ライフサイエンスコーパス: hypercapnia

1 (room air enhanced with carbon dioxide, ie, hypercapnia).

2 pheral (hypoxia) and central chemoreceptors (hypercapnia).

3 ination of apnoea, attributed in part to the hypercapnia.

4 ons) are critical for causing arousal during hypercapnia.

5 is important for the ventilatory response to hypercapnia.

6 s is reflected in progressive hypoxaemia and hypercapnia.

7 g the deterioration of dynamic CA induced by hypercapnia.

8 ntilation in hypoxia but respond normally to hypercapnia.

9 n in patients with advanced lung disease and hypercapnia.

10 ndices were found between CB normocapnia and hypercapnia.

11 nificance in patients with lung diseases and hypercapnia.

12 njury, and critical care illness may develop hypercapnia.

13 te ventilatory (VE) responses to hypoxia and hypercapnia.

14 uency tissue CBFv, which were insensitive to hypercapnia.

15 approximately 0.12 Hz) and was sensitive to hypercapnia.

16 hemoglobin oscillations were insensitive to hypercapnia.

17 mends increasing respiratory rate to prevent hypercapnia.

18 I) correlated with injury and was reduced in hypercapnia.

19 at normocapnia (ie, breathing room air) and hypercapnia.

20 ro-ORX have blunted respiratory responses to hypercapnia.

21 anxiety and sympathetic mobilization during hypercapnia.

22 in the chemoreflex responses to hypoxia and hypercapnia.

23 ilatory chemoreflex activation by hypoxia or hypercapnia.

24 ructive pulmonary disease (COPD) and chronic hypercapnia.

25 H hamsters exposed to normoxia, hypoxia, and hypercapnia.

26 ess to chemoreflex activation by hypoxia and hypercapnia.

27 ocked NO increase in endothelial cells under hypercapnia.

28 was used to induce brain acidosis induced by hypercapnia.

29 potentially life-saving arousal response to hypercapnia.

30 in the brainstem also prevented arousal from hypercapnia.

31 peradditive ventilatory responses to central hypercapnia.

32 rotonin neurons cause arousal in response to hypercapnia.

33 tivity, preceding PN bursts, occurred during hypercapnia.

34 adaptive neurobiological effects of chronic hypercapnia.

35 arousal to hypoxia and, to a lesser extent, hypercapnia.

36 the CR activation is achieved by hypoxia or hypercapnia.

37 tch that is necessary to arouse animals from hypercapnia.

38 in/pre-pro-enkephalin, and do not respond to hypercapnia.

39 iratory frequency increased with progressive hypercapnia.

40 rted changes with adenosine (11.2% +/- 10.6 [hypercapnia, 10 mm Hg] vs 12% +/- 12.3 [adenosine]; P =

41 te nucleus after 24 h, but not after 30 d of hypercapnia; 2) the number of serotonergic and total neu

42 mocapnia and normal pH, 110,104; compensated hypercapnia, 20,463; and hypercapnic acidosis, 122,245)

43 photostimulation were largely unaffected by hypercapnia (3 and 6% CO(2)).

44 During quiet wake or non-REM sleep, hypercapnia (3 or 6% FI,CO2 ) increased both fR and VT w

45 Hypercapnia (3-6% FiCO2 ) increased FR and VT in CBD rat

46 o 0.094 +/- 0.040 Hz at the highest level of hypercapnia (41.7 +/- 5.4 mmHg), showing a correlation o

47 eduction that was only slightly larger under hypercapnia (6% FiCO2), but was greatly enhanced during

48 Late-E activity generated during hypercapnia (7-10% CO(2)) was abolished with pontine tra

49 Hypercapnia, a surrogate state of depressed CA, leads to

50 We found that hypercapnia activated genes that regulate Wnt signaling

51 ypercapnia), it has yet to be elucidated how hypercapnia activates genes and signaling pathways, or w

52 mission or death in patients with persistent hypercapnia after an acute COPD exacerbation.

53 rols), normoxic air with 5% CO2 (therapeutic hypercapnia), air and endotoxemia (5 mg/kg endotoxin), a

54 Hypercapnia also reduced forskolin-stimulated CFTR-depen

55 Hypercapnia also reduced macrophage killing of Pseudomon

56 Hypercapnia also reduced the volume of forskolin-stimula

57 We previously reported that hypercapnia alters expression of host defense genes, inh

58 (82)Rb injected 3 min after the beginning of hypercapnia and a 1-tissue-compartment model with flow-d

59 The duration of hypercapnia and acidosis was longer in thoracoscopy comp

60 ted with prolonged and severe intraoperative hypercapnia and acidosis, compared with open surgery.

61 paired thoracoscopically, but this may cause hypercapnia and acidosis, which are potentially harmful.

62 onary stenosis, MBF increased in response to hypercapnia and adenosine (P < 0.05, all territories), b

63 changes in canines with LAD stenosis during hypercapnia and adenosine infusion were not different (1

64 (LAD) underwent vasodilator challenges with hypercapnia and adenosine.

65 anterior descending coronary territory (with hypercapnia and adenosine; both P < 0.05).

66 inicians strike a balance between permissive hypercapnia and adequate ventilation.

67 mage to the lungs is accompanied by systemic hypercapnia and associated acidosis, which are associate

68 itions and NO production is increased during hypercapnia and decreased during hypocapnia independent

69 ptors because they are strongly activated by hypercapnia and express high levels of proton sensors (K

70 mb-high RTN neurons do not express Fos after hypercapnia and have low-to-undetectable levels of Kcnk5

71 Patients with compensated hypercapnia and hypercapnic acidosis had higher Acute Ph

72 dy aimed to assess the impact of compensated hypercapnia and hypercapnic acidosis in patients receivi

73 e clinical studies evaluating the effects of hypercapnia and hypercapnic acidosis in patients requiri

74 d to identify the independent association of hypercapnia and hypercapnic acidosis with hospital morta

75 wever, lung-protective ventilation can cause hypercapnia and hypercapnic acidosis.

76 on of photoperiodic perception, tolerance to hypercapnia and hypoxia and resistance to cancer.

77 entral chemoreceptors.SIGNIFICANCE STATEMENT Hypercapnia and hypoxia during sleep elicit arousal, whi

78 Hypercapnia and hypoxia produce arousal in mammals by ac

79 iration during metabolic challenges (such as hypercapnia and hypoxia) improves pulmonary ventilation.

80 s predicted by increased chemosensitivity to hypercapnia and is associated with worse clinical condit

81 g the diaphragm, using electromyography with hypercapnia and optogenetic photoactivation.

82 ung disease, who frequently suffer from both hypercapnia and respiratory infections.

83 e changes of pHi and [Cl(-)]i in response to hypercapnia and seizure activity.

84 ally, C1 neurons are marginally activated by hypercapnia and the large breathing stimulation caused b

85 hanisms underlying the beneficial effects of hypercapnia and the relative contribution of elevated CO

86 r blockade and artificial ventilation, under hypercapnia and under either anaesthesia or decerebratio

87 scles of the caudal intercostal spaces, with hypercapnia and under either anaesthesia or decerebratio

88 sment of chemoreflex response to hypoxia and hypercapnia, and 24-h cardiorespiratory recording.

89 release transmitters in response to hypoxia, hypercapnia, and acidemia to activate afferent sensory f

90 ngement (hypoxemia, hyperoxemia, hypocapnia, hypercapnia, and acidosis) was associated with multiple

91 ng capacity, resulting in chronic hypoxemia, hypercapnia, and increased erythropoietin synthesis.

92 potential metabolic threat, such as hypoxia, hypercapnia, and reduced perfusion.

93 nts who benefit from flavanols intake during hypercapnia are also those who do so in the cognitive ch

94 sion: approximately 58.7 mmHg), but not mild-hypercapnia (arterial CO2 tension: approximately 46.3 mm

95 O2 tension: approximately 38.4 mmHg), severe hypercapnia (arterial CO2 tension: approximately 58.7 mm

96 creased the latency of mice to arouse during hypercapnia, as did silencing DR(Sert) terminals in the

97 r and greater brain oxygenation responses to hypercapnia, as well as higher performance only when cog

98 etabolic responses under extreme hypoxia and hypercapnia associated with prolonged apnoea.

99 g respiratory neuroplasticity during chronic hypercapnia but alone do not account for ventilatory acc

100 rent and severe ventilatory insensitivity to hypercapnia but also exhibit relatively normal ventilati

101 The latter input operates during normo- or hypercapnia but fails to activate RTN neurons under hypo

102 vision had minimal effects on arousal during hypercapnia but instead increased non-rapid eye movement

103 ion during exposure to normoxia, hypoxia, or hypercapnia, but comparable ventilatory responsiveness t

104 Namely they are activated by hypercapnia, but not by hypoxia, and express proton sens

105 vated (Fos) following 2 hours of exposure to hypercapnia, but not by hypoxia.

106 w properties influence levels of hypoxia and hypercapnia, but their effects on ventilation and oxygen

107 levels in endothelial cells increased during hypercapnia by 36% in 8hours and remained 25% above base

108 ibute little to resting BP under normoxia or hypercapnia, C1 neuron discharge is restrained continuou

109 cterial loads were observed, indicating that hypercapnia can decrease host resistance.

110 g at the same level of hypoxia suggests that hypercapnia can partly explain the cerebral metabolic re

111 These data indicate that hypercapnia can partly explain the reduction in CMRO2 ne

112 show that both of these insults, hypoxia and hypercapnia, can trigger SLA in wild-type flies as well.

113 t of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body PCO2 approximately 22, 41 and

114 nide, but only mildly activated by hyperoxic hypercapnia (central chemoreceptor stimulation).

115 ted this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nu

116 noea experience chronic intermittent hypoxia-hypercapnia (CIHH) during sleep that elicit sympathetic

117 The hypercapnia condition is achieved by breathing 5% carbon

118 ring baseline breathing, but particularly in hypercapnia, confirming a significant increase in inspir

119 pathway, and illustrate a mechanism by which hypercapnia could contribute to worse outcomes of patien

120 im of the current work was to investigate if hypercapnia could modulate cAMP-regulated ion and fluid

121 Based on these results, we hypothesize that hypercapnia counter-regulates activation of the HIF path

122 velocity (MCAv(mean) ) and its reactivity to hypercapnia (CVR(HYPER) ) and hypocapnia (CVR(HYPO) ), r

123 ther patients had exposure to hypocapnia and hypercapnia (defined as Paco(2) </=30 mm Hg and Paco(2)

124 Refractory hypoxemia and/or uncompensated hypercapnia despite optimal conventional management were

125 Notably, hypercapnia did not affect LPS-induced degradation of Ik

126 In contrast, hypercapnia did not down-regulate IL-10 or interferon-be

127 ther trials should focus on whether moderate hypercapnia during postcardiac arrest care improves outc

128 The combination of hypoxia and hypercapnia during sleep produces arousal, which helps r

129 Acute hypercapnia (elevated arterial CO(2)/H(+)) is a suffocat

130 Hypercapnia (elevated blood pCO2 > approximately 50 mm H

131 we show that two novel insults, hypoxia and hypercapnia (elevated CO(2) levels) are potent triggers

132 Hypercapnia, elevated partial pressure of CO2 in blood a

133 xposed to increased temperature, reduced pH, hypercapnia, elevated shear stress and augmented mechani

134 ask to total face mask because of refractory hypercapnia, encephalopathy score (3 [3-4] vs. 2 [2-3];

135 ultiple stressors such as darkness, hypoxia, hypercapnia, energetics and high pathonecity.

136 nts with heart failure (HF), and hypoxia and hypercapnia episodes activate chemoreceptors stimulating

137 o, blockers with selectivity for Cx26 reduce hypercapnia-evoked ATP release and the consequent adapti

138 capnia only, 18 (9%) had both hypocapnia and hypercapnia exposure, and 60 (31%) had no exposure; 74%

139 g that Zfh2's role in mediating responses to hypercapnia extends beyond the immune system.

140 (eupnoea) and during hypoxia (FIO2 =0.12) or hypercapnia (FICO2 =0.07) before and up to 23 days after

141 Among patients with persistent hypercapnia following an acute exacerbation of COPD, add

142 Therapeutic hypercapnia following endotoxemic challenge was associat

143 Elevated CO(2) levels (hypercapnia) frequently occur in patients with obstructi

144 transmission to CVNs evoked by acute hypoxia-hypercapnia (H-H) and CIHH.

145 adipose mass and reduced central response to hypercapnia have been implicated as pathophysiological d

146 Hypercapnia (HC), elevation of the partial pressure of C

147 ion strategies in these patients may lead to hypercapnia (HC).

148 Hypoxia (low oxygen) and hypercapnia (high carbon dioxide) are co-incidental feat

149 this meta-analysis of patients with COPD and hypercapnia, home BPAP, compared with no device, was ass

150 inspiratory activity induced by hypoxia and hypercapnia; however, hyperpolarizing pFL neurons attenu

151 ted active expiration when it was induced by hypercapnia, hypoxia, or disinhibition of the pFL.

152 ted cerebral perfusion and vasoreactivity to hypercapnia, impaired cognition and, in CMS+, symptoms o

153 ysis of available transcriptomic datasets of hypercapnia in a human bronchial cell line, flies and ne

154 the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 19% of control

155 the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 223% of control

156 thesis that the ventilatory insensitivity to hypercapnia in BN rats is due to altered raphe gene expr

157 Chronic hypercapnia in COPD patients does not exaggerate this re

158 to the ventilatory response to specific CNS hypercapnia in eight unanaesthetized, awake dogs.

159 A 24-hr exposure to therapeutic hypercapnia in endotoxin-stimulated, spontaneously breat

160 and inflammatory adaptations during chronic hypercapnia in goats.

161 s the response of MBF to different levels of hypercapnia in healthy humans with PET.

162 may contribute to the beneficial effects of hypercapnia in inflammatory diseases of the lung.

163 he increased sensitivity to both hypoxia and hypercapnia in these BS mutants suggests possible physio

164 ons are glutamatergic, strongly activated by hypercapnia in vivo and by CO(2) or protons in slices.

165 increased astrocyte [Ca(2+)]iin vitro and by hypercapnia in vivo is inhibited.

166 A5 neurons respond weakly to hypercapnia in vivo or to changes in pH in slices sugges

167 During quiet wake or non-REM sleep, hypercapnia increased both breathing frequency (fR ) and

168 tor of adenosine, resting MBF decreased; and hypercapnia increased MBF but not adenosine (P < 0.05).

169 nd tidal volume (VT ) whereas, in REM sleep, hypercapnia increased VT exclusively.

170 reased both fR and VT whereas, in REM sleep, hypercapnia increased VT exclusively.

171 r are observed with even very mild levels of hypercapnia (increased arterial CO2).

172 We demonstrate that hypercapnia (increased CO2) evokes an increase in astroc

173 of the vasodilator PgE2 We demonstrate that hypercapnia (increased CO2) evokes increases in astrocyt

174 Relish IkappaB-like domain is unaffected by hypercapnia, indicating that immunosuppression acts down

175 d for 5 min at rest (normocapnia) and during hypercapnia induced by breathing 5% CO(2) in air.

176 (AMPK) activation is required for high CO2 (hypercapnia)-induced Na,K-ATPase endocytosis in alveolar

177 During co-activation of the EPR and the hypercapnia-induced CR (CO(2) -CR), the haemodynamic res

178 The EPR and hypercapnia-induced CR interaction results in a simple a

179 Zfh2 mutations also partially rescue hypercapnia-induced delays in egg hatching, suggesting t

180 the interaction/integration/conservation of hypercapnia-induced genomic responses in mammals (mice a

181 nteraction may hold promise for ameliorating hypercapnia-induced immunosuppression and improving resi

182 lated activity, attenuating the hypoxia- and hypercapnia-induced increase in inspiratory activity, an

183 5 rescued both LMO7b phosphorylation and the hypercapnia-induced Na,K-ATPase endocytosis.

184 A hypercapnia-induced oxygen-conserving response may prote

185 elB was observed in vivo and correlated with hypercapnia-induced protection against LPS-induced lung

186 ne and metabolic organ of the fly, mitigates hypercapnia-induced reductions in Dipt and other antimic

187 Hypercapnia-induced RelB processing was sensitive to pro

188 yperoxygenation-induced vasoconstriction and hypercapnia-induced vasodilatation.

189 (LPS) and other Toll-like receptor ligands, hypercapnia inhibited expression of tumor necrosis facto

190 In the present study we show that hypercapnia inhibits autophagy induced by starvation, ra

191 To explore whether hypercapnia interferes with host defense, we studied the

192 ently develop bacterial lung infections, and hypercapnia is a risk factor for mortality in such indiv

193 Hypercapnia is associated with increased susceptibility

194 Hypercapnia is clinically defined as an arterial blood p

195 AbN late-E activity during hypercapnia is coupled with augmented pre-I discharge in

196 Hypercapnia is demonstrated to be a useful tool to induc

197 ulness, the ventilatory response to normoxic hypercapnia is higher in young SHRs (mean +/- SEM: 179 +

198 As hypercapnia is known to suppress neuronal activity, we s

199 nic obstructive pulmonary disease (COPD) and hypercapnia is uncertain.

200 Elevated arterial CO(2) (hypercapnia) is encountered in a range of clinical condi

201 Elevated blood and tissue CO(2), or hypercapnia, is common in severe lung disease.

202 organisms are responsive to CO(2) elevation (hypercapnia), it has yet to be elucidated how hypercapni

203 on ( approximately 0.12 Hz) was decreased by hypercapnia, its lower-frequency component ( approximate

204 Here, we provide evidence that during hypercapnia, JNK promotes the phosphorylation of LMO7b,

205 Collectively, our data suggest that hypercapnia leads to JNK-induced LMO7b phosphorylation a

206 Here, we investigated whether hypercapnia leads to skeletal muscle atrophy.

207 l innate immune functions in the macrophage, hypercapnia may cause a previously unrecognized defect i

208 Therefore, hypercapnia may play a key role in the pathophysiology o

209 eurons, and the activation of RTN neurons by hypercapnia may ultimately derive from their intrinsic p

210 MBF increased with increasing levels of hypercapnia; MBF at a PETco2 of 60 mm Hg was double that

211 n previous studies we have demonstrated that hypercapnia modulates agonist-stimulated cAMP levels thr

212 n (heliox) reduces the work of breathing and hypercapnia more than air/O2, but its impact on clinical

213 vels (normocapnia and normal pH, compensated hypercapnia [normal pH with elevated carbon dioxide], an

214 Elevated CO(2) concentrations (hypercapnia) occur in patients with severe lung diseases

215 Significant hypercapnia occurred more frequently during anesthetic c

216 io, 1.74; 95% CI, 1.62-1.88) and compensated hypercapnia (odds ratio, 1.18; 95% CI, 1.10-1.26) when c

217 pared myocardial BOLD MR imaging showed that hypercapnia of 10 mm Hg may provide a cardiac hyperemic

218 Patients with hypercapnia often develop lung infections and have an in

219 However, the effect of hypercapnia on autophagy, a conserved process by which c

220 et study with the same divers, the impact of hypercapnia on cerebral metabolism was determined using

221 however, little is known about the impact of hypercapnia on gene transcription.

222 The suppressive effects of hypercapnia on HIF-alpha protein stability could be mimi

223 However, the effects of hypercapnia on non-neuronal tissues and the mechanisms t

224 d hypercapnia, we investigated the effect of hypercapnia on the HIF pathway.

225 nd mechanistic perspective on the effects of hypercapnia on the lungs and discuss the recent understa

226 and pathophysiological effects of high CO2 (hypercapnia) on the lungs and specific lung cells, which

227 , 52 (27%) had hypocapnia only, 63 (33%) had hypercapnia only, 18 (9%) had both hypocapnia and hyperc

228 roposed to affect ventilation in response to hypercapnia, only the retrotrapezoid nucleus, a portion

229 ith a significant increase in intraoperative hypercapnia [open 68 mm Hg; thoracoscopy 96 mm Hg; diffe

230 sympathetic activity in rats in normocapnia, hypercapnia or after CIH.

231 al manipulations of the BotC and pFRG during hypercapnia or after the exposure to short-term sustaine

232 ion during active expiration observed during hypercapnia or after the exposure to short-term sustaine

233 Intermittent hypoxia, reoxygenation, and hypercapnia or hypocapnia occur in both adults and child

234 In contrast, hypercapnia or hypoxia-induced enhanced expiratory-relat

235 usal from sleep and respiratory responses to hypercapnia or hypoxia.

236 to the stimulation of breathing elicited by hypercapnia or metabolic acidosis.

237 ncreased hospital mortality than compensated hypercapnia or normocapnia.

238 ute volume did not neurologically respond to hypercapnia or optogenetic photoactivation of the C4 cer

239 for death associated with severe hypoxemia, hypercapnia, or both not responding to maximized convent

240 for death associated with severe hypoxemia, hypercapnia, or both not responding to maximized convent

241 Vt was not associated with hypercapnia (P = 1.00).

242 hypoxia (P=0.024) and tended to be higher to hypercapnia (P=0.066) in the SDB group.

243 .70 +/- 1.58 (normocapnia) to 4.14 +/- 2.05 (hypercapnia; P < 0.0001).

244 d clinical trial of patients with persistent hypercapnia (Paco2 >53 mm Hg) 2 weeks to 4 weeks after r

245 We use a graded hypercapnia paradigm and participant feedback to rule ou

246 Hypercapnia (PCO2 90-100 mm Hg) was established in mecha

247 induced hypercapnia, we hypothesized chronic hypercapnia per se will lead to similar changes.

248 Under high chemical drive (hypercapnia), postinspiratory discharge was nearly aboli

249 r pocket, but limited in time as hypoxia and hypercapnia rapidly develop.

250 Our data reveal that hypercapnia reduces CFTR-dependent, electrogenic Cl(-) a

251 vs. 296.0 +/- 43.9% LF/HFHRV , normoxia vs. hypercapnia, respectively), incidence of cardiac arrhyth

252 Hypercapnia-responsive Wnt pathway homologues were simil

253 t ventilation during exposure to hypoxia and hypercapnia, resulting in reduced ventilatory responsive

254 P(a) CO(2) ~33 mmHg, pH ~7.39), or normoxic hypercapnia (S(a) O(2) ~98%, P(a) O(2) ~105 mmHg, P(a) C

255 nt effect on any of the parameters; however, hypercapnia seemed to nonsignificantly attenuate the hyp

256 Severe hypercapnia, seen in respiratory disorders (eg, asthma o

257 We show that hypercapnia significantly impairs embryonic morphogenesi

258 We found that acute exposure to hypercapnia significantly reduced forskolin-stimulated e

259 In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exe

260 se results are of relevance to patients with hypercapnia such as those with chronic obstructive pulmo

261 Hypercapnia suppressed HIF-alpha protein stability and H

262 We previously demonstrated that hypercapnia suppresses induction of NF-kappaB-regulated

263 e muscle vasoconstriction during hypoxia and hypercapnia than HF patients without SDB, which seems to

264 Hypercapnia, the elevation of CO2 in blood and tissue, c

265 ute isocapnic hypoxia (G(pO2)) and hyperoxic hypercapnia, the latter divided into peripheral (G(pCO2)

266 Similarly, during hypercapnia, the vascular responses (forearm blood flow,

267 Recent reports suggest that permissive hypercapnia, therapeutic paralysis, sedation, and contro

268 following these insults and, in the case of hypercapnia, they exhibit SLA at a lower threshold.

269 MBF increased significantly at each level of hypercapnia to 1.92-fold over baseline (0.86 +/- 0.24 vs

270 ue chemosensor for detecting and translating hypercapnia to fear-associated behavioral and physiologi

271 ic rats (p < .001) and by 33% in therapeutic hypercapnia-treated endotoxemic rats (p < .001).

272 significantly increased only in therapeutic hypercapnia-treated endotoxemic rats (p < .05).

273 ignificantly high in the lung of therapeutic hypercapnia-treated endotoxemic rats compared to the lun

274 In the spleen, therapeutic hypercapnia-treated endotoxemic rats had low expression

275 t for an appropriate ventilatory response to hypercapnia up until P15.

276 four progressive levels of systemic arterial hypercapnia via increased fractional inspired CO(2) for

277 BOLD MR (17% +/- 14 [hypercapnia] vs 14% +/- 24 [adenosine]; P = .80) and cor

278 nd coronary blood flow velocity (21% +/- 16 [hypercapnia] vs 26% +/- 27 [adenosine]; P > .99) respons

279 osine infusion were not different (1% +/- 4 [hypercapnia] vs 6% +/- 4 [adenosine]; P = .12).

280 In the absence of stenosis, mean MBF under hypercapnia was 2.1 +/- 0.9 mL/min/g and adenosine was 2

281 In this multicenter study, hypercapnia was associated with good 12-month outcome in

282 The extent of effect on MBF due to hypercapnia was compared with adenosine.

283 Inhibition of IL-6 expression by hypercapnia was concentration dependent, rapid, reversib

284 latency to arousal in response to hypoxia or hypercapnia was determined along with changes in ventila

285 aptive changes in ventilation in response to hypercapnia, we have studied the mechanisms of CO(2)-dep

286 ling during carotid body denervation-induced hypercapnia, we hypothesized chronic hypercapnia per se

287 ause of the relationship between hypoxia and hypercapnia, we investigated the effect of hypercapnia o

288 Hypocapnia and hypercapnia were common after cardiac arrest and were in

289 rn of spontaneous circulation hypocapnia and hypercapnia were independent predictors of poor neurolog

290 Hypocapnia and hypercapnia were independently associated with poor neur

291 n defect volumes measured with adenosine and hypercapnia were significantly correlated (R = 0.85) and

292 changes in the CBFV response, resulting from hypercapnia, which led to a reduction in the autoregulat

293 nsitivity of the higher CBFV oscillations to hypercapnia, which triggers blood vessel vasodilation, s

294 natriuretic peptide, and chemosensitivity to hypercapnia, which was the only independent predictor of

295 which we randomly assigned patients without hypercapnia who had acute hypoxemic respiratory failure

296 studies that enrolled adults with COPD with hypercapnia who used home NIPPV for more than 1 month we

297 -base balance during exposure to therapeutic hypercapnia with and without endotoxemia before and at 4

298 toxemia (5 mg/kg endotoxin), and therapeutic hypercapnia with endotoxemia.

299 e activity (MSNA) in response to hypoxia and hypercapnia would be more pronounced in patients with HF

300 eduction in fluid secretion, associated with hypercapnia, would be predicted to have important conseq