ライフサイエンスコーパス: hypercapnic

1 ir breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake you

2 O(2) in N(2)), hypoxic (10% O(2)in N(2)) and hypercapnic (5% CO(2) in O(2))air.

3 Hyperoxic (100% O(2)) and hypercapnic (5% CO(2), 21% O(2), balance N(2)) challenge

4 odilatation in these regions to a subsequent hypercapnic (5% CO2 ) challenge.

5 air as well as acute hypoxic (10% O(2)) and hypercapnic (6% CO(2)) conditions, we describe breathing

6 Hypoxic (10% O(2)/5% CO(2)/85% N(2)) and hypercapnic (7% CO(2)/93% O(2)) stimuli were delivered t

7 pocapnic (2% CO2), normocapnic (5% CO2), and hypercapnic (7% CO2) conditions, with and without endoto

8 3.44 1.05% per mmHg PaCO2 ; P = 0.499), nor hypercapnic (7.45 1.85 vs. 6.37 2.23% per mmHg PaCO2 ; P

9 Hypercapnic acidosis (15 % CO(2), pH(o) 6.8) resulted in

10 n, can be associated with the development of hypercapnic acidosis (HCA).

11 -reperfusion group (FICO(2), 5%; n = 6), and hypercapnic acidosis (ischemia-reperfusion + hypercapnic

12 Hypercapnic acidosis (P(CO2) 9 %; pH(o) 7.17) induced an

13 (Pa(CO(2)) approximately 40 mm Hg; n = 6) or hypercapnic acidosis (Pa(CO(2)) 80-100 mm Hg; n = 6).

14 s, and found that their response to moderate hypercapnic acidosis (pH 7.4 to ~7.2) was markedly reduc

15 ount (to 384 % of control) as in response to hypercapnic acidosis (to 327 % of control).

16 Hypercapnic acidosis activated an inward rectifier curre

17 s are consistent with a protective effect of hypercapnic acidosis against ventilator-associated lung

18 Significant improvement in hypercapnic acidosis along with reduction in ventilation

19 Hypercapnic acidosis also directly reduced DNA binding o

20 Neurones with no response to hypercapnic acidosis also had no response to isocapnic a

21 suggest a dose-response association between hypercapnic acidosis and 28-day mortality in the 12 mL/k

22 Hypercapnic acidosis and IkappaBalpha-SuperRepressor tra

23 Diverse effects of hypercapnic acidosis are mediated via inhibition of nucl

24 Hypercapnic acidosis attenuated moderate and severe vent

25 Hypercapnic acidosis attenuated ventilation-induced lung

26 ase ADAM17, suggesting stretch activates and hypercapnic acidosis blocks stretch-mediated activation

27 Consistent with previous reports that hypercapnic acidosis can suppress mammalian NF-kappaB-re

28 ith a beta-blocker, esmolol, during a severe hypercapnic acidosis challenge.

29 I) for 28-day mortality rate associated with hypercapnic acidosis defined as day 1 pH <7.35 and Pa(CO

30 Hypercapnic acidosis during the first 24 hours of intens

31 Patients with compensated hypercapnia and hypercapnic acidosis had higher Acute Physiology and Chr

32 fects of and the signal pathway regulated by hypercapnic acidosis in ischemia-reperfusion-induced lun

33 ss the impact of compensated hypercapnia and hypercapnic acidosis in patients receiving mechanical ve

34 es evaluating the effects of hypercapnia and hypercapnic acidosis in patients requiring mechanical ve

35 determine whether the beneficial effects of hypercapnic acidosis in reducing stretch-induced injury

36 ve effect on the LV systolic function during hypercapnic acidosis in situ.

37 Hypercapnic acidosis induces mitochondrial dysfunction a

38 Hypercapnic acidosis inhibited canonical nuclear factor-

39 We tested the hypothesis that hypercapnic acidosis is associated with reduced mortalit

40 We conclude that hypercapnic acidosis is protective against VILI in this

41 Hypercapnic acidosis may attenuate lung ischemia-reperfu

42 e of this study was to assess the effects of hypercapnic acidosis on lung cell injury and repair by c

43 f this study was to establish the effects of hypercapnic acidosis on mitogen-activated protein kinase

44 uent in vitro studies examined the effect of hypercapnic acidosis on specific nuclear factor-kappaB c

45 We aim to examine the effect of hypercapnic acidosis on the nuclear factor-kappaB pathwa

46 The effect of hypercapnic acidosis on the p50/p65 nuclear factor-kappa

47 , but the underlying mechanisms of action of hypercapnic acidosis on this pathway is unclear.

48 s ratio for hospital mortality was higher in hypercapnic acidosis patients (odds ratio, 1.74; 95% CI,

49 The mortality was higher in hypercapnic acidosis patients when compared with other g

50 Hypercapnic acidosis protects against ventilation-induce

51 To investigate whether hypercapnic acidosis protects against ventilator-induced

52 Hypercapnic acidosis reduced cyclic mechanical stretch-i

53 Hypercapnic acidosis reduced E. coli inflammation and lu

54 Hypercapnic acidosis reduced indices of inflammation suc

55 Hypercapnic acidosis reduced the decrement of the nuclea

56 ingly being deployed for severe hypoxemia or hypercapnic acidosis refractory to conventional ventilat

57 Our results also showed that hypercapnic acidosis significantly inhibited the ischemi

58 Other definitions of hypercapnic acidosis spanning a range of magnitudes sugg

59 arate experimental series, the potential for hypercapnic acidosis to attenuate moderate and severe ve

60 vitro experiments examined the potential for hypercapnic acidosis to reduce pulmonary epithelial infl

61 normally augments ventilation in response to hypercapnic acidosis to restore normal pH and PCO2Tac1-P

62 uction in the ventilatory response to graded hypercapnic acidosis vs. controls.

63 Hypercapnic acidosis was associated with reduced 28-day

64 nsitivity in these neurones, the response to hypercapnic acidosis was quantified and compared with th

65 None of our definitions of hypercapnic acidosis were associated with reduction in 2

66 e independent association of hypercapnia and hypercapnic acidosis with hospital mortality.

67 3.63, 95% CI 1.36-9.67; p value = 0.01) and hypercapnic acidosis x TTI 10.4 min (OR: 2.27, 95% CI 1.

68 normal pH with elevated carbon dioxide], and hypercapnic acidosis) during the first 24 hours of ICU s

69 hypercapnic acidosis (ischemia-reperfusion + hypercapnic acidosis) group (FICO(2), 10%; n = 6).

70 10,104; compensated hypercapnia, 20,463; and hypercapnic acidosis, 122,245) were included in analysis

71 mechanical ventilation under normocapnia or hypercapnic acidosis, and nuclear factor-kappaB activati

72 Hypercapnic acidosis, common in mechanically ventilated

73 To experimentally induce severe hypercapnic acidosis, mice were exposed to a 40% CO(2) c

74 In patients with hypercapnic acidosis, the mortality increased with incre

75 ATP isoform(s) and elucidate its response to hypercapnic acidosis, we performed these studies on vasc

76 role of the nuclear factor-kappaB pathway in hypercapnic acidosis-mediated protection from stretch in

77 r in the regulation of vascular tones during hypercapnic acidosis.

78 c hypercapnia in the same way as they did to hypercapnic acidosis.

79 her reduction in the ventilatory response to hypercapnic acidosis.

80 have a significant effect on the response to hypercapnic acidosis.

81 firing rate by more than 20% in response to hypercapnic acidosis.

82 ective ventilation can cause hypercapnia and hypercapnic acidosis.

83 randomized to (normocapnia; FICO2 0.00) or (hypercapnic acidosis; FICO2 0.05), subjected to high str

84 mask to total face mask included refractory hypercapnic acute respiratory failure (n = 24, 66.7%), p

85 tertiary referral thoracic center for severe hypercapnic acute respiratory failure and persistent bil

86 tertiary referral thoracic center for severe hypercapnic acute respiratory failure and persistent bil

87 In patients in hypercapnic acute respiratory failure, for whom escalati

88 nt process and that the released uPA impairs hypercapnic and hypotensive dilation through an LRP- and

89 ecorded under baseline conditions and during hypercapnic and hypoxic challenge in C(2) hemisected, no

90 tio < 70%), 9 also classified as chronically hypercapnic, and 9 age- and gender-matched controls.

91 cterized by repeated occurrences of hypoxic, hypercapnic, and transient blood pressure elevation epis

92 rges occurred only during eucapnic anoxia or hypercapnic anoxia.

93 a similar trend was noted for patients with hypercapnic ARF (5.41 intubations versus 18.52 intubatio

94 tly in response to apnea during hyperoxic or hypercapnic baseline conditions with both anesthetics.

95 We used a hypercapnic breath-holding task to evoke a systemic vaso

96 subsequent response to acute hypoxia during hypercapnic breathing (targeted end-tidal partial pressu

97 A subset study with mild and severe hypercapnic breathing at the same level of hypoxia sugge

98 olism was determined using varying levels of hypercapnic breathing, against the background of similar

99 Hypercapnic buffer (pH 6.9) for the first 2 minutes of r

100 Exposing conscious rats to such hypercapnic, but not atmospheric air, resulted in respir

101 ed as the percent increase of normocapnic to hypercapnic CBF normalized by the change in end-tidal ca

102 Although diminished global hypercapnic CBF reactivity (P < .02) was suggestive of a

103 e studies does not define its normal role in hypercapnic cerebral vasodilation, but rather is a uniqu

104 The use of a hypercapnic challenge (5% CO2 ) confirmed that these red

105 y, was attenuated during quiet breathing and hypercapnic challenge in Gaa(-/-) mice (6 to >21 months

106 blood oxygen level-dependent MRI response to hypercapnic challenge in normal-appearing white matter f

107 hat prostaglandin E2 (PGE2), released during hypercapnic challenge, increases calcium oscillations in

108 sia or by transient global vasodilation in a hypercapnic challenge.

109 minute ventilation (V E) at rest and during hypercapnic challenges, as well as peak oxygen consumpti

110 athing in air and in response to hypoxic and hypercapnic challenges.

111 ontribute, via OX(1)Rs in the region, to the hypercapnic chemoreflex control during wakefulness and t

112 Hypoxic and hypercapnic chemosensitivity (n=38), heart rate variabil

113 ar resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing bloo

114 heral plant decreased, especially during the hypercapnic condition (-4.1 +/- 0.8 to -2.0 +/- 0.2 mmHg

115 i-inflammatory cytokine interleukin-10 under hypercapnic condition were significantly decreased (p <

116 rleukin-6 were significantly decreased under hypercapnic condition when compared with hypocapnic cond

117 l pH from 7.4 to 7.0 in both normocapnic and hypercapnic conditions decreased Ca(2+) wave activity, a

118 during NREM sleep (p < 0.001); isocapnic and hypercapnic conditions did not differ (p = 0.95).

119 Groups exposed to hypercapnic conditions without LPS did not manifest thes

120 yte production of NO under hypo-, normo- and hypercapnic conditions.

121 f trachea displacement under either hypo- or hypercapnic conditions.

122 urements were made in normoxic, hypoxic, and hypercapnic conditions.

123 he indirect pathway operates under normo- or hypercapnic conditions; under respiratory alkalosis (e.g

124 usual care for patients with chronic stable hypercapnic COPD (conditional recommendation, moderate c

125 2 in reducing NIV failure (25-15%) in severe hypercapnic COPD exacerbations.

126 normalization of Pa(CO(2)) in patients with hypercapnic COPD on long-term NIV (conditional recommend

127 we suggest that patients with chronic stable hypercapnic COPD undergo screening for obstructive sleep

128 titrate NIV in patients with chronic stable hypercapnic COPD who are initiating NIV (conditional rec

129 ve hypocapnic CVR was higher (P = 0.019) and hypercapnic CVR was lower (P = 0.025) following NaHCO(3)

130 es head-down tilt bed rest (HDTBR) in a mild hypercapnic environment ( PCO2 = ~4 mmHg), we investigat

131 Our data suggest that the mild hypercapnic environment does not contribute to the devel

132 ile a (supra-)optimal brain perfusion during hypercapnic exercise coincides with a suppressed sympath

133 The VA(BF) and posterior CDO2 responses to hypercapnic exercise were not different from the summate

134 and sympathetic discharge constrained during hypercapnic exercise.

135 The number of NTS and AP neurons with FOS in hypercapnic-exposed animals was significantly greater th

136 stigation was performed to determine whether hypercapnic exposure elicited expression of the c-fos pr

137 of ventilation in air and during hypoxia and hypercapnic exposures.

138 the ventilatory responses during and after a hypercapnic gas challenge (HCC, 5% CO(2), 21% O(2), 74%

139 or antagonist (30 mg/kg SB334867) attenuated hypercapnic gas-induced pressor and anxiety responses, w

140 Two groups of animals were studied: a hypercapnic group (n = 10) and a normocapnic control gro

141 Cardiac function, hypercapnic (HCVR) and hypoxic (HVR) ventilatory respons

142 TN neurons expressed c-Fos after exposure to hypercapnic hyperoxia (6-7% end-tidal CO(2); 3.5 h; no h

143 (100% oxygen), two levels of mild and severe hypercapnic hyperoxia (inspired Pco2 of 30 and 60 torr;

144 in breathing cycles, each comprising 40 s of hypercapnic hypoxia ( PETCO2 : +4 +/- 3 mmHg above basel

145 erwent 40 consecutive 1 min bouts of 40 s of hypercapnic hypoxia ( PETO2 : 48 mmHg; PETCO2 : +5 mmHg)

146 Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations

147 Acute intermittent hypercapnic hypoxia (IHH) evokes persistent increases in

148 that recurring cycles of acute intermittent hypercapnic hypoxia characteristic of obstructive sleep

149 Acute intermittent hypercapnic hypoxia evokes persistent sympathoexcitation

150 blood pressure following acute intermittent hypercapnic hypoxia in men.

151 lity manifest acutely following intermittent hypercapnic hypoxia is unknown.

152 However, we show that, during hypercapnic hypoxia, a population of rVRC expiratory-aug

153 ve hypovolaemia following acute intermittent hypercapnic hypoxia.

154 ested the hypothesis that acute intermittent hypercapnic-hypoxia (AIHH) enhances cortico-phrenic neur

155 ested the hypotheses that acute intermittent hypercapnic-hypoxia (AIHH): (1) enhances cortico-phrenic

156 amines are coreleased by the carotid body at hypercapnic, hypoxic and high-potassium stimulus, are si

157 t required for normal baseline breathing and hypercapnic, hypoxic chemosensory reflexes.

158 However, the molecular mediators of hypercapnic immune suppression are undefined.

159 Our results suggest that hypercapnic immune suppression is mediated by a conserve

160 Hypercapnic immune suppression is not mediated by acidos

161 entify Zfh2 as the first in vivo mediator of hypercapnic immune suppression.

162 This hypercapnic-induced oxygen conservation may protect the

163 -2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy and bacterial killin

164 of wound repair was significantly reduced in hypercapnic lungs (63 versus 38%; p < 0.02).

165 -stimulated human whole blood cultures under hypercapnic, normocapnic, and hypocapnic conditions.

166 during wakefulness and during isocapnic and hypercapnic NREM sleep.

167 blood perfusing it is hypoxic, hypoglycemic, hypercapnic, or acidic.

168 Hypercapnic patients had lower FEV(1) (0.60 +/- 0.24 ver

169 ost defense and improve clinical outcomes in hypercapnic patients with advanced lung disease.

170 tment are similarly impaired in eucapnic and hypercapnic patients with severe COPD.

171 ent (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic

172 can contribute under certain circumstances (hypercapnic patients).

173 ventilation after extubation in high-risk or hypercapnic patients, and the other is steroid administr

174 ve explanation for CO(2) retention in stable hypercapnic patients.

175 19 eucapnic (PCO(2) 40 +/- 3 mm Hg), and 13 hypercapnic (PCO(2) 52 +/- 10 mm Hg) patients with sever

176 Hg), normocapnic (pCO(2) 40.1+/-0.9mmHg) and hypercapnic (pCO(2) 56.3+/-8.7mmHg) conditions.

177 a protective ventilatory strategy in severe hypercapnic pediatric respiratory failure.

178 extracellular, acidification to the measured hypercapnic pH levels lowered the currents as effectivel

179 ted in 48 subjects (11.1% of studies) during hypercapnic phases only.

180 aging was performed at rest and during 6-min hypercapnic plateaus (baseline; PETco2 at 50, 55, and 60

181 of VILI; its inhibition is one mechanism of hypercapnic protection and may be a target for clinical

182 liorated any negative effects of hypoxic and hypercapnic pulmonary vasoconstriction.

183 Three groups of normocapnic, hypocapnic, and hypercapnic rat lungs were perfused ex vivo, either duri

184 OS-derived NO is critically important to the hypercapnic reactivity of cerebral arterioles, and that

185 ave any worsening in symptoms, her hyperoxic hypercapnic rebreathing ventilatory response was not dif

186 on (NIV) is widely used in episodes of acute hypercapnic respiratory failure (AHRF) in patients with

187 Hypercapnic respiratory failure (end-tidal CO2 of 75 mm

188 -chronic obstructive pulmonary disease acute hypercapnic respiratory failure (n = 35), postextubation

189 was mildly hypotensive and was experiencing hypercapnic respiratory failure and acute renal failure

190 was mildly hypotensive and was experiencing hypercapnic respiratory failure and acute renal failure

191 extracorporeal CO2 removal in patients with hypercapnic respiratory failure and respiratory acidosis

192 leep function of patients surviving an acute hypercapnic respiratory failure episode requiring admiss

193 support (invasive or noninvasive) for acute hypercapnic respiratory failure in the ICU.

194 Severe hypercapnic respiratory failure requiring ICU admission

195 Two patients died in follow-up from hypercapnic respiratory failure secondary to neuromuscul

196 Surviving acute hypercapnic respiratory failure should be an opportunity

197 ve patients admitted for an episode of acute hypercapnic respiratory failure underwent an assessment

198 NIV during an admission for acute-on-chronic hypercapnic respiratory failure, favoring instead reasse

199 tion in such critical care settings as acute hypercapnic respiratory failure, particularly related to

200 ased in the plasma of patients with COPD and hypercapnic respiratory failure.

201 cid/base disturbances resulting from chronic hypercapnic respiratory failure.

202 rst line intervention to treat patients with hypercapnic respiratory failure.

203 gies to reduce excess CO(2) in patients with hypercapnic respiratory failure.

204 jor comorbidities known to precipitate acute hypercapnic respiratory failure.

205 NIV in patients with COPD and chronic stable hypercapnic respiratory failure.

206 optical BFI, not absorption, shows a graded hypercapnic response consistent with human cerebrovascul

207 emoreflex in adults, causing a difference in hypercapnic response of approximately 50% after neuron p

208 triggered local PGE2 release and blunted the hypercapnic response.

209 (10 mg/kg, i.v.) also significantly reduced hypercapnic responses (mean decrease of 44%).

210 f voltage-gated Ca2+ channels suppressed the hypercapnic responses, thereby supporting the membrane p

211 p gain) with increased controller gain (high hypercapnic responsiveness) generally being the cause.

212 t change from the observed baseline for each hypercapnic state, significantly decreased (P<0.05) with

213 hetic drive seen during panic attacks and in hypercapnic states such as COPD.

214 reshold for panic attacks during hypoxic and hypercapnic states.

215 Our findings demonstrated that prolonged hypercapnic stimulation elicited FOS expression in AP an

216 Accordingly, hypercapnic stimulation in HFpEF rats exacerbated increa

217 fNIRS signals collected during cognitive and hypercapnic stimuli to characterize effects of functiona

218 stigated whether a physiologically tolerable hypercapnic stimulus ( approximately 25 mm Hg increase i

219 ificantly greater than that with the maximal hypercapnic stimulus (2.00 vs. 0.86 mL/min/g; P < 0.0001

220 n VLF, myogenic and respiratory bands, while hypercapnic stimulus induced a global response across bo

221 entilatory response to oxygen deprivation or hypercapnic stimulus.

222 channels during cognitive stimulus, but not hypercapnic stimulus.

223 blocks lysosomal degradation, prevented the hypercapnic suppression of HIF-alpha protein.

224 with human orthologs whose knockdown reduced hypercapnic suppression of the gene encoding the antimic

225 artery pressure was increased throughout the hypercapnic trial.

226 During hypercapnic trials, the PaO2 remained at the normal rang

227 nt returned to baseline values 30 mins after hypercapnic trials.

228 PaCO2 and pH became normalized 15 mins after hypercapnic trials.

229 the ability to survive extremely hypoxic and hypercapnic underground conditions.

230 of the KATP channels greatly eliminated the hypercapnic vasodilation.

231 approximately twice the variance in morning hypercapnic vasomotor reactivity relative to overnight C

232 etention during sleep predicted a diminished hypercapnic vasomotor response in the morning.

233 n (8-OH DPAT) (250 microg/kg, i.p.) restored hypercapnic Ve at 2 and 4 weeks after injury (i.e., appr

234 Improvements in hypercapnic Ve response after single administration of 8

235 As a secondary outcome, mean hypercapnic ventilation was significantly decreased on d

236 The mean hypercapnic ventilation was significantly decreased with

237 ion at end-tidal carbon dioxide of 55 mm Hg (hypercapnic ventilation) using rebreathing methodology a

238 ll minute of hypoxia and the fifth minute of hypercapnic ventilation) were similar in the three group

239 n female obesity is even more detrimental to hypercapnic ventilatory control during wakefulness and N

240 The concentration-dependence of the hypercapnic ventilatory effect might be due to differenc

241 ry edema, 68% in nine patients with non-COPD hypercapnic ventilatory failure, 77% in 13 post-extubati

242 CO(2)-evoked increase in respiration is the hypercapnic ventilatory reflex (HCVR).

243 s study explores the state dependence of the hypercapnic ventilatory reflex (HCVR).

244 ructure that mediates a large portion of the hypercapnic ventilatory reflex, regulates breathing diff

245 The acute hypercapnic ventilatory response (AHCVR) arises from bot

246 d female C57BL/6J-Lep(ob) mice had depressed hypercapnic ventilatory response (HCVR) in comparison wi

247 EM1 and EM2 attenuated the hypercapnic ventilatory response (HCVR) only in high dos

248 ilation, metabolism and the magnitude of the hypercapnic ventilatory response (HCVR) were measured ev

249 e models, IDDM resulted in depression of the hypercapnic ventilatory response (HCVR).

250 ave found that sleep deprivation reduces the hypercapnic ventilatory response (HCVR).

251 patients caused a prolonged decrease in the hypercapnic ventilatory response (HCVR; a measure of res

252 stress and contributes significantly to the hypercapnic ventilatory response and thermoregulatory co

253 ed PCO2 , cerebrovascular reactivity and the hypercapnic ventilatory response in 11 healthy subjects

254 Here, we show that the hypercapnic ventilatory response in adult Lmx1b(f/f/p) m

255 hypoxic depression of breathing at P21, but hypercapnic ventilatory response is normal.

256 ctivity to CO(2) and tested the steady-state hypercapnic ventilatory response to CO(2) in nine normal

257 etrotrapezoid nucleus (RTN) that mediate the hypercapnic ventilatory response, but functional support

258 aseline ventilation, and rescued the blunted hypercapnic ventilatory response.

259 ep fragmentation are associated with blunted hypercapnic ventilatory response.

260 , cerebrovascular reactivity to CO(2) or the hypercapnic ventilatory response.

261 ith type 1 diabetes, we measured hypoxic and hypercapnic ventilatory responses (HCVRs), ventilatory r

262 ethysmograph was used to measure hypoxic and hypercapnic ventilatory responses of the unanaesthetized

263 In contrast, hypercapnic ventilatory responses were not altered by ad

264 sustained during exercise, despite hyperoxic-hypercapnic ventilatory responsiveness being normal and

265 t determinant of eupnoeic ventilation and of hypercapnic ventilatory responsiveness in humans, primar

266 rate (VT /TI ) (P </= 0.05) when the CB was hypercapnic vs. hypocapnic; central CO2 response slopes