ライフサイエンスコーパス: cerebral blood flow

1 unction, decrease inflammation, and increase cerebral blood flow).

2 g of basilar and carotid arteries to measure cerebral blood flow.

3 eGFR is independently associated with lower cerebral blood flow.

4 ions cause vasoconstriction that would limit cerebral blood flow.

5 zheimer's disease is associated with reduced cerebral blood flow.

6 e areas of high or low metabolic activity or cerebral blood flow.

7 n, which assume that only arterioles control cerebral blood flow.

8 relation between blood pressure and regional cerebral blood flow.

9 lature in response to changes in pressure or cerebral blood flow.

10 ent positron emission tomography of regional cerebral blood flow.

11 of white matter pathology, and a measure of cerebral blood flow.

12 trols, and is associated with alterations in cerebral blood flow.

13 matter abnormalities and changes in regional cerebral blood flow.

14 l artery occlusion (MCAO) with monitoring of cerebral blood flow.

15 fusion magnetic resonance imaging to measure cerebral blood flow.

16 on choice of reference region and changes in cerebral blood flow.

17 ratio of mean arterial pressure to regional cerebral blood flow.

18 ribes the link between neuronal activity and cerebral blood flow.

19 5)O-H2O PET showed no significant changes in cerebral blood flow.

20 vessels could be used as a means to increase cerebral blood flow.

21 es in cutaneous vasodilatation, sweating and cerebral blood flow.

22 t, the HBV compartment showed similar median cerebral blood flow (17 [range, 11-40] vs 14 [range, 6-2

23 0) relative to controls (interquartile range cerebral blood flow = 40.8-46.3 ml/100 g/min; oxygen ext

24 thly blood transfusions (interquartile range cerebral blood flow = 46.2-56.8 ml/100 g/min; oxygen ext

25 associated with 0.42 ml/min per 100 ml lower cerebral blood flow (95% confidence interval, 0.01 to 0.

26 is closely followed by a localised change in cerebral blood flow, a process termed neurovascular coup

27 Averaging regional cerebral blood flow across all tasks, the organic dyston

28 isease stage, amyloid-beta pathology affects cerebral blood flow across the span from controls to dem

29 Furthermore, despite an increase in cerebral blood flow after 2 hours of hypoxia (hypoxia vs

30 of arterial CO2 (Paco(2)) is a regulator of cerebral blood flow after brain injury.

31 Levosimendan increased cerebral blood flow after experimental cardiac arrest/ca

32 eater number of brain regions than those for cerebral blood flow alone.

33 d associations with Alzheimer's disease than cerebral blood flow alone.

34 ere assessed and haemodynamic variables (ie, cerebral blood flow and CBV) were measured in affected a

35 erebrovascular abnormalities such as altered cerebral blood flow and cerebral microinfarcts.

36 e aim of the present study was to assess the cerebral blood flow and cerebral oxygen extraction in ad

37 Hence, cerebral blood flow and cerebral oxygenation are importa

38 an arterial pressure, and reductions in mean cerebral blood flow and end-tidal CO2 during OLBNP.

39 was associated with a mild increase in both cerebral blood flow and femoral blood flow (P<0.05 versu

40 [(18)F]-fluorodeoxyglucose, to map regional cerebral blood flow and glucose metabolism, and with [(1

41 amyloid-beta had different associations with cerebral blood flow and grey matter volume.

42 Thus, pericytes are major regulators of cerebral blood flow and initiators of functional imaging

43 Moreover, we observed higher cerebral blood flow and lower oxygen saturation in femal

44 cosity early after cardiac arrest may reduce cerebral blood flow and may contribute to secondary brai

45 ted cancer survivors had significantly lower cerebral blood flow and metabolic activity in key brain

46 aemic penumbra suggested imaging of regional cerebral blood flow and metabolism would be required to

47 entration, oxygen saturation, and indices of cerebral blood flow and metabolism.

48 brain function is the tight coupling between cerebral blood flow and neuronal activity.

49 the long-term impact of low-grade GM-IVH on cerebral blood flow and neuronal health have not been fu

50 Prospective study measuring cerebral blood flow and oxygen extraction fraction using

51 Cerebral blood flow and oxygen extraction fraction were

52 o compare the effects of these strategies on cerebral blood flow and oxygenation.

53 lly undermine the capacity for regulation of cerebral blood flow and probably underlie several cerebr

54 all parameters had decreased in both groups, cerebral blood flow and regional cerebral blood flow (in

55 The changes in regional cerebral blood flow and regional metabolism can be asses

56 e was associated with sustained reduction in cerebral blood flow and restored DMN thalamo-cortical fu

57 apnoea and hypopnoea, along with changes in cerebral blood flow and sleep fragmentation.

58 easibility of using the relationship between cerebral blood flow and the BOLD signal to improve dynam

59 lations exhibited significant improvement in cerebral blood flow and the neurovascular coupling respo

60 ive metabolism, measured from the product of cerebral blood flow and the radial artery-jugular venous

61 The associations of amyloid-beta with cerebral blood flow and volume differed across the disea

62 ta pathology has different associations with cerebral blood flow and volume, and may cause more loss

63 lities are combined with long periods of low cerebral blood flow and/or circulatory arrest.

64 Brain hemodynamics (cerebral and regional cerebral blood flow) and cerebral oxygen metabolism (cer

65 termined by transcranial Doppler ultrasound (cerebral blood flow) and constant infusion thermodilutio

66 rea around intracranial monitoring (regional cerebral blood flow) and in bilateral supra-ventricular

67 ateral supra-ventricular brain areas (global cerebral blood flow) and was matched to cerebral physiol

68 reased cerebral vascular resistance, reduced cerebral blood flow, and a higher incidence of lacunar t

69 ional connection strength that is related to cerebral blood flow, and a phase shift parameter that is

70 MCA pseudofeeders are the result of impaired cerebral blood flow, and are thus a risk factor for furt

71 ionships between oxygen extraction fraction, cerebral blood flow, and clinical markers of cerebrovasc

72 ated with lower cognitive performance, lower cerebral blood flow, and greater white matter hyperinten

73 Cardiac index, local cerebral blood flow, and hemodynamic variables were meas

74 time, reproducibility and quantification of cerebral blood flow, and to measure cerebrovascular rese

75 ion tomography scans with H2(15)O to measure cerebral blood flow as a marker of neuronal activity.

76 The primary outcome was cerebral blood flow as a measure of resting brain activi

77 ce software segmentation was used to compare cerebral blood flow as measured with ASL.

78 CA) is a protective mechanism that maintains cerebral blood flow at a relatively constant level despi

79 l that different signaling cascades regulate cerebral blood flow at the capillary and arteriole level

80 with increased blood pressure and decreased cerebral blood flow both linked to in vivo biomarkers an

81 tly more accurate in predicting low regional cerebral blood flow (both p < 0.05).

82 imilar to those in the general population on cerebral blood flow, brain volumes, and dementia.

83 ght link between neuronal activity and local cerebral blood flow, but their precise identity, cellula

84 Between 2005 and 2012, we measured cerebral blood flow by 2-dimensional phase-contrast magn

85 tentials by electrophysiological recordings, cerebral blood flow by laser Doppler flowmetry, and oxyg

86 Little attention has been paid to cerebral blood flow (CBF) alterations in IGE detected by

87 Here, cerebral blood flow (CBF) and blood oxygen-level depende

88 ble to quantitatively measure the changes in cerebral blood flow (CBF) and cerebral oxygen metabolism

89 alized to the brain, resulting in changes in cerebral blood flow (CBF) and metabolism in these patien

90 responses in rat barrel cortex, measured by cerebral blood flow (CBF) and neurophysiological recordi

91 The role of pericytes in the regulation of cerebral blood flow (CBF) and neurovascular coupling rem

92 Cerebral blood flow (CBF) and oxygen extraction fraction

93 This pilot study aims to evaluate cerebral blood flow (CBF) and oxygen metabolism (CMRO2)

94 and to assess potential correlations between cerebral blood flow (CBF) and quantitative histologic mi

95 o produce spatial maps displaying changes in cerebral blood flow (CBF) and RSFC after MDMA administra

96 Resting cerebral blood flow (CBF) and task-related activation of

97 tion ratios taking into account an increased cerebral blood flow (CBF) at a Gp of less than 2 mmol/L

98 ; and (2) that pharmacological reductions in cerebral blood flow (CBF) at baseline would lower the 'C

99 nerve induces pressor response and improves cerebral blood flow (CBF) by activating the rostral vent

100 Resting-state regional cerebral blood flow (CBF) can be measured noninvasively

101 brain voxelwise analysis of the ASL relative cerebral blood flow (CBF) data, receiver operating chara

102 Disease-related phenotypes, including cerebral blood flow (CBF) deficits, white matter lesions

103 blood oxygenation level-dependent (BOLD) and cerebral blood flow (CBF) fMRI during unilateral median

104 ental properties of brain physiology such as cerebral blood flow (CBF) have never been investigated.

105 n labeling provided measurements of regional cerebral blood flow (CBF) in 12 alcoholics and 12 contro

106 ial spin labeling, we measured resting-state cerebral blood flow (CBF) in 29 adult smokers across fou

107 dy, we showed that a high-fat meal decreased cerebral blood flow (CBF) in homeostatic brain areas (hy

108 e first study to show regional reductions in cerebral blood flow (CBF) in response to decreased oxyge

109 aining a spontaneous and instant increase of cerebral blood flow (CBF) in response to neural activati

110 O2, which has previously been shown to evoke cerebral blood flow (CBF) increases via the release of t

111 In our study, we found that Cerebral Blood Flow (CBF) is 90.91% sensitive and 100% s

112 Cerebral blood flow (CBF) is controlled by arterial bloo

113 Animal models suggest that reduced cerebral blood flow (CBF) is one of the most enduring ph

114 Cessation of cerebral blood flow (CBF) leads to cell death in the inf

115 Decreased cerebral blood flow (CBF) may contribute to the patholog

116 Changes in cerebral blood flow (CBF) may occur with acute exposure

117 ional anisotropy (FA), fiber number (FN) and cerebral blood flow (CBF) measurements.

118 his approach may be influenced by changes in cerebral blood flow (CBF) or radiotracer clearance.

119 determine whether cocaine-induced changes in cerebral blood flow (CBF) reflect neuronal activation or

120 nkage between elevated TIMP3 and compromised cerebral blood flow (CBF) remains unknown.

121 ly induced BOLD responses decreased, whereas cerebral blood flow (CBF) responses increased.

122 which dilate arterioles, increasing in turn cerebral blood flow (CBF) to areas with increased metabo

123 Cerebral blood flow (CBF) was measured at the internal c

124 Following this training period, hippocampal cerebral blood flow (CBF) was measured by functional mag

125 Cerebral blood flow (CBF) was measured using colour-code

126 Infarct volume and cerebral blood flow (CBF) were measured.

127 orrhagic hypotension (HH) and resuscitation, cerebral blood flow (CBF) would decrease more in aged co

128 indicators: (1) global and regional resting cerebral blood flow (CBF), (2) oxygen extraction fractio

129 to determine MB's effect on glucose uptake, cerebral blood flow (CBF), and cerebral metabolic rate o

130 were used to study structural connectivity, cerebral blood flow (CBF), and corticospinal excitabilit

131 r Hb, higher brain blood density, lower mean cerebral blood flow (CBF), and significant cerebral circ

132 ated the local relationships between DVR and cerebral blood flow (CBF), as well as relative CBF (R1),

133 e exercise is associated with a reduction in cerebral blood flow (CBF), but regulation of CBF during

134 opathy have abnormal vascular reactivity and cerebral blood flow (CBF), but, to our knowledge, abnorm

135 impaired neurovascular coupling, and reduced cerebral blood flow (CBF), caused by cortical vasoconstr

136 Increased visual cortex cerebral blood flow (CBF), decreased visual cortex alpha

137 adrenalin (NA), modulates cortical activity, cerebral blood flow (CBF), glucose metabolism, and blood

138 DWLS enabled rapid identification of cerebral blood flow (CBF), prediction of infarct area an

139 very (R1) parameters as surrogate indices of cerebral blood flow (CBF), with a secondary goal of dire

140 er (BBB) disruption, cerebral apoptosis, and cerebral blood flow (CBF).

141 e facial nerve for the purpose of increasing cerebral blood flow (CBF).

142 erstitial brain tissue (Pbto2), and regional cerebral blood flow (CBF).

143 n vivo validation was performed, in which 3D cerebral-blood-flow (CBF) networks in mouse brain over a

144 bral oxygen saturation (SO2) and an index of cerebral blood flow (CBFi) at the infant's bedside and c

145 ume ratios, apparent diffusion coefficients, cerebral blood flow, cerebral blood volume, and intratum

146 ence standard were 4.5%, 5.0%, and 1.9%, for cerebral blood flow, cerebral blood volume, and mean tra

147 Cerebral blood flow, cerebral blood volume, cerebral oxy

148 ress syndrome, cerebral blood flow, regional cerebral blood flow, cerebral oxygen delivery, and cereb

149 ct diagnosis, APOE epsilon4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and p

150 TMPAP expression had no effect on resting cerebral blood flow, cerebrovascular reactivity, and neu

151 Basal and activity-dependent cerebral blood flow changes are coordinated by the actio

152 resulted in elevated cardiac index and local cerebral blood flow compared with vehicle after cardiac

153 Regional cerebral blood flow correlated significantly with global

154 educed intracerebral thrombosis and improved cerebral blood flow could be identified as underlying me

155 jects, neither positive clinical effects nor cerebral blood flow decreases were detected.

156 sess whole-brain oxygen extraction fraction, cerebral blood flow, degree of vasculopathy, severity of

157 mechanism responsible for relatively stable cerebral blood flow despite changes of systemic blood pr

158 hock is associated with severe impairment of cerebral blood flow despite correction of arterial hypot

159 gies in different trajectories, we tested if cerebral blood flow differed between amyloid-beta-negati

160 relative to both non-demented groups, but no cerebral blood flow differences between non-demented amy

161 sodilatation, sweating and the reductions in cerebral blood flow during a hot flush.

162 in cutaneous vasodilatation, sweat rate and cerebral blood flow during a hot flush.

163 e last two decades, physiological studies of cerebral blood flow dynamics have demonstrated that subs

164 ed diminished inferior parietal and temporal cerebral blood flow for patients with Alzheimer's diseas

165 (5% CO2 ) confirmed that these reductions in cerebral blood flow from hypoxia were related to vasocon

166 lowing 4-6 days at high altitude (HA) global cerebral blood flow (gCBF) increases to preserve cerebra

167 While the effect of neural activity on cerebral blood flow has been extensively studied, whethe

168 the association between kidney function and cerebral blood flow has yet to be determined.

169 ypertonic saline on neuronal survival and on cerebral blood flow have been shown in several animal mo

170 BF), but, to our knowledge, abnormalities in cerebral blood flow have not been reported for healthy i

171 Reduced cerebral blood flow impairs cognitive function and ultim

172 a and orbitofrontal cortex; altered regional cerebral blood flow in a pattern reminiscent of the obse

173 LDL-C variability was associated with lower cerebral blood flow in both trial arms (P=0.031 and P=0.

174 e hyperactivity and hypoactivity of regional cerebral blood flow in brain regions in cocaine-dependen

175 gnetic resonance imaging to measure regional cerebral blood flow in brain regions susceptible to agei

176 Isoflurane increases regional cerebral blood flow in comparison to propofol.

177 d associations of amyloid-beta with regional cerebral blood flow in healthy controls (n = 51), early

178 ositron emission topographic measurements of cerebral blood flow in humans have consistently reported

179 in the brain to couple neuronal activity and cerebral blood flow in normal and pathologic states.

180 t could account in part for the reduction in cerebral blood flow in patients with Alzheimer's disease

181 cytes are not contractile, and regulation of cerebral blood flow in physiological and pathological co

182 urements of BOLD, cerebral blood volume, and cerebral blood flow in regions of positive and negative

183 technology that provides a direct measure of cerebral blood flow in response to cognitive activity.

184 vent of transcranial Doppler, measurement of cerebral blood flow in response to transient changes in

185 h -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, includ

186 igher amyloid-beta load was related to lower cerebral blood flow in several regions, independent of d

187 , while there is reliably increased regional cerebral blood flow in sgPFC in MDD, no such abnormality

188 level, diabetes is associated with abnormal cerebral blood flow in surviving brain regions and great

189 h muscle cells are key players in regulating cerebral blood flow in the healthy state and contribute

190 r diseases showed decreased resting regional cerebral blood flow in the lateral parieto-occipital ass

191 The decrease in cerebral blood flow in the primary auditory cortex corre

192 Successful therapy corresponded to decreased cerebral blood flow in the primary auditory cortex, supp

193 AI accompanied by locally increased regional cerebral blood flow in the right ventral AI); and distur

194 ntional individuals showed increased resting cerebral blood flow in the ventral striatum and ventrome

195 Cerebral blood flow in these brain regions correlated wi

196 oth groups, cerebral blood flow and regional cerebral blood flow (in inner and cerebellum brainstem r

197 hanisms must be playing hand in hand, namely cerebral blood flow increase and microvascular flow homo

198 ating effect on cerebral vessels producing a cerebral blood flow increase.

199 Similar to seizures, cerebral blood flow increases in patients with PDs to co

200 that an elevated ratio of blood pressure to cerebral blood flow, indicative of cerebrovascular resis

201 Evidence indicates that cerebral blood flow is both increased and diminished in

202 The precise regulation of cerebral blood flow is critical for normal brain functio

203 Continuous cerebral blood flow is essential for neuronal survival,

204 Cerebral blood flow is highly sensitive to changes in CO

205 Cerebral blood flow is one brain phenotype that is known

206 erebral oximetry index approaches 1, because cerebral blood flow is pressure passive.

207 Impaired oxygen delivery due to reduced cerebral blood flow is the hallmark of delayed cerebral

208 erval: 0.92, 0.98]) and with delay-corrected cerebral blood flow less than 30% in patients with compl

209 mm (P = .04) and the core volume measured as cerebral blood flow less than 30% was underestimated whe

210 with a delay time of more than 2 seconds and cerebral blood flow less than 40% provided the most accu

211 o-creatinine ratio was associated with lower cerebral blood flow level (difference in cerebral blood

212 tient selection and ancillary assessments of cerebral blood flow likely have a significant role.

213 poperfusion (defined as an oligemic regional cerebral blood flow < 35 mL/100 g/min) was examined usin

214 tients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling

215 obe, apparently normal tissue) combined with cerebral blood flow measurements using perfusion CT.

216 ted whether developmental sex differences in cerebral blood flow mediated sex differences in anxiety

217 wer cerebral blood flow level (difference in cerebral blood flow [milliliters per minute per 100 ml]

218 l cerebral blood flow (n = 16), low regional cerebral blood flow (n = 14) measurements had a higher p

219 Compared with normal regional cerebral blood flow (n = 16), low regional cerebral bloo

220 at levosimendan exerts beneficial effects on cerebral blood flow, neuronal injury, neurological outco

221 onance (MR) imaging technique used to assess cerebral blood flow noninvasively by magnetically labeli

222 ume (nrCBV) and Gaussian-normalized relative cerebral blood flow (nrCBF) maps.

223 results when hypoxia-associated increases in cerebral blood flow occur in the context of restricted v

224 s greater than 3 seconds and delay-corrected cerebral blood flow of less than 30% (P = .34 and .33, r

225 l reconstruction and their relationship with cerebral blood flow, oxygen delivery, and carbon dioxide

226 circle had greater asymmetry in hemispheric cerebral blood flow (p = 0.05).

227 icit, intracellular pH (P < 0.0001), but not cerebral blood flow (P = 0.31), differed between tissue

228 44%, respectively) with increasing amount of cerebral blood flow (P<0.05).

229 od flow correlated significantly with global cerebral blood flow (Pearson r = 0.70, p < 0.01).

230 irment, alterations in neural activation and cerebral blood flow perturbations can occur and may cont

231 t was obtained with oxygen-15 water regional cerebral blood flow PET in 39 healthy women genotyped fo

232 d by quantifying metabolic RSN expression in cerebral blood flow PET scans acquired at rest and durin

233 or blood-brain barrier damage and had higher cerebral blood flow postreoxygenation compared with the

234 Regional cerebral blood flow (rCBF) and volume (rCBV) were measur

235 Using regional cerebral blood flow (rCBF) as a marker of basal neuronal

236 s study was undertaken to determine regional cerebral blood flow (rCBF) changes representing ongoing

237 rtial brain tissue oxygenation, and regional cerebral blood flow (rCBF) did not reach significance, b

238 tudy was to determine if changes in regional cerebral blood flow (rCBF) during hypoglycemia relative

239 ngitudinal changes in resting state regional cerebral blood flow (rCBF) during normal aging and inves

240 als with H(2) (1)(5)O PET to assess regional cerebral blood flow (rCBF) during rest and tested for be

241 re IN-OT-induced changes in resting regional cerebral blood flow (rCBF) in 32 healthy men.

242 imaging was used to measure resting regional cerebral blood flow (rCBF) in 52 individuals at ultra-hi

243 effect of age and diagnosis on glutamate and cerebral blood flow (rCBF) in adults with SZ and healthy

244 face area, subcortical volumes, and regional cerebral blood flow (rCBF) in healthy controls (HC) (n =

245 itivity and high resolution, and of regional cerebral blood flow (rCBF) in the brain of transgenic AP

246 We measured regional cerebral blood flow (rCBF) using pseudo-continuous arter

247 Regional cerebral blood flow (rCBF) was measured within and outsi

248 We compared longitudinal changes in regional cerebral blood flow (rCBF), assessed by (15)O-water PET,

249 asures of brain physiology, such as regional cerebral blood flow (rCBF), remains incompletely underst

250 ting for an AD-related reduction in regional cerebral blood flow (rCBF).

251 working memory-related hippocampal regional cerebral blood flow (rCBF).

252 g the previously validated measure (relative cerebral blood flow [rCBF], <30%), thrombectomy patients

253 h amyloid-beta being associated with greater cerebral blood flow reduction in controls and greater vo

254 gside ventricular and venous vessel volumes, cerebral blood flow, regional brain volumes, and intracr

255 rm lambs with respiratory distress syndrome, cerebral blood flow, regional cerebral blood flow, cereb

256 Moreover, the stroke effects on multiscale cerebral blood flow regulation could not be detected by

257 of stroke, cognitive decline and diminished cerebral blood flow regulation.

258 eable binding potential [BPND]) and relative cerebral blood flow (relative delivery [R1]) at voxel le

259 Cerebral blood flow required for tissue survival was hig

260 Change in the cerebral blood flow response to an acute challenge with

261 s of methylphenidate treatment increased the cerebral blood flow response to methylphenidate within t

262 d cerebrospinal fluid by 60-80% and improved cerebral blood flow responses and hippocampal function a

263 Therefore, we examined cerebral blood flow responses to augmented arterial pres

264 These effects might induce cerebral blood flow responses to brain inflammation.

265 To test this, we measured NBG, BOLD, and cerebral blood flow responses to stimuli that either cor

266 otective effects in morality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm o

267 untreated hypertensive patients (n=20) had a cerebral blood flow similar to age-matched controls (n=2

268 Mean arterial pressure, cardiac output, cerebral blood flow, skeletal muscular oxygen partial pr

269 y demonstrated that BDG patients had greater cerebral blood flow than did Fontan patients and that an

270 BDG patients had significantly higher cerebral blood flow than did Fontan patients.

271 and also elicits dynamic changes in regional cerebral blood flow that range from physiological neurov

272 PET allows the quantification of regional cerebral blood flow, the regional oxygen extraction frac

273 ain brain homeostasis, and the regulation of cerebral blood flow to adequately couple energy supply t

274 eostatic processes, including matching local cerebral blood flow to neuronal metabolism (neurovascula

275 the CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-i

276 oride application followed by measurement of cerebral blood flow using a combination of laser Doppler

277 the acetazolamide-induced change in regional cerebral blood flow using SPECT with (99m)Tc-labeled hex

278 lood volume and Gaussian-normalized relative cerebral blood flow values (area under the receiver oper

279 compared with pH-stat strategy and decreases cerebral blood flow velocities in survivors.

280 fTCD can be gained when considering the raw cerebral blood flow velocity (CBFV) recordings.

281 In contrast, cerebral-blood-flow velocity (CBFv) in arteries and vein

282 moglobin was 9.7 g/dL (range, 6.9-12.9), and cerebral blood flow was 43 +/- 11 mL/100 g/min.

283 tion between circle of Willis variations and cerebral blood flow was also analyzed.

284 Cerebral blood flow was higher in the cerebral perfusion

285 gen extraction fraction (P < 0.0001) but not cerebral blood flow was increased in participants with h

286 Cerebral blood flow was measured using perfusion CT in t

287 with subdural electrode strips and regional cerebral blood flow was measured with a parenchymal ther

288 y 10 hours, when AMS symptoms had developed, cerebral blood flow was normal (Delta-51ml/min(-1) , 95%

289 Cerebral blood flow was reduced in patients with dementi

290 Cerebral blood flow was significantly decreased in the p

291 t blood viscosity plays an important role in cerebral blood flow, we investigated the feasibility to

292 In addition, (15)O-H2O scans to measure cerebral blood flow were acquired before each (11)C-erlo

293 Protocol B: Myocardial and cerebral blood flow were measured in seven pigs before v

294 ness, cerebral metabolic rate of glucose and cerebral blood flow were preferentially decreased in the

295 , pro-inflammatory signalling, and protected cerebral blood flow, when determined 1 to 3 days post-in

296 gnals provide valuable information about the cerebral blood flow which can be utilized in further val

297 STRACT: Hypoxia causes an increase in global cerebral blood flow, which maintains global cerebral oxy

298 Hypoxia causes an increase in global cerebral blood flow, which maintains global cerebral oxy

299 iological effects of TMS on AVH, we measured cerebral blood flow with pseudo-continuous magnetic reso

300 rse association exists of various indexes of cerebral blood flow with these brain lesions.