (FI,O1), 0.1-0.1

41 uctance (FVC) responses to steady-state (SS) isocapnic hypoxia (O(2) saturation ~85%).

42 re, during and after three episodes of 5 min isocapnic hypoxia (P(a,O2) = 30-45 mmHg), separated by 5

43 Phrenic responses to isocapnic hypoxia (P(a,O2) = 60, 50 and 40 +/- 2 mmHg) w

44 ition (Pa(O2), 160 +/- 12 mm Hg) and in mild isocapnic hypoxia (Pa(O2), 69 +/- 7.2 mm Hg), with and w

45 and for 60 min after three 5 min episodes of isocapnic hypoxia (Pa,O2 35-45 mmHg) separated by 5 min

46 successive days: normoxia followed by acute isocapnic hypoxia (Pa,O2 to ca 12 mmHg) with infusion of

47 station) we investigated the effect of acute isocapnic hypoxia (Pa,O2, 12 +/- 0.6 mmHg) on the fetal

48 d eight healthy human participants to 8 h of isocapnic hypoxia and 8 h of air as a control.

49 Isocapnic hypoxia decreased the autocorrelation coeffici

50 ted phrenic responses to strictly controlled isocapnic hypoxia in urethane-anaesthetized, vagotomized

51 Compared with air, isocapnic hypoxia increased the gross variability of min

52 activation of peripheral chemoreceptors with isocapnic hypoxia resets arterial baroreflex control of

53 tion of peripheral chemoreceptors with acute isocapnic hypoxia resets arterial baroreflex control of

54 activation of peripheral chemoreceptors with isocapnic hypoxia resets baroreflex control of both hear

55 ncrease in total variational activity during isocapnic hypoxia was found to result from increases in

56 The respiratory response to isocapnic hypoxia was measured again post-lesioning.

57 Isocapnic hypoxia was repeated 10 min later.

58 and was identical to the first, except that isocapnic hypoxia was replaced with normoxia.

59 essive hyperoxic hypercapnia and progressive isocapnic hypoxia were associated with recruitment of ph

60 nt activity, integrated phrenic responses to isocapnic hypoxia were investigated in urethane-anaesthe

61 tery flow velocity (MCFV) during progressive isocapnic hypoxia, progressive hyperoxic hypercapnia, an

62 group were exposed to two 6-hour periods of isocapnic hypoxia.

63 frequency-90 (SEF(90)) in response to 40 min isocapnic hypoxia.

64 e during euoxia and during a short period of isocapnic hypoxia.

65 and 60 min following three 5-min episodes of isocapnic hypoxia.

66 the same breathing rate and depth as during isocapnic hypoxia.

67 ram during and after three 5 min episodes of isocapnic hypoxia.

68 jects, we described ventilatory responses to isocapnic-hypoxia, hyperoxic-hypercapnia, and exercise;

69 ventilation (VI) increased during the first isocapnic hypoxic episode and reached progressively high

70 e of phrenic nerve activity following brief, isocapnic hypoxic episodes in rats is diminished by prio

71 rmittent isocapnic hypoxia (AIH, three 5 min isocapnic hypoxic episodes).

72 od was drawn for hormone measurement and the isocapnic hypoxic ventilatory response was measured.

73 ventilatory responsiveness being normal and isocapnic-hypoxic ventilatory responsiveness being low r

74 nd-tidal CO2 was monitored and maintained at isocapnic levels; arterial blood gases were determined.

75 nspired gas mixtures were alternated between isocapnic normoxia and hypoxia (arterial partial pressur

76 contributed to the augmented VI during both isocapnic normoxia and hypoxia.

77 se to mild-to-moderate exercise in humans is isocapnic, or 'error-free'.

78 capnic level that existed prior to exercise (isocapnic post-exercise protocol, IPE).

79 n V I, VT, and TE despite wakefulness and an isocapnic state, suggesting that neural responses may ha

80 P ET , CO 2) was clamped at baseline levels (isocapnic trial) or uncontrolled.

81 In study 1, during the isocapnic trial, P ET , CO 2 was successfully clamped at

82 Compared to the isocapnic trial, the decline in mean MCAv was 15 +/- 4 c

83 unter-regulatory hormones, a 54% increase in isocapnic ventilation, and a 108% increase in the hypoxi