ライフサイエンスコーパス: hypoxaemia

1 is modified at high altitude (i.e. prolonged hypoxaemia).

2 ents with disorders that are associated with hypoxaemia.

3 ns might have on the fetal response to acute hypoxaemia.

4 the fetal cardiovascular responses to acute hypoxaemia.

5 n and all died within 20 min of the onset of hypoxaemia.

6 in femoral blood flow measured during acute hypoxaemia.

7 in-1 concentration ([ET-1]) was unaltered by hypoxaemia.

8 k ventilatory response, led to a progressive hypoxaemia.

9 ive and maladaptive processes in response to hypoxaemia.

10 lic and endocrine defence responses to acute hypoxaemia.

11 ion and the cardiovascular response to acute hypoxaemia.

12 om each group were subjected to 1 h of acute hypoxaemia.

13 of the fetal cardiovascular defence to acute hypoxaemia.

14 om each group were subjected to 1 h of acute hypoxaemia.

15 nstrictor and catecholaminergic responses to hypoxaemia.

16 d enhanced chemoreflex function during acute hypoxaemia.

17 Notably, we find that exposure to hypoxaemia 1 week after induction of myocardial infarcti

18 In fetuses subjected to acute hypoxaemia 48 h following dexamethasone treatment, femor

19 /- 4 days, a 1 h episode of acute, isocapnic hypoxaemia (9 % O(2) in N(2), to reduce carotid P(a,O2)

20 rise the effects of prevailing and sustained hypoxaemia, acidaemia or hypoglycaemia on the fetal card

21 aemia; however, the partial contributions of hypoxaemia, acidaemia or hypoglycaemia to mediating thes

22 During acute hypoxaemia all fetuses elicited hypertension, bradycardi

23 Hypoxaemia also induced hyperlactacaemia and hypocarbia

24 fetal treatment with vitamin C during acute hypoxaemia also significantly increased fetal plasma SOD

25 d flow and vascular conductance during acute hypoxaemia and (2) determine the effects of nitric oxide

26 d to a 3 h protocol: 1 h of normoxia, 1 h of hypoxaemia and 1 h of recovery during fetal I.V. infusio

27 to a 3 h experiment: 1 h of normoxia, 1 h of hypoxaemia and 1 h of recovery while on slow i.v. infusi

28 bjected to a 3 h protocol: 1 h normoxia, 1 h hypoxaemia and 1 h recovery.

29 re the primary sites of chemotransduction of hypoxaemia and acidosis in peripheral arterial chemorece

30 owth restriction (IUGR) fetuses have chronic hypoxaemia and elevated plasma catecholamine concentrati

31 apnoea in humans is reflected in progressive hypoxaemia and hypercapnia.

32 ics in neonates, and seems to reduce rebound hypoxaemia and production of toxic byproducts.

33 Treatment started 30 min before hypoxaemia and ran continuously until the end of the cha

34 Treatment started 30 min before hypoxaemia and ran continuously until the end of the cha

35 apnoea, through the effects of intermittent hypoxaemia and sleep fragmentation, could contribute ind

36 er 5 who are hospitalized for pneumonia have hypoxaemia and that around 1.5 million children with sev

37 ncentration of cortisol in response to acute hypoxaemia and to exogenous ACTH were blunted in twins r

38 modified in utero by anaemia (high flow and hypoxaemia) and that the remodelled coronary tree persis

39 l vasoconstrictor and glycaemic responses to hypoxaemia, and attenuated the increases in haemoglobin,

40 reactivated by exposure to gradual systemic hypoxaemia, and highlight the potential therapeutic role

41 Release of cellular mediators in hypoxaemia, and the relation between anaemia and oxyhaem

42 diovascular responses to an episode of acute hypoxaemia; and (2) to determine the effects of these ad

43 plasma noradrenaline and vasopressin during hypoxaemia; and (3) basal upward resetting of hypothalam

44 sults indicate that ventilatory responses to hypoxaemia are greatly attenuated in adult rats that had

45 d the vasodilatation elicited by normocapnic hypoxaemia (arterial O2 pressure, Pa,O2, approximately 2

46 e investigated the effect of acute isocapnic hypoxaemia (arterial Po2, 12.5 +/- 0.6 mmHg) on heart ra

47 rvation may protect the brain against severe hypoxaemia associated with prolonged apnoea.

48 Modulation of CBF and CVR persists during hypoxaemia but ETA receptors do not appear to contribute

49 used to alleviate pulmonary hypertension and hypoxaemia, but generates toxic free radicals and oxides

50 etal cardiovascular and metabolic defence to hypoxaemia by affecting sympathetic outflow.

51 lar and metabolic defence responses to acute hypoxaemia by affecting sympathetic outflow.

52 Patients with severe hypoxaemia can be managed with early short-term use of n

53 We tested the hypothesis that nocturnal hypoxaemia can predict CNS events better than clinical o

54 Hypoxaemia caused a rapid and sustained vasodilation, wh

55 eshi children with very severe pneumonia and hypoxaemia compared with standard low-flow oxygen therap

56 activity and, instead, it may be a result of hypoxaemia directly.

57 In marked contrast, hypoxaemia during CGRP antagonist treatment led to prono

58 In fetuses subjected to acute hypoxaemia during dexamethasone treatment, the increase

59 days later, fetuses were subjected to 0.5 h hypoxaemia during either i.v. saline or a selective CGRP

60 days later, fetuses were subjected to 0.5 h hypoxaemia during either i.v. saline or a selective CGRP

61 ess of sex, those who developed the greatest hypoxaemia during exercise demonstrated the most attenua

62 Hypoxaemia during intrauterine life may be important in

63 Hypoxaemia during saline led to significant increases in

64 k of breathing and exercise-induced arterial hypoxaemia (EIAH) can decrease O2 delivery and exacerbat

65 ing or eliminating exercise-induced arterial hypoxaemia (EIAH) during exercise decreases the severity

66 questioned whether exercise-induced arterial hypoxaemia (EIAH) occurs in healthy active women, who ha

67 Abstract Hypoxaemia elicits adrenergic suppression of fetal gluco

68 rease in carotid vascular conductance during hypoxaemia failed to reach statistical significance both

69 During hypoxaemia, fetuses treated with phentolamine did not el

70 bilical vascular conductance at the onset of hypoxaemia followed by a sustained increase in umbilical

71 tment on the fetal cardiovascular defence to hypoxaemia following nitric oxide (NO) synthase blockade

72 Two episodes of hypoxaemia (H) were induced in all animals by reducing t

73 to respond to a subsequent episode of acute hypoxaemia; however, the partial contributions of hypoxa

74 The surges in hypoxaemia, hypercapnia, and catecholamine associated wi

75 gement but anaesthetists should aim to avoid hypoxaemia, hypotension, aspiration and limit blood and

76 tal care to pre-empt or more rapidly reverse hypoxaemia, hypovolaemia, and onset of shock.

77 renaline and adrenaline were observed during hypoxaemia in both groups; however, both the increments

78 nvestigated physiological responses to acute hypoxaemia in fetal sheep during and following maternal

79 normal femoral constrictor response to acute hypoxaemia in the fetus (5.2 +/- 1.0 vs. 1.1 +/- 0.3 mmH

80 e umbilical haemodynamic defence response to hypoxaemia in the late gestation fetus.

81 hanced femoral vasoconstriction during acute hypoxaemia in the llama fetus is not mediated by stimula

82 s are indispensable to fetal survival during hypoxaemia in the llama since their abolition leads to c

83 the fetal cardiovascular responses to acute hypoxaemia in the llama were investigated.

84 nism producing a fall in RO during isocapnic hypoxaemia in the neonate.

85 Further more, hypoxaemia in the older child also occurs during the day

86 olic or endocrine defence responses to acute hypoxaemia in the twin fetus.

87 f myocardial work, tended to decrease during hypoxaemia in twins, in contrast to the increase observe

88 es in newborns following exposure to chronic hypoxaemia in utero.

89 in mice, gradual exposure to severe systemic hypoxaemia, in which inspired oxygen is gradually decrea

90 rine responses to a further episode of acute hypoxaemia, including: (1) enhanced pressor and femoral

91 Hypoxaemia increased plasma adrenaline (26-fold) and nor

92 During saline infusion, hypoxaemia induced hypertension, bradycardia, femoral va

93 In fetuses whose mothers received saline, hypoxaemia induced significant increases in fetal arteri

94 al chromaffin cells are the source for acute hypoxaemia-induced elevations in fetal plasma catecholam

95 The fetal defence to hypoxaemia involves a redistribution of blood flow away

96 The fetal defence to acute hypoxaemia involves cardiovascular and metabolic respons

97 KEY POINTS: Chronic fetal hypoxaemia is a common pregnancy complication associated

98 ABSTRACT: Chronic fetal hypoxaemia is a common pregnancy complication that may a

99 n of rCBF produced in the cerebral cortex by hypoxaemia is in large measure neurogenic, mediated tran

100 y support for severe childhood pneumonia and hypoxaemia is low-flow oxygen therapy.

101 ncrease in umbilical blood flow after 15 min hypoxaemia is predominantly pressure driven, and (3) dem

102 In contrast to other models of chronic fetal hypoxaemia, late gestation onset fetal hypoxaemia promot

103 In all fetuses, acute hypoxaemia led to a progressive increase in mean arteria

104 In saline-infused fetuses, acute hypoxaemia led to a rapid, but transient, decrement in u

105 In control fetuses, acute hypoxaemia led to transient bradycardia, femoral vasocon

106 or, and appropriate management of, nocturnal hypoxaemia might be a safe and effective alternative to

107 al cardiovascular defence responses to acute hypoxaemia, occurring either during or 48 h following th

108 Repeated acute hypoxaemia of a moderate degree over a period of 2 weeks

109 on the fetal cardiovascular defence to acute hypoxaemia of fetal treatment with the antioxidant vitam

110 esis that enhanced NO synthesis during acute hypoxaemia offsets fetal peripheral vasoconstrictor resp

111 ons for understanding the chronic impacts of hypoxaemia on exercise, and the interactions between the

112 fect of timing and duration of fetal chronic hypoxaemia on fetal lung maturation, which supports the

113 to either the physiological stress of acute hypoxaemia or to an exogenous ACTH test, and on the feta

114 h FR139317 than with vehicle infusion during hypoxaemia (P < 0.01) and recovery (P < 0.05).

115 animals were given repeated acute isocapnic hypoxaemia (Pa,O2 reduced to ca. 13 mmHg) for 1 h every

116 fetal hypoxaemia, late gestation onset fetal hypoxaemia promotes molecular regulation of fetal lung m

117 After the 1 h recovery period of the acute hypoxaemia protocol, withdrawal of the sodium nitropruss

118 xamethasone-treated fetuses during the acute hypoxaemia protocols.

119 erfusion of the umbilical circulation during hypoxaemia remain unknown.

120 During hypoxaemia, similar falls in Pa,O2 occurred in all fetus

121 ces in obstetric practice, undiagnosed fetal hypoxaemia still contributes to a high incidence of peri

122 odilation and increased nitrosylation during hypoxaemia that could not be reversed by NO scavenging.

123 diating the fetal defence responses to acute hypoxaemia that occur during dexamethasone treatment may

124 During hypoxaemia the rapid initial bradycardia, the increase i

125 amethasone, bradycardia persisted throughout hypoxaemia, the magnitude of the femoral vasoconstrictio

126 During acute hypoxaemia, the reduction in arterial partial pressure o

127 unger than 5 years with severe pneumonia and hypoxaemia to receive oxygen therapy by either bubble CP

128 /- 2 days, a 1 h episode of acute, isocapnic hypoxaemia (to reduce carotid P(O(2)) to 12 +/- 1 mmHg)

129 eripheral vasoconstrictor responses to acute hypoxaemia via actions involving the carotid chemoreflex

130 etal peripheral vasoconstrictor responses to hypoxaemia via chemoreflex and adrenomedullary actions.

131 In the HbSS group who had sleeping hypoxaemia, waking SaO2 measurements showed continuing h

132 Fetal hypoxaemia was induced during either fetal infusion with

133 the increase in umbilical blood flow during hypoxaemia was similar to that in fetuses infused with s

134 lure (pedal frequency < 70% target) arterial hypoxaemia was surreptitiously reversed via acute O2 sup

135 Temporary hypoxaemia was the most frequent non-severe complication

136 ockade of the de novo synthesis of NO during hypoxaemia while compensating for the tonic production o

137 e Wistar rats undergoing short-term systemic hypoxaemia, who received pharmacological inhibitors and

138 nfusion all llama fetuses responded to acute hypoxaemia with intense femoral vasoconstriction.

139 Twins responded to acute hypoxaemia with similar pressor and vasopressor response

140 During saline infusion, fetuses responded to hypoxaemia with transient bradycardia, femoral vasoconst

141 The increase in CBF during hypoxaemia with vehicle (P < 0.01) was absent with FR139

142 , waking SaO2 measurements showed continuing hypoxaemia, with similar correlation between SaO2 and ce

143 ing aerobic respiration by inducing systemic hypoxaemia would alleviate oxidative DNA damage, thereby