ライフサイエンスコーパス: hyperventilation

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

2 n but increased significantly after inducing hyperventilation.

3 rtical tissue oxygenation is impaired during hyperventilation.

4 temperature (Bt) simultaneously during acute hyperventilation.

5 s studied during apnoea caused by mechanical hyperventilation.

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

7 o show impaired tissue oxygenation following hyperventilation.

8 were available in case of hypoventilation or hyperventilation.

9 ing lung inflation pressures and eliminating hyperventilation.

10 in cerebral flow velocity that occurs during hyperventilation.

11 flow velocity decreased significantly during hyperventilation.

12 Apnoea was commonly preceded by hyperventilation.

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

14 f the response were altered significantly by hyperventilation.

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

16 measured during two sequences of hypocapnic hyperventilation.

17 l amplitudes were significantly increased by hyperventilation.

18 No subject had a panic attack before hyperventilation.

19 panic disorder were studied during regulated hyperventilation.

20 d the associated breathlessness reflects the hyperventilation.

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

22 overed in bronchoalveolar lavage fluid after hyperventilation.

23 inical management includes a role for modest hyperventilation.

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

25 14.6 +/- 3.8 nmol; apnoea 47.1 +/- 8.5 nmol; hyperventilation 23.3 +/- 6.0 nmol, n = 14.

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

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

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

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

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

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

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

33 Hyperventilation and alkalization remain common therapie

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

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

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

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

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

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

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

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

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

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

44 Both hyperventilation and hypoventilation were associated wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 The physiologic results of hyperventilation are discussed.

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

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

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

67 The hyperventilation associated increases in extracellular g

68 1.0, 2.0, 4.0, and 8.0 ppm) during eucapnic hyperventilation at 20 L/min.

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

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

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

72 Hypocapnic hyperventilation, but not eucapnic hyperventilation or a

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

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

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

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

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

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

79 Hyperventilation challenge with warm humidified air (WAC

80 Following CO2 or hyperventilation challenges, respiratory rate dropped sh

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

82 Hyperventilation consistently reduced cerebral blood flo

83 This study suggests that hyperventilation disrupts mechanisms mediating vestibula

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

85 newly identified and deadly consequences of hyperventilation during CPR.

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

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

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

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

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

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

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

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

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

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

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

97 After passive hyperventilation, hypocapnia was associated with apnea i

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

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

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

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

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

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

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

105 % of cases and because of hypoventilation or hyperventilation in 9%.

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

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

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

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

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

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

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

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

114 Voluntary hyperventilation increased body sway in normal subjects,

115 Hyperventilation increases the volume of severely hypope

116 Hyperventilation induced a longer hypocapnia-induced apn

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

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

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

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

121 Hyperventilation-induced bronchoconstriction (HIB) is a

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

123 These hyperventilation-induced changes are much more common du

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

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

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

127 Hyperventilation-induced hypocapnia affects hemodynamic

128 Hyperventilation-induced increases in HypoBV were appare

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

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

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

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

133 Isocapnic hyperventilation is a promising therapy for CO poisoning

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 Mechanical hyperventilation of acidemic patients with acute lung in

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

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

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

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

154 Hyperventilation of hot humid air induces transient bron

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

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

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

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

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

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

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

162 The effect of hyperventilation on postural balance was investigated.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 Hyperventilation resulted in increases in cerebral perfu

181 Hyperventilation resulted in significant decreases in ar

182 Hyperventilation seems to spare vestibular reflex activi

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

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

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

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

187 Hyperventilation significantly impairs systemic oxygenat

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

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

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

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

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

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

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

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

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

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

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

199 Hyperventilation trials were done 24-36 hrs after injury

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

201 Isocapnic hyperventilation utilizing mechanical ventilation may de

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

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

204 Hyperventilation was maintained during exercise, at the

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

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

207 Hyperventilation was sustained during exercise, despite

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

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

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

211 Hyperventilation, which is standard therapy for postoper

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

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

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

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

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

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

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

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

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

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

222 Hyperventilation with mixtures of O2 and CO2 has long be

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

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

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