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

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

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

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

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

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

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

12 Hypercapnic acidosis activated an inward rectifier curre

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

14 Hypercapnic acidosis also directly reduced DNA binding o

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

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

17 Hypercapnic acidosis and IkappaBalpha-SuperRepressor tra

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

19 Hypercapnic acidosis attenuated moderate and severe vent

20 Hypercapnic acidosis attenuated ventilation-induced lung

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

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

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

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

25 Hypercapnic acidosis during the first 24 hours of intens

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

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

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

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

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

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

32 Hypercapnic acidosis inhibited canonical nuclear factor-

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

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

35 Hypercapnic acidosis may attenuate lung ischemia-reperfu

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

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

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

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

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

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

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

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

44 Hypercapnic acidosis protects against ventilation-induce

45 To investigate whether hypercapnic acidosis protects against ventilator-induced

46 Hypercapnic acidosis reduced cyclic mechanical stretch-i

47 Hypercapnic acidosis reduced E. coli inflammation and lu

48 Hypercapnic acidosis reduced indices of inflammation suc

49 Hypercapnic acidosis reduced the decrement of the nuclea

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

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

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

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

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

55 Hypercapnic acidosis was associated with reduced 28-day

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

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

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

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

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

61 10,104; compensated hypercapnia, 20,463; and hypercapnic acidosis, 122,245) were included in analysis

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

63 Hypercapnic acidosis, common in mechanically ventilated

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

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

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

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

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

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

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

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

72 ective ventilation can cause hypercapnia and hypercapnic acidosis.

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

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

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

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

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

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

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

80 rges occurred only during eucapnic anoxia or hypercapnic anoxia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 2 in reducing NIV failure (25-15%) in severe hypercapnic COPD exacerbations.

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

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

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

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

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

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

116 (100% oxygen), two levels of mild and severe hypercapnic hyperoxia (inspired Pco2 of 30 and 60 torr;

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

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

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

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

121 Hypercapnic immune suppression is not mediated by acidos

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

123 This hypercapnic-induced oxygen conservation may protect the

124 -2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy and bacterial killin

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

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

127 during wakefulness and during isocapnic and hypercapnic NREM sleep.

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

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

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

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

132 can contribute under certain circumstances (hypercapnic patients).

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

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

135 19 eucapnic (PCO(2) 40 +/- 3 mm Hg), and 13 hypercapnic (PCO(2) 52 +/- 10 mm Hg) patients with sever

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 Severe hypercapnic respiratory failure requiring ICU admission

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

154 Surviving acute hypercapnic respiratory failure should be an opportunity

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

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

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

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

159 jor comorbidities known to precipitate acute hypercapnic respiratory failure.

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

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

162 triggered local PGE2 release and blunted the hypercapnic response.

163 (10 mg/kg, i.v.) also significantly reduced hypercapnic responses (mean decrease of 44%).

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

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

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

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

168 reshold for panic attacks during hypoxic and hypercapnic states.

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

170 Accordingly, hypercapnic stimulation in HFpEF rats exacerbated increa

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

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

173 entilatory response to oxygen deprivation or hypercapnic stimulus.

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

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

176 artery pressure was increased throughout the hypercapnic trial.

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

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

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

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

181 of the KATP channels greatly eliminated the hypercapnic vasodilation.

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

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

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

185 Improvements in hypercapnic Ve response after single administration of 8

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 ep fragmentation are associated with blunted hypercapnic ventilatory response.

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

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

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

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

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

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