ライフサイエンスコーパス: hyperventilation

1 CO(2), 3 and 5%), and hypocapnia (voluntary hyperventilation).

2 ments decreases in cerebral perfusion during hyperventilation.

3 n but increased significantly after inducing hyperventilation.

4 rtical tissue oxygenation is impaired during hyperventilation.

5 temperature (Bt) simultaneously during acute hyperventilation.

6 s studied during apnoea caused by mechanical hyperventilation.

7 al blood pressure (BP) did not change during hyperventilation.

8 o show impaired tissue oxygenation following hyperventilation.

9 in cerebral flow velocity that occurs during hyperventilation.

10 flow velocity decreased significantly during hyperventilation.

11 Apnoea was commonly preceded by hyperventilation.

12 CO2 was a more potent stimulus to panic than hyperventilation.

13 f the response were altered significantly by hyperventilation.

14 tly enhanced for > or = 60 s after voluntary hyperventilation.

15 measured during two sequences of hypocapnic hyperventilation.

16 were available in case of hypoventilation or hyperventilation.

17 gement using dantrolene, active cooling, and hyperventilation.

18 g may play a subsidiary role in cold-induced hyperventilation.

19 .001) and better depicted regional hypo- and hyperventilation.

20 xia also provides a dose- and time-dependent hyperventilation.

21 ing lung inflation pressures and eliminating hyperventilation.

22 g of calming meditation and anxiety-inducing hyperventilation.

23 rs included head-up-tilt, head-down-tilt and hyperventilation.

24 ted the magnitude of the tachycardia and the hyperventilation.

25 avior, microcephaly, hypotonia, epilepsy and hyperventilation.

26 ction might contribute to thermally mediated hyperventilation.

27 plays a primary role in driving heat-induced hyperventilation.

28 rting its role in driving thermally mediated hyperventilation.

29 l amplitudes were significantly increased by hyperventilation.

30 period, reaching values consistent with mild hyperventilation.

31 No subject had a panic attack before hyperventilation.

32 panic disorder were studied during regulated hyperventilation.

33 d the associated breathlessness reflects the hyperventilation.

34 baseline (by 20 +/- 2 %) during post-apnoea hyperventilation.

35 overed in bronchoalveolar lavage fluid after hyperventilation.

36 inical management includes a role for modest hyperventilation.

37 rrowed (-4.1 mm Hg) despite the accompanying hyperventilation.

38 14.6 +/- 3.8 nmol; apnoea 47.1 +/- 8.5 nmol; hyperventilation 23.3 +/- 6.0 nmol, n = 14.

39 essure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation th

40 ne and estradiol than did patients with mild hyperventilation (30 < PaCO2 < or = 35) or normal ventil

41 of this study was to determine the effect of hyperventilation (40 L/min) with room air (25 degrees C;

42 ollectively, these observations suggest that hyperventilation activates pH-sensitive neurons of the i

43 t rapidly accumulates in hypoxia and induces hyperventilation, activates Olfr78 in heterologous expre

44 here was a mild but significant trend toward hyperventilation, albeit within safe clinical levels, wh

45 of a background apnoea caused by mechanical hyperventilation an average of 34 s after the onset of R

46 and sensation were assessed during eucapnic hyperventilation and abdominal compression.

47 ty in the carotid sinus nerve (CSN), causing hyperventilation and activation of the sympathoadrenal s

48 Hyperventilation and alkalization remain common therapie

49 pared with 29 previous patients treated with hyperventilation and alkalization, 13 before and 16 afte

50 In 1992, the authors prospectively abandoned hyperventilation and alkalization.

51 nd strongly suggests the negative effects of hyperventilation and alkalization.

52 rovascular reactivity to CO(2) would lead to hyperventilation and an increased ventilatory responsive

53 -dependent breathing irregularities, such as hyperventilation and apnea.

54 y low-frequency periodic alternation between hyperventilation and apnoea.

55 ls with increasing exercise intensity during hyperventilation and during hypoxic exercise (p < 0.05).

56 of impending herniation, the routine use of hyperventilation and high-dose barbiturates is no longer

57 y was to investigate the degree to which the hyperventilation and hypocapnia can induce the changes k

58 Thus, hyperventilation and hypocapnia, per se, widened the Del

59 addition, the independent outcome effect of hyperventilation and hypoventilation was assessed.

60 Both hyperventilation and hypoventilation were associated wit

61 with a 13% overlap of patients who had both hyperventilation and hypoventilation.

62 y fibers whose activation by hypoxia elicits hyperventilation and increased cardiac output.

63 t ventilator-induced lung injury by avoiding hyperventilation and lung over inflation are the strateg

64 ely with plant gain, i.e. it is widened with hyperventilation and narrowed with hypoventilation, rega

65 of the VE-PET,CO2 relationship is due to the hyperventilation and not the alkalosis; and (iii) ventil

66 that the ability of the secondary effects of hyperventilation and of the baroreceptor reflex to maint

67 equent use of vasopressors and lesser use of hyperventilation and osmotherapy, was superior to intrac

68 When breathing 12% O2, CH rats showed hyperventilation and raised haematocrit (52%) relative t

69 flex is an important determinant of exercise hyperventilation and reduced exercise tolerance.

70 ow the CO(2) reserve despite an accompanying hyperventilation and reduced plant gain.

71 with panic disorder had lower pCO(2) during hyperventilation and slower pCO(2) recovery across the p

72 haly, seizures, autism, ataxia, intermittent hyperventilation and stereotypic hand movements.

73 pressure monitoring, use of osmotic agents, hyperventilation, and computed tomography scan utilizati

74 xygenation especially in conditions of acute hyperventilation, and deeper brain regions other than th

75 first during normal ventilation, then during hyperventilation, and finally again during normal ventil

76 athophysiologic relationships among dyspnea, hyperventilation, and panic anxiety.

77 ycine (PPG) blunted or abolished the hypoxic hyperventilation, and the addition of Na2S to the water

78 st of the apnoeic response without affecting hyperventilation, and unmasked a vasopressor response.

79 er, the increases in V NO during exercise or hyperventilation are a function of high airflow rates, w

80 The physiologic results of hyperventilation are discussed.

81 colonic tone and sensation during hypocapnic hyperventilation are not caused by colonic compression.

82 These effects of hyperventilation are not mediated humorally but may resu

83 appreciation for the deleterious effects of hyperventilation as well as an attempt to increase bysta

84 The hyperventilation associated increases in extracellular g

85 1.0, 2.0, 4.0, and 8.0 ppm) during eucapnic hyperventilation at 20 L/min.

86 n of CO(2) as well as by voluntary hypo- and hyperventilation at rest and during steady-state exercis

87 Patients demonstrated hyperventilation at rest, with hypocapnia (28 +/- 3.8 mm

88 reflected a reduction in oxygenation during hyperventilation; b) Pbto2 was affected more by changes

89 Hypocapnic hyperventilation, but not eucapnic hyperventilation or a

90 The presence of prior hyperventilation, but not prior hypocapnia, caused an in

91 Mean CMRO2 was slightly increased following hyperventilation, but responses were extremely variable,

92 ated by a clinical observation of consistent hyperventilation by professional rescuers in out-of-hosp

93 either during or over a 30-min period after hyperventilation; by 60 min, Qaw had returned toward bas

94 ng subdural hematomas, even brief periods of hyperventilation can significantly increase extracellula

95 presence of prior hypocapnia, but not prior hyperventilation, caused a reduction in air-breathing PE

96 Hyperventilation challenge with warm humidified air (WAC

97 Following CO2 or hyperventilation challenges, respiratory rate dropped sh

98 decreased (P = 0.028) during 5 minutes after hyperventilation, consistent with homeostatic responses.

99 Moreover, hyperventilation consistently activated neurons within t

100 Hyperventilation consistently reduced cerebral blood flo

101 is research was to examine the prevalence of hyperventilation (defined by pCO(2) value) among acute h

102 apnoea hypoxaemic hypercapnia, and hyperoxic hyperventilation designed to ablate hypoxaemia, resultin

103 This study suggests that hyperventilation disrupts mechanisms mediating vestibula

104 eral vestibular loss in order to evaluate if hyperventilation disrupts vestibular compensation.

105 newly identified and deadly consequences of hyperventilation during CPR.

106 f HPA axis activity, self-reported fear, and hyperventilation during the period before lactate infusi

107 yperventilation era and 7 of 16 (44%) in the hyperventilation/ECMO era (p < 0.0001).

108 survived compared with 2 of 13 (15%) in the hyperventilation era and 7 of 16 (44%) in the hyperventi

109 ]) and airway reactivity (eucapnic voluntary hyperventilation [EVH] challenge).

110 s at baseline (five scans), during regulated hyperventilation (five scans), and across recovery (10 s

111 ete a CMR study with a breathing maneuver of hyperventilation followed by a voluntary apnea.

112 and breathing problems involving episodes of hyperventilation followed by apnea.

113 itation), breathing techniques (i.a., cyclic hyperventilation followed by breath retention), and expo

114 hy subjects arousal is associated with brief hyperventilation followed by more prolonged hypoventilat

115 t by having eight subjects perform isocapnic hyperventilation for 1, 2, 4, and 8 min at a constant le

116 rotid sinus nerve (CSN) activity and ensuing hyperventilation greater than expected from the prevaili

117 (61.7 4.3 kg) were randomized to 48 hours of hyperventilation (group "Hyper," n = 4); 48 hours of hyp

118 Neither type of hyperventilation had an effect on airway resistance.

119 chemoreceptors with systemic hypoxia causes hyperventilation, hypertension and tachycardia.

120 After passive hyperventilation, hypocapnia was associated with apnea i

121 spect to the following potential triggers of hyperventilation: hypoxia (sO(2) 92.5 +/- 5.2 vs 92 +/-

122 similar cerebral blood flow reductions with hyperventilation, hypoxic regions achieved significantly

123 We conclude that following 6 h of passive hyperventilation: (i) the left shift of the VE-PET,CO2 r

124 Idiopathic hyperventilation (IH) is a poorly understood condition o

125 relationship is due to alkalosis and not to hyperventilation; (ii) the increase in slope of the VE-P

126 nd hyperoxaemic hypercapnia (prior hyperoxic hyperventilation) impact free radical-mediated nitric ox

127 ic disorder demonstrate greater alkalosis to hyperventilation, implicating increased lactate as direc

128 effects predominates and, therefore, whether hyperventilation improves or impairs systemic oxygenatio

129 re basilar artery flow during rest and after hyperventilation in 16 patients with panic disorder and

130 % of cases and because of hypoventilation or hyperventilation in 9%.

131 ne and estradiol appear to contribute to the hyperventilation in cirrhotic patients.

132 local cerebral blood flow was observed with hyperventilation in five of 20 patients at 24-36 hrs (ra

133 small organ that is responsible for driving hyperventilation in hypoxia, was assessed under incremen

134 Passively induced hypocapnic hyperventilation in NREM sleep was not associated with P

135 the response of basilar artery blood flow to hyperventilation in patients with panic disorder.

136 f magnitude lower than those associated with hyperventilation in pregnant patients, the increased ven

137 Sway was also enhanced by hyperventilation in these patients, particularly in the

138 in each group], and one case of anxiety and hyperventilation [in the chromocolonoscopy group]), colo

139 ration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging-c

140 Isocapnic hyperventilation, in our animal model, did not alter art

141 Voluntary hyperventilation increased body sway in normal subjects,

142 Hyperventilation increases the volume of severely hypope

143 Hyperventilation induced a longer hypocapnia-induced apn

144 ess, SB-334867 caused a 30% reduction of the hyperventilation induced by 7% CO(2) (mean +/- S.E.M., 1

145 fluence resting blood pressure but amplifies hyperventilation-induced blood pressure elevations.

146 contribute to the development of repetitive hyperventilation-induced bronchial obstruction and hyper

147 s study was to determine if heparin inhibits hyperventilation-induced bronchoconstriction (HIB) in a

148 neurokinin (NK) receptor activity modulates hyperventilation-induced bronchoconstriction (HIB) in ca

149 Hyperventilation-induced bronchoconstriction (HIB) is a

150 Inhalation of heparin attenuates hyperventilation-induced bronchoconstriction in humans a

151 These hyperventilation-induced changes are much more common du

152 bserved kinetics support the hypothesis that hyperventilation-induced changes in ASF osmolality initi

153 d (2) NK receptor activity is stimulated via hyperventilation-induced eicosanoid production and relea

154 e development of HIB and appear to do so via hyperventilation-induced eicosanoid production and relea

155 Hyperventilation-induced hypocapnia affects hemodynamic

156 Hyperventilation-induced increases in HypoBV were appare

157 with heparin either attenuated or abolished hyperventilation-induced leukotriene, prostaglandin, and

158 The possibility that this hyperventilation-induced unsteadiness is due to interfer

159 sis that changes in airway osmolality during hyperventilation initiate peripheral airway constriction

160 Exercise-induced hyperventilation is a negative prognostic factor in CHF.

161 Isocapnic hyperventilation is a promising therapy for CO poisoning

162 However, hyperventilation is associated with changes in end-expir

163 certain whether chemosensitivity is altered, hyperventilation is maintained during exercise, and the

164 Hyperventilation is relatively frequent in AHF and is re

165 Isocapnic cold air hyperventilation (ISH) is believed to cause airway narro

166 At 24-36 hrs, hyperventilation led to a >or=10% increase in the extrac

167 high plasma cortisol levels) and evidence of hyperventilation (low PCO2 levels) in comparison with NP

168 A possible mechanism for this effect is that hyperventilation lowers arterial PCO2, raising cerebral

169 ation was reversed by using a combination of hyperventilation, mannitol and hypertonic saline.

170 The effect of 30 mins of hyperventilation (mean PaCO2, 24.6 mm Hg) on the extrace

171 towards baseline, substantively because of a hyperventilation-mediated reduction in the partial press

172 icus (n = 5), severe to profound impairment, hyperventilation (n = 3), and obstructive sleep apnea (n

173 al ventilation, n = 10) or active (voluntary hyperventilation, n = 9) profound hypocapnia.

174 e study, to simulate the clinically observed hyperventilation, nine pigs in cardiac arrest were venti

175 domain are neither sufficient to prevent the hyperventilation nor abnormal hypoxic ventilatory respon

176 reases were not significantly greater during hyperventilation, nor was pH return to baseline slowed d

177 tion status was more evenly distributed with hyperventilation observed in 38%, normoventilation in 29

178 antagonist DPCPX did not affect the resting hyperventilation of 1-7CH rats breathing 12% O2 and incr

179 Mechanical hyperventilation of acidemic patients with acute lung in

180 glycosylation of the diaphragm; and (2) the hyperventilation of DKA is leptin dependent.

181 including bronchoprovocations with isocapnic hyperventilation of frigid air, methacholine and/or exer

182 SR(aw) increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patie

183 In contrast, hyperventilation of HA did not cause cough and increased

184 Hyperventilation of hot humid air induces transient bron

185 determine the airway responses to isocapnic hyperventilation of humidified air at hot (49 degrees C;

186 Criteria postulated to document hyperventilation of the pulmonary blood flow due to a ri

187 canine model of EIA to examine the effect of hyperventilation on airway surface fluid (ASF) volume an

188 r, it is important to quantify the effect of hyperventilation on brain tissue PO(2) and cerebrovenous

189 were to determine the effects of hypocapnic hyperventilation on colonic motility and sensation in he

190 We studied the effects of isocapnic hyperventilation on five adult mechanically ventilated s

191 (i) The effect of hyperventilation on peripheral compound sensory action p

192 The effect of hyperventilation on postural balance was investigated.

193 s the potential negative role of inadvertent hyperventilation on survival outcome.

194 lectrophysiology and examined the effects of hyperventilation on the amplitude of the cortical somato

195 six normal subjects to assess the effect of hyperventilation on the vestibulo-ocular reflex and its

196 c reflex was recorded to study the effect of hyperventilation on vestibulo-spinal activity.

197 ypocapnic hyperventilation, but not eucapnic hyperventilation or abdominal compression, significantly

198 chemoreflex gain and delay time (rather than hyperventilation or hypocapnia) as causes of PB.

199 ny of the conditions investigated (exercise, hyperventilation, or hypoxia).

200 micromol/L, with no change during exercise, hyperventilation, or hypoxia.

201 icantly greater than that for bradycardia or hyperventilation (P < 0.05).

202 Patients with severe hyperventilation (PaCO2 < or = 30 mm Hg) had statistical

203 A transient hyperventilation (PET,CO2 -7 +/- 1 mmHg vs. baseline) oc

204 On the other hand, after 60 mins of hyperventilation, Pico2 - Paco2 increased to 37.9+/-3.6

205 iological responses to high altitude include hyperventilation, polycythemia, hypoxic pulmonary vasoco

206 RTN inhibition probably limits the degree of hyperventilation produced by hypocapnic hypoxia.

207 The 1, 3 and 7CH rats showed resting hyperventilation relative to N rats, but baseline heart

208 Hyperventilation reliably provokes seizures in patients

209 reduction and increase in CMRO2 secondary to hyperventilation represent physiologic challenges to the

210 n persisted in 7 cases (3 and 6 after active hyperventilation, respectively).

211 Hyperventilation resulted in increases in cerebral perfu

212 Hyperventilation resulted in significant decreases in ar

213 Hyperventilation seems to spare vestibular reflex activi

214 d with 5% and 7% CO2 inhalation and room air hyperventilation separated by room air breathing with co

215 However, despite these beneficial effects, hyperventilation shifted the cerebral blood flow distrib

216 After BSCC, normal ventilation rather than hyperventilation should be used to improve systemic oxyg

217 The greater basilar artery sensitivity to hyperventilation shown by panic disorder patients sugges

218 Hyperventilation significantly impairs systemic oxygenat

219 Despite their resting hyperventilation, SS (Kcnj16-/-) rats showed up to 45% r

220 overy in subjects with panic disorder during hyperventilation suggested altered acid-base regulation.

221 atory disorders including Congenital Central Hyperventilation Syndrome (CCHS), Sudden Infant Death Sy

222 thing manoeuvres: 5% and 8% CO(2) in air and hyperventilation targeting reductions of 5 and 10 mmHg c

223 (EIB) was assessed by the eucapnic voluntary hyperventilation test.

224 everal mechanisms: the anxiogenic effects of hyperventilation, the catastrophic misinterpretation of

225 unction, repeated episodes of hypercapnia or hyperventilation, the use of anxiogenic medications, and

226 During hyperventilation, the volume of NO rose in both groups.

227 panic disorder had greater hypocapnea during hyperventilation, their observed pH response, not altere

228 ease in the proportion who used prophylactic hyperventilation therapy (83% vs. 36%) and steroids (64%

229 perfusion pressure was kept at >50 mm Hg and hyperventilation to a PaCO2 of 25-30 torr (3.33-4.00 kPa

230 Although hyperventilation to a Paco2 of 26 to 30 torr (3.5 to 4.0

231 esponse): condition III, volitionally driven hyperventilation to match that achieved in condition II

232 patient response, the mechanisms that enable hyperventilation to powerfully activate absence seizure-

233 percapnia, and during recovery from moderate hyperventilation (to simulate changes leading to respira

234 Hyperventilation trials were done 24-36 hrs after injury

235 were measured before and for 4 hrs after the hyperventilation trials.

236 Isocapnic hyperventilation utilizing mechanical ventilation may de

237 e (30%, 60%, and 90% V O2max), two levels of hyperventilation (V E = 42.8 +/- 9.1 L/min and 84.2 +/-

238 peak VO(2), P<0.05), and pronounced exercise hyperventilation (VE/VCO(2), P<0.01).

239 Hyperventilation was maintained during exercise, at the

240 Hyperventilation was observed in only six of 14 C57BL/6J

241 st-apnoea decrease in CFV did not occur when hyperventilation was prevented.

242 Hyperventilation was sustained during exercise, despite

243 d neuronal activation and breathing; hypoxic hyperventilation was unchanged.

244 y might contribute to heat- and cold-induced hyperventilation, we indirectly measured carotid body to

245 apeutic response with caffeine, ketamine, or hyperventilation were used in 14 of the 24 patients, and

246 heparin inhibits the late-phase response to hyperventilation, which is characterized by increased pe

247 Hyperventilation, which is standard therapy for postoper

248 eripheral SAP amplitude were observed during hyperventilation, which reversed during the recovery per

249 nses to hypocapnia were studied by voluntary hyperventilation with (P(ET,O2)) clamped at 100 and 50 m

250 pocapnia (PET(CO(2)) = 35 mm Hg, induced via hyperventilation with an iron lung ventilator); (4) hypo

251 idence of asthma, suggesting that repetitive hyperventilation with cold air may predispose individual

252 irways responsiveness (elicited via eucapnic hyperventilation with cold air or methacholine challenge

253 hyperpnea to examine the effects of repeated hyperventilation with cool, dry air (i.e., dry air chall

254 id mediator production and release caused by hyperventilation with dry air, and significantly attenua

255 In contrast, eucapnic hyperventilation with frigid air (thermal stress, 720 ca

256 nd 13 asthmatic subjects performed isocapnic hyperventilation with frigid air while the fractional co

257 , Qaw increases during and/or after eucapnic hyperventilation with frigid air, and that this response

258 Hyperventilation with mixtures of O2 and CO2 has long be

259 ange significantly during and after eucapnic hyperventilation with room air (thermal stress, 224 cal/

260 e healthy volunteers: (1) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (PET,CO2)

261 low the eupnoeic value; (2) passive eucapnic hyperventilation, with PET,CO2 maintained eucapnic; (3)