ライフサイエンスコーパス: hypoxaemia

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

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

3 nstrictor and catecholaminergic responses to hypoxaemia.

4 d enhanced chemoreflex function during acute hypoxaemia.

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

6 the fetal cardiovascular responses to acute hypoxaemia.

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

8 in femoral blood flow measured during acute hypoxaemia.

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

10 k ventilatory response, led to a progressive hypoxaemia.

11 with hypoxic cerebral vasodilatation during hypoxaemia.

12 flow, highlighting a key catalytic role for hypoxaemia.

13 ve stress, a consequence of the magnitude of hypoxaemia.

14 xygenation (V-A ECMO) and can cause cerebral hypoxaemia.

15 ntanyl becomes more lethal in the context of hypoxaemia.

16 e total ventilatory response to steady-state hypoxaemia.

17 .11-5.69) times higher odds of death than no hypoxaemia.

18 pathways controlling FHRV during labour-like hypoxaemia.

19 y associated with the individual severity of hypoxaemia.

20 me was mortality within 48 h of detection of hypoxaemia.

21 f which occurred within 48 h of detection of hypoxaemia.

22 ponses in critical illnesses associated with hypoxaemia.

23 in clinical decisions of diseases related to hypoxaemia.

24 eater OSA-related heart rate acceleration or hypoxaemia.

25 uirements despite significant improvement in hypoxaemia.

26 ents with disorders that are associated with hypoxaemia.

27 ive and maladaptive processes in response to hypoxaemia.

28 lic and endocrine defence responses to acute hypoxaemia.

29 ion and the cardiovascular response to acute hypoxaemia.

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

31 of the fetal cardiovascular defence to acute hypoxaemia.

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

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

34 /- 4 days, a 1 h episode of acute, isocapnic hypoxaemia (9 % O(2) in N(2), to reduce carotid P(a,O2)

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

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

37 Children with hypoxaemia admitted to wards meeting minimum standards f

38 During acute hypoxaemia all fetuses elicited hypertension, bradycardi

39 Hypoxaemia also induced hyperlactacaemia and hypocarbia

40 nic input from the CB, reveals that extra-CB hypoxaemia also provides dose-dependent ventilatory stim

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

42 The pooled prevalence of hypoxaemia among admitted patients was 24.5% (95% CI 19.

43 The high prevalence of hypoxaemia among children with severe pneumonia, particu

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

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

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

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

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

49 cantly reduces the incidence and severity of hypoxaemia and decreases the need for airway rescue inte

50 rlie variation in the presentation of silent hypoxaemia and define priorities for subsequent investig

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

52 ugh the role of pulse oximeters in detecting hypoxaemia and guiding oxygen therapy is widely recognis

53 of burial, an avalanche victim is exposed to hypoxaemia and hypercapnia, which have important effects

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

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

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

57 unger than 5 years admitted to hospital with hypoxaemia and respiratory signs were included.

58 nths who presented with severe pneumonia and hypoxaemia and six hospitals to standard low-flow oxygen

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

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

61 te onset of noncardiogenic pulmonary oedema, hypoxaemia and the need for mechanical ventilation.

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

63 nder five years of age" AND "pneumonia" AND "hypoxaemia" AND "low- and middle-income countries" by se

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

65 d peripheral perfusion and peripheral tissue hypoxaemia, and (iii) pressurized calcified arteries pre

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

67 Age, severity of hypoxaemia, and duration and intensity of mechanical ven

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

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

70 ly suppressed between periods of labour-like hypoxaemia, and thus, that the parasympathetic system is

71 on admission, documented oxygen therapy for hypoxaemia, and whether minimum standards for availabili

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

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

74 Early detection and treatment of hypoxaemia are critical, but there are few data to quant

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

76 Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidn

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

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

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

80 function and exercise capacity under chronic hypoxaemia at high altitude.

81 es the importance of rapid identification of hypoxaemia at the first point of contact and referral fo

82 critical, but there are few data to quantify hypoxaemia burden outside the child pneumonia population

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

84 on of oxygen can rescue patients from severe hypoxaemia, but at the risk of microvascular obstruction

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

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

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

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

89 Differential hypoxaemia can lead to cerebral damage after only a few

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

91 Hypoxaemia caused a rapid and sustained vasodilation, wh

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

93 tality in children with severe pneumonia and hypoxaemia compared with use of standard low-flow oxygen

94 fection or exposure, severe malnutrition, or hypoxaemia despite antibiotics and oxygen.

95 multicomponent health-system intervention on hypoxaemia detection, oxygen therapy, and mortality amon

96 Differential hypoxaemia (DH) is common in patients supported by femor

97 gen, patients with exercise-induced arterial hypoxaemia did not have an augmented haemodynamic respon

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

99 ation that result in moderate (but not mild) hypoxaemia do not elicit increased inspiratory output, s

100 l chest radiographical opacities with severe hypoxaemia due to non-cardiogenic pulmonary oedema.

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

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

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

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

105 Hypoxaemia during intrauterine life may be important in

106 This indicates that the impacts of hypoxaemia during opioid-induced respiratory depression

107 Hypoxaemia during saline led to significant increases in

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

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

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

111 trated evidence of exercise-induced arterial hypoxaemia (EIAH).

112 Abstract Hypoxaemia elicits adrenergic suppression of fetal gluco

113 Using MRI, this study quantifies the chronic hypoxaemia experienced by growth-restricted fetuses due

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

115 During hypoxaemia, fetuses treated with phentolamine did not el

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

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

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

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

120 UCO caused a rapid onset of fetal hypoxaemia, hypercapnia, and acidosis; however, by 6 h,

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

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

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

124 ted risk of death for children with moderate hypoxaemia (ie, peripheral oxygen saturations [SpO(2)] 9

125 ygen saturations [SpO(2)] 90-93%) and severe hypoxaemia (ie, SpO(2) <90%).

126 sonable agreement with the WHO definition of hypoxaemia in all regions except for Peru (the highest a

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

128 ospital admission rates of ALRI or ALRI with hypoxaemia in children with laboratory-confirmed hPIV; p

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

130 herapy in children with severe pneumonia and hypoxaemia in general hospitals in Ethiopia.

131 ent in alertness or sleepiness, or overnight hypoxaemia in OSA.

132 und a high proportion of false positives for hypoxaemia in Peru (11.6%, 95% CI 7.0-14.7).

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

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

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

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

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

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

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

140 We suggest that moderate hypoxaemia in the primary care setting should prompt car

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

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

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

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

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

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

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

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

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

150 st that a physiological continuum exists for hypoxaemia-induced OXINOS in HA dwellers that when exces

151 st that a physiological continuum exists for hypoxaemia-induced systemic OXINOS in HA dwellers that w

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

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

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

155 Chronic fetal hypoxaemia is a common pregnancy complication that incre

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

157 Hypoxaemia is common across all age groups and a range o

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

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

160 High altitude-induced hypoxaemia is often associated with peripheral vascular

161 Hypoxaemia is one of the strongest predictors of these d

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

163 of upper airway obstruction and intermittent hypoxaemia, is prevalent in patients with cardiovascular

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

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

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

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

168 Hypoxaemia (low oxygen saturation in blood) is a key pre

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

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

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

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

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

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

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

176 Given the effects of hypoxaemia on pulmonary vasoconstriction, cardiorespirat

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

178 WHO cutoffs for fast breathing and hypoxaemia overlap with RR and SpO(2) values that are no

179 In swine with profound hypoxaemia owing to acute and temporary (12 min) upper-a

180 lure, ICU admission, intubation/ventilation, hypoxaemia, oxygen requirement, hypercoagulopathy/venous

181 Of patients with hypoxaemia, oxygen therapy was documented for 88% (79-97

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

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

184 The primary outcome was incidence of hypoxaemia (peripheral oxygen saturation (SpO(2)) <=90%)

185 n either group at rest or during exaggerated hypoxaemia ( PIO2 = 67 mmHg).

186 We present an updated estimate of hypoxaemia prevalence among children with pneumonia in l

187 us, and Google Scholar for studies reporting hypoxaemia prevalence among patients attending health fa

188 excluded protocol papers, articles reporting hypoxaemia prevalence based on less than 100 pneumonia c

189 We aimed to estimate hypoxaemia prevalence for adults and children with acute

190 Hypoxaemia prevalence was highest in neonatal and primar

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

192 Chronic fetal hypoxaemia promotes oxidative stress, and maternal antio

193 In turn, chronic fetal hypoxaemia promotes oxidative stress, and maternal antio

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

195 xamethasone-treated fetuses during the acute hypoxaemia protocols.

196 re associated with the magnitude of arterial hypoxaemia (R(2) = 0.60, P = 0.008 and R(2) = 0.63, P =

197 erfusion of the umbilical circulation during hypoxaemia remain unknown.

198 yperoxic hyperventilation designed to ablate hypoxaemia, resulting in hyperoxaemic hypercapnia.

199 r exercise-induced lung congestion, arterial hypoxaemia, RV-PA uncoupling, ventricular interdependenc

200 Based on hypoxaemia severity at PARDS diagnosis, mortality was si

201 d elements of PARDS (ie, PARDS risk factors, hypoxaemia severity metrics, type of ventilation), comor

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

203 We reported pooled prevalence of hypoxaemia (SpO(2) <90%) by classification of clinical s

204 ay rescue interventions, incidence of severe hypoxaemia (SpO(2) <=85%), lowest oxygen saturation reco

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

206 t high altitude (HA) characterised by severe hypoxaemia that carries a higher risk of stroke and migr

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

208 Acute respiratory failure can cause profound hypoxaemia that leads to organ injury or death within mi

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

210 During hypoxaemia the rapid initial bradycardia, the increase i

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

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

213 xic ventilatory response and greater resting hypoxaemia, they had similar hypoxic pulmonary vasoconst

214 RR and SpO(2) thresholds for tachypnoea and hypoxaemia to determine agreement.

215 in human COPD to target prolonged, nocturnal hypoxaemia to prevent sarcopenia in these patients.

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

217 /- 2 days, a 1 h episode of acute, isocapnic hypoxaemia (to reduce carotid P(O(2)) to 12 +/- 1 mmHg)

218 We reported pooled prevalence of hypoxaemia (typically defined as SpO(2) <90%) overall an

219 1; P<0.001), had a lower incidence of severe hypoxaemia v 4.8%; adjusted risk ratio 0.16, 0.07 to 0.3

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

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

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

223 The prevalence of hypoxaemia was 31% (95% CI 26-36; 101 775 children) amon

224 Hypoxaemia was associated with 4.84 (95% CI 4.11-5.69) t

225 Fetal hypoxaemia was induced during either fetal infusion with

226 The incidence of hypoxaemia was significantly lower in the lateral group

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

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

229 Temporary hypoxaemia was the most frequent non-severe complication

230 Nocturnal hypoxaemia, which is common in chronic obstructive pulmo

231 incidence (42%) of exercise-induced arterial hypoxaemia, which is likely to be a consequence of hypov

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

233 Among non-critically ill patients with hypoxaemia who were admitted to hospital with covid-19,

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

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

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

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

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

239 ted EVALI in our cohort had life-threatening hypoxaemia, with 67% requiring management in the intensi

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

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