ライフサイエンスコーパス: hypercapnia

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

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

3 tch that is necessary to arouse animals from hypercapnia.

4 n in patients with advanced lung disease and hypercapnia.

5 ndices were found between CB normocapnia and hypercapnia.

6 nificance in patients with lung diseases and hypercapnia.

7 njury, and critical care illness may develop hypercapnia.

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

9 uency tissue CBFv, which were insensitive to hypercapnia.

10 approximately 0.12 Hz) and was sensitive to hypercapnia.

11 hemoglobin oscillations were insensitive to hypercapnia.

12 mends increasing respiratory rate to prevent hypercapnia.

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

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

15 ro-ORX have blunted respiratory responses to hypercapnia.

16 anxiety and sympathetic mobilization during hypercapnia.

17 in the chemoreflex responses to hypoxia and hypercapnia.

18 ilatory chemoreflex activation by hypoxia or hypercapnia.

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

20 ess to chemoreflex activation by hypoxia and hypercapnia.

21 ocked NO increase in endothelial cells under hypercapnia.

22 was used to induce brain acidosis induced by hypercapnia.

23 potentially life-saving arousal response to hypercapnia.

24 peradditive ventilatory responses to central hypercapnia.

25 rotonin neurons cause arousal in response to hypercapnia.

26 tivity, preceding PN bursts, occurred during hypercapnia.

27 reflex gain was not altered by hyperpnoea or hypercapnia.

28 support the potential benefits of permissive hypercapnia.

29 ls affected neuronal response to more severe hypercapnia.

30 ed neuronal responses to hypocapnia and mild hypercapnia.

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

32 iratory frequency increased with progressive hypercapnia.

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

34 is important for the ventilatory response to hypercapnia.

35 s is reflected in progressive hypoxaemia and hypercapnia.

36 ntilation in hypoxia but respond normally to hypercapnia.

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

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

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

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

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

42 During exposure to hypercapnia (5% CO(2) in 95% O(2)), frequency of breathi

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

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

45 Correspondingly, modest hypercapnia (7-13%) increases mortality of flies inocula

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

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

48 f central chemoreceptors with mild hyperoxic hypercapnia also causes resetting of the arterial barore

49 Hypercapnia also reduced forskolin-stimulated CFTR-depen

50 Hypercapnia also reduced macrophage killing of Pseudomon

51 Hypercapnia also reduced the volume of forskolin-stimula

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

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

54 nd intravenous magnesium, marked progressive hypercapnia and acidosis rapidly developed requiring hig

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

56 removal to mechanical ventilation corrected hypercapnia and acidosis, allowing reduction of other su

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

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

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

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

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

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

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

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

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

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

67 Post-MTBI fMRI responses to hypercapnia and forepaw stimulation were significantly i

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

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

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

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

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

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

74 impairment of cerebrovasodilation induced by hypercapnia and hypotension after hypoxia/ischemia (H/I)

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

76 ontrol of automatic breathing in response to hypercapnia and hypoxia.

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

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

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

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

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

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

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

84 wed an attenuated hyperaemic response during hypercapnia and whisker stimulation compared to wild-typ

85 Carotid body chemoreceptors sense hypoxemia, hypercapnia, and acidosis and play an important role in

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

87 gh potassium concentrations, during normoxic hypercapnia, and during hypoxia is demonstrated using th

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

89 Quantitative baseline blood flow, and hypercapnia- and hyperoxia-induced blood flow changes in

90 ate quantitative basal blood flow as well as hypercapnia- and hyperoxia-induced blood flow changes in

91 Permissive hypercapnia appears as a safe and effective management s

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

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

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

95 +/- 2.8 beats min(-1) during hyperpnoea and hypercapnia (both P < 0.017).

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

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

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

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

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

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

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

103 Heart rate is elevated during hyperoxic hypercapnia, but this response is not different from the

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

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

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

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

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

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

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

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

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

113 While neither hyperpnoea nor hypercapnia changed mean arterial pressure (92.0 +/- 1.8

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

115 The hypercapnia condition is achieved by breathing 5% carbon

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

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

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

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

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

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

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

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

124 f central chemoreceptors with mild hyperoxic hypercapnia does not affect arterial pressure, sympathet

125 Further, hypercapnia does not induce responses characteristic of

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

127 The hypercapnia effects were independent of intracellular RO

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

129 Hypercapnia (elevated blood pCO2 > approximately 50 mm H

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

131 Hypercapnia (elevated CO(2) levels) occurs as a conseque

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 Hypercapnia (end-expiratory CO(2) from 5% to 10%) increa

136 eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tidal P(CO(2)) + 5 mmHg above eucapnia)

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

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

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

140 provide a likely neurochemical mechanism for hypercapnia-evoked bradycardia and the dysregulation of

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

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

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

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

145 Therapeutic hypercapnia following endotoxemic challenge was associat

146 Exposure of rats to hypercapnia for up to 7 days caused a sustained decrease

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

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

149 report that neonates managed with permissive hypercapnia have a shorter duration of mechanical ventil

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

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

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

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

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

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

156 Chronic hypercapnia in COPD patients does not exaggerate this re

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

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

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

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

161 d diminished BOLD responses to hyperoxia and hypercapnia in the Royal College of Surgeons rat retinas

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

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

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

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

166 eased blood flow due to vasoconstriction and hypercapnia increased blood flow due to vasodilation in

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

170 nd tidal volume (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 (AMPK) activation is required for high CO2 (hypercapnia)-induced Na,K-ATPase endocytosis in alveolar

176 Interestingly, absolute hyperoxia- and hypercapnia-induced blood flow changes in the RCS retina

177 cerebral blood flow were used to control for hypercapnia-induced changes in blood oxygen level-depend

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

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

180 proterenol, or a cAMP analog ameliorated the hypercapnia-induced impairment of AFR.

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

182 5 rescued both LMO7b phosphorylation and the hypercapnia-induced Na,K-ATPase endocytosis.

183 A hypercapnia-induced oxygen-conserving response may prote

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

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

186 Hypercapnia-induced RelB processing was sensitive to pro

187 yperoxygenation-induced vasoconstriction and hypercapnia-induced vasodilatation.

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

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

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

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

192 Hypercapnia is associated with increased susceptibility

193 Hypercapnia is clinically defined as an arterial blood p

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

195 Hypercapnia is demonstrated to be a useful tool to induc

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

197 Hypercapnia is known to modulate inflammation in lungs.

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

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

200 ucing brief (< 30 s) episodes of hypoxia and hypercapnia, it is unknown if repetitive apnoeas also el

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

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

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

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

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

206 Ictal hypoxemia and hypercapnia may contribute to SUDEP.

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

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

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

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

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

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

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

214 Significant hypercapnia occurred more frequently during anesthetic c

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

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

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

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

219 However, the effect of hypocapnia and hypercapnia on blood cytokine production during sepsis i

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

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

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

234 ncreased hospital mortality than compensated hypercapnia or normocapnia.

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

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

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

238 e gas exchange during environmental hypoxia, hypercapnia, or both; and (iii) the oxidative-damage hyp

239 increase in CBF produced by neural activity, hypercapnia, or by the endothelium-dependent vasodilator

240 sgow Coma Scale) and respiratory (hypoxemia, hypercapnia, or nursing requirements for complex respira

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 and 90.7 +/- 1.4 mmHg during hyperpnoea and hypercapnia; P = 0.427) or muscle sympathetic nerve acti

244 tegrated units min(-1) during hyperpnoea and hypercapnia; P = 0.653), heart rate was increased from 5

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

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

247 ented, impaired responses to hypotension and hypercapnia post H/I, but none of these antagonists affe

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

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

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

255 We show that hypercapnia significantly impairs embryonic morphogenesi

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

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

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

259 Hypercapnia suppressed HIF-alpha protein stability and H

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

261 phagocytic immune-responsive S2* cell line, hypercapnia suppresses induction of specific antimicrobi

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

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

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

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

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

267 In hypercapnia, there is a reduced ventilatory response (ex

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 Therefore, under hypercapnia, total respiratory loop gain was markedly re

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

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

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

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

276 pH 0.03; 95% CI, 0.02 to 0.04; P<0.001), and hypercapnia (treatment difference, 0.7 kPa [5.2 mm Hg];

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

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

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

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

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

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

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

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

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

286 f pial arterioles in response to hypoxia and hypercapnia was significantly reduced in alcohol-fed rat

287 reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 +/- 0.2

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

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

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

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

292 Hypocapnia and hypercapnia were independently associated with poor neur

293 etal pial arterioles to systemic hypoxia and hypercapnia were measured using a cranial window techniq

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

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

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

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