ライフサイエンスコーパス: hypoperfusion

1 yperaemia) to pathological inverse coupling (hypoperfusion).

2 core of ischemia to the areas of less severe hypoperfusion.

3 , and reduce end-organ injury from prolonged hypoperfusion.

4 EEG silence during transient global cerebral hypoperfusion.

5 EEG silence during transient global cerebral hypoperfusion.

6 oid-beta are differentially impacted by mild hypoperfusion.

7 Time to peak (TTP) was employed to detect hypoperfusion.

8 (AKI) occurred at 24 h in rats subjected to hypoperfusion.

9 r after only 5 mins of cerebral ischemia and hypoperfusion.

10 Base deficit was used as a measure of tissue hypoperfusion.

11 and assess its relationship with acute-stage hypoperfusion.

12 rtional to both injury severity and systemic hypoperfusion.

13 pendently with severity of injury and tissue hypoperfusion.

14 correlation between FMZ binding and initial hypoperfusion.

15 products, reductions in microcirculation and hypoperfusion.

16 d failed to show a relationship with initial hypoperfusion.

17 ith intracranial stenosis to protect against hypoperfusion.

18 deficit (BD) was used as a measure of tissue hypoperfusion.

19 with normal vital signs but ongoing, occult hypoperfusion.

20 vascular lumen, resulting in prolonged renal hypoperfusion.

21 racellular potassium, and in part because of hypoperfusion.

22 when organ dysfunction occurs as a result of hypoperfusion.

23 l velocities did not identify subendocardial hypoperfusion.

24 cardiac output are associated with cerebral hypoperfusion.

25 zation, heparin-induced thrombocytopenia, or hypoperfusion.

26 associated with different sites of cortical hypoperfusion.

27 to increase oxygen extraction in response to hypoperfusion.

28 r procedures and are at risk for spinal cord hypoperfusion.

29 e oxygen unloading during hypocapnia-induced hypoperfusion.

30 lt of experimental atherosclerosis and renal hypoperfusion.

31 adiol augments the PGHS response to cerebral hypoperfusion.

32 therwise modify the Fos response to cerebral hypoperfusion.

33 at it modulates the Fos response to cerebral hypoperfusion.

34 rking memory and white matter function after hypoperfusion.

35 phasia or neglect showed concurrent cortical hypoperfusion.

36 or neglect, and for the presence of cortical hypoperfusion.

37 strongly predicts cortical ischaemia and/or hypoperfusion.

38 can be accounted for by concurrent cortical hypoperfusion.

39 stroke can be largely explained by cortical hypoperfusion.

40 availability regulate fatty acid use during hypoperfusion.

41 idence of occlusive vasculopathy or cerebral hypoperfusion.

42 ymptoms, such as syncope and end-stage organ hypoperfusion.

43 nd regained in the setting of acute cerebral hypoperfusion.

44 ble in 39 of the 47 patients with asymmetric hypoperfusion.

45 rysm can be one possible cause of pancreatic hypoperfusion.

46 d is driven by significant tissue injury and hypoperfusion.

47 groups: Group A = no pulmonary congestion/no hypoperfusion = 14 (3%), Group B = isolated pulmonary co

48 ary congestion = 32 (6%), Group C = isolated hypoperfusion = 158 (28%) and Group D = congestion with

49 shed ARDS who do not have evidence of tissue hypoperfusion (1C); protocols for weaning and sedation (

50 face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% to 57%) to compensate for reductions

51 on = 158 (28%) and Group D = congestion with hypoperfusion = 367 (64%).

52 rarefaction of brain microvessels, cerebral hypoperfusion, a disrupted blood-brain barrier (BBB), an

53 Hypoperfusion abnormalities evidenced by SPECT are more

54 rometabolic and cerebrovascular responses to hypoperfusion after traumatic brain injury.

55 We hypothesized that estrogen and cerebral hypoperfusion alone would augment Fos abundance in vario

56 erence between stress and rest TPD or stress hypoperfusion analysis.

57 Recent data suggest that cerebral hypoperfusion and activation of cerebral ion transporter

58 tribute, BR14 can define regions of relative hypoperfusion and also discriminate between infarcted an

59 opathy occurs only in the presence of tissue hypoperfusion and appears to occur without significant c

60 ngle density despite greater left-hemisphere hypoperfusion and atrophy during life.

61 graine and stroke might both be triggered by hypoperfusion and could therefore exist on a continuum o

62 n-dependent increase in severity of cerebral hypoperfusion and extension of ischaemic pathology beyon

63 erentiate intrinsic renal disease from renal hypoperfusion and helps guide the decision for OHT alone

64 ma and hemorrhage are associated with tissue hypoperfusion and hypoxemia, changes in oxygen delivery

65 Acute renal failure resulting from hypoperfusion and hypoxia is a significant clinical prob

66 Although interictal hypoperfusion and ictal hyperperfusion are established l

67 ects is similar to the pattern of interictal hypoperfusion and ictal hyperperfusion that has been obs

68 o study patients with unilateral hemispheric hypoperfusion and impaired vasomotor reactivity from cri

69 irculation in patients with septic shock are hypoperfusion and increased flow heterogeneity.

70 zer of nNOS, reverses PAF-induced intestinal hypoperfusion and injury.

71 onal changes in the vasculature that promote hypoperfusion and ischemia, while also affecting the ext

72 resonance (MR) imaging to detect myocardial hypoperfusion and microinfarction in a swine model of co

73 ascular uncoupling, vessel regression, brain hypoperfusion and neurovascular inflammation.

74 ly conflicting data showing microcirculatory hypoperfusion and normal or even increased blood flow in

75 ts exposed to hypoxia, which may result from hypoperfusion and placental injury.

76 onse syndrome and contribute to distal organ hypoperfusion and pulmonary hypertension.

77 consistent with possible effects of cerebral hypoperfusion and reperfusion injury.

78 decreased blood flow, mucosal ischemia, and hypoperfusion and reperfusion injury.

79 oagulopathy occurs in the presence of tissue hypoperfusion and severe traumatic injury and is mediate

80 Patients with tissue hypoperfusion and severe traumatic injury showed a stron

81 mentia since it may lead to chronic cerebral hypoperfusion and stroke.

82 We identified areas of hypoperfusion and structural damage with magnetic resona

83 ed RBC alterations will directly cause organ hypoperfusion and suggest that T/HS-induced RBC damage c

84 lenge in patients with sepsis-induced tissue hypoperfusion and suspicion of hypovolemia to achieve a

85 Chronic cerebral hypoperfusion and VaD was induced by bilateral common ca

86 eurological consequences of chronic cerebral hypoperfusion and VaD.

87 ction in an animal model of chronic cerebral hypoperfusion and vascular dementia (VaD).

88 er this is attributable to peripheral tissue hypoperfusion and/or cellular hypoxia, simultaneous meas

89 sent study, we tested the effect of cerebral hypoperfusion and/or estradiol on the expression of Fos,

90 The data collected at baseline, peak hypoperfusion, and 5 and 10 min post hypoperfusion was a

91 oangiopathy with destruction of capillaries, hypoperfusion, and inflammatory cell stress on the perif

92 rrant angiogenesis, vessel regression, brain hypoperfusion, and inflammatory responses, may initiate

93 zed that early coagulopathy is due to tissue hypoperfusion, and investigated derangements in coagulat

94 ay include ischemic injury from microemboli, hypoperfusion, and other factors resulting from major su

95 erin on PAF-induced bowel injury, mesenteric hypoperfusion, and systemic inflammation.

96 Both amyloid-beta accumulation and hypoperfusion are likely to cause the upregulation of VE

97 ological mechanisms, such as anaesthesia and hypoperfusion, are also involved.

98 egion linked to infarcts suggested transient hypoperfusion as a pathogenic mechanism, a hypothesis pr

99 el-fluid phase induces vascular collapse and hypoperfusion as a primary mechanism of treatment resist

100 posterior circulation stroke, with regional hypoperfusion as an important potential contributor to s

101 They found resting hypoperfusion at 1 hour that persisted at 1 week.

102 partially reversed the HS/CR-induced hepatic hypoperfusion at 3 and 4 hours postresuscitation compare

103 ssure monitoring alone in detecting cerebral hypoperfusion at the bedside in patients with severe tra

104 patients with severe sepsis with evidence of hypoperfusion at the time of ED presentation.

105 patients with severe sepsis with evidence of hypoperfusion at the time of emergency department (ED) p

106 s infection/inflammation (INF), air trapping/hypoperfusion (AT), normal/hyperperfusion (NOR), and bul

107 te that CE in DKA is accompanied by cerebral hypoperfusion before treatment and suggest that blocking

108 ocardial thinning suggests an early stage of hypoperfusion, before the development of local wall moti

109 on was defined as >50% reduction in critical hypoperfusion between the baseline CT perfusion and the

110 ritical stenosis of medullary arterioles and hypoperfusion (Binswanger's disease).

111 ch as the kidneys are challenged not only by hypoperfusion but also by the high concentrations of pla

112 , patients with global left ventricular (LV) hypoperfusion but normal RV perfusion may have increased

113 sion/stenosis with sparse collaterals showed hypoperfusion by both of the two approaches, one with ab

114 uroimaging studies show that cocaine-induced hypoperfusion can persist even after 6 months of abstine

115 Hypoperfusion can result in deficits on complex and simp

116 much more strongly associated with cortical hypoperfusion (chi(2) = 57.3 for aphasia; chi(2) = 28.7

117 ssive intestinal vasoconstriction and tissue hypoperfusion compared to baseline flow.

118 The AD group showed significant regional hypoperfusion, compared with the CN group, in the right

119 In the absence of tissue hypoperfusion, coronary artery disease, or acute hemorrh

120 her ictal perfusion changes, both hyper- and hypoperfusion, correspond to electrically connected brai

121 posterior cerebral circulation and cerebral hypoperfusion could partially explain the pathogenesis o

122 Mortality was associated with relative "hypoperfusion" (CPP<CPPopt), severe disability with "hyp

123 racranial pressure and treatment of cerebral hypoperfusion decrease secondary injury.

124 intracranial monitoring to predict cerebral hypoperfusion (defined as an oligemic regional cerebral

125 d low cardiac output, or b) ongoing signs of hypoperfusion despite achieving adequate intravascular v

126 and T2WI findings following MTBI, persistent hypoperfusion developed that was not associated with cyt

127 f migraine auras may belong to a spectrum of hypoperfusion disorders along with transient ischemic at

128 e, we suggest that changes in blood vessels, hypoperfusion disorders, and microembolisation can cause

129 ular disease, theoretically because systemic hypoperfusion disrupts cerebral perfusion, contributing

130 , patients with no evidence of congestion or hypoperfusion (dry-warm, n = 123); profile B, congestion

131 d as WMH, is associated with posterior brain hypoperfusion during acute increase in arterial pressure

132 Kidney hypoperfusion during episodes of systemic hypotension or

133 Interestingly, however, cerebral blood flow hypoperfusion during the generalization phase (but not p

134 controls but no evidence of deoxygenation or hypoperfusion during vasodilatory stress.

135 verely injured trauma patients with signs of hypoperfusion (eg, base deficit, hypotension) and need f

136 essure (</=65 mm Hg) accompanied by signs of hypoperfusion (eg, oliguria, hyperlactemia, poor periphe

137 In summary, cerebral hypoperfusion either at rest or induced by hypocapnia at

138 tudy indicates that a single, mild, cerebral hypoperfusion event produces profound and long lasting e

139 ment should not remain underfilled if tissue hypoperfusion exists, acknowledging the above difficulti

140 independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on cerebral oxygen delive

141 measured in rats to test the hypotheses that hypoperfusion follows severe ischemia in the retina and

142 is event lasted over an hour, is mediated by hypoperfusion, generalizes to people with epilepsy, and

143 The 37 patients with evidence of resting hypoperfusion had evidence of improved resting perfusion

144 Cerebral hypoperfusion has previously been associated with mild c

145 branch retinal vein occlusion (BRVO) causes hypoperfusion, high levels of vascular endothelial growt

146 We also propose inflammatory and hypoperfusion hypotheses, concepts that link underlying

147 ry to anaerobic glycolysis induced by tissue hypoperfusion, hypoxia, or both.

148 seizures, since the occurrence of postictal hypoperfusion/hypoxia results in a separate set of neuro

149 We hypothesized that episodes of hypoperfusion/hypoxia, as observed during acute chest sy

150 pairments are the consequence of this severe hypoperfusion/hypoxic event.

151 elay in BOLD signal corresponded to areas of hypoperfusion identified by contrast-based perfusion MRI

152 both filling status and the degree of tissue hypoperfusion (if present), and a precise evaluation of

153 of alpha-synuclein, (2) OH-mediated cerebral hypoperfusion impairs cognition and (3) the two act syne

154 onuclide lung scan reports showed asymmetric hypoperfusion in 47 of 410 consecutive patients referred

155 directly from an area of infarction or from hypoperfusion in adjacent tissue, to more global cogniti

156 ent hemodynamic treatment of hypotension and hypoperfusion in critically ill patients is directed at

157 specific dynamics following chronic cerebral hypoperfusion in mice.

158 ometabolism extended over wider regions than hypoperfusion in patient groups compared with controls.

159 h was seen in 34.5% of our patients; and (c) hypoperfusion in PISPECT did have localizing value when

160 T in our series was due to the occurrence of hypoperfusion in PISPECT, which was seen in 34.5% of our

161 omising alternative to DSC-PWI for detecting hypoperfusion in subacute stroke patients who had obviou

162 cal infarctions are associated with cortical hypoperfusion in subjects with aphasia/neglect; (ii) tha

163 , we developed an oligemic model of cerebral hypoperfusion in the 3xTg-AD mouse model of AD.

164 Although cerebral hypoperfusion in the aged rats was not associated with i

165 sociated with atrophy, hypometabolism and/or hypoperfusion in the dorsolateral prefrontal cortex, the

166 and physiological responses to white matter hypoperfusion in the human brain.

167 A transient hypoperfusion in the injured cerebral region, followed b

168 ge,.43 to.60), especially when patients with hypoperfusion in the lung adjacent to a central mediasti

169 reflect changes in neurotransmitters and/or hypoperfusion in the midbrain.

170 The pattern of hypoperfusion in the placebo state followed by heightene

171 (OH) is a common cause of transient cerebral hypoperfusion in the population.

172 ere accounted for, the AD group still showed hypoperfusion in the right inferior parietal lobe extend

173 inant function analysis, using the degree of hypoperfusion in various Brodmann's areas--BA 22 (includ

174 e compared the relative localizing values of hypoperfusion in video-electroencephalographically (EEG)

175 eto-occipital dysfunction (hypometabolism or hypoperfusion) in all 7 tested patients CONCLUSIONS: Vis

176 this binding loss is proportional to initial hypoperfusion, in keeping with the hypothesis that the r

177 d from myocardial microvascular rarefaction, hypoperfusion, increased deposition of interstitial fibr

178 is laboratory has demonstrated that cerebral hypoperfusion increases the expression of prostaglandin

179 rct (or dense ischaemia) on DWI and cortical hypoperfusion indicated by PWI, was evaluated with chi-s

180 e white matter tract there was an absence of hypoperfusion-induced alterations in the proportion of 5

181 mination the same day to identify regions of hypoperfusion/infarct of 16 Brodmann areas.

182 mechanisms for the disorder include cerebral hypoperfusion, inflammation, gene polymorphisms, and mol

183 the molecular and cellular pathways by which hypoperfusion influenced tau and amyloid-beta proteins.

184 although the underlying mechanisms by which hypoperfusion influences AD neuropathology remains unkno

185 espite the mild and transient nature of this hypoperfusion injury, the pattern of decreased total tau

186 novel finding that a single, mild, transient hypoperfusion insult acutely increases Abeta levels by e

187 Inducible hypoperfusion is a common finding in hypertrophic cardio

188 Chronic cerebral hypoperfusion is a major cause of age-related vascular c

189 There is clinical evidence that intestinal hypoperfusion is a major factor in progressive organ fai

190 Cerebral hypoperfusion is among the mechanisms that may explain t

191 Cerebral hypoperfusion is associated with accelerated cognitive d

192 diminished vasodilatory capacity and tissue hypoperfusion is associated with impaired wound healing,

193 asia/neglect; (ii) that reversal of cortical hypoperfusion is associated with resolution of the aphas

194 f these studies indicates that chronic brain hypoperfusion is linked to AD risk factors, AD preclinic

195 into the pathophysiology of CAD; myocardial hypoperfusion is not necessarily commensurate with deoxy

196 The significance of ictal hypoperfusion is not well understood.

197 Postischemic hypoperfusion is present in the rat retina 60 minutes af

198 Cerebral hypoperfusion is widely implicated in cognitive impairme

199 HS-2 gene expression in response to cerebral hypoperfusion/ischemia in neurons, we used a cell cultur

200 oform of this enzyme, is induced by cerebral hypoperfusion/ischemia.

201 target of 7-9 g/dL in the absence of tissue hypoperfusion, ischemic coronary artery disease, or acut

202 remains a useful method for detecting global hypoperfusion its sensitivity to regional ischaemia is l

203 pericyte constrictions were a major cause of hypoperfusion leading to thrombosis and distal microvasc

204 an result in thromboembolism with or without hypoperfusion leading to transient or permanent cerebral

205 erebral blood volume (VLCBV), diffusion, and hypoperfusion lesion volumes have been proposed as predi

206 owerful predictor than baseline diffusion or hypoperfusion lesion volumes.

207 selective impairment in each case was due to hypoperfusion (low blood flow) in left posterior inferio

208 e significant only in AHF (signs of cerebral hypoperfusion, low serum sodium, chronic obstructive pul

209 In contrast, transient hypoperfusion markedly decreases total tau levels, coinc

210 this presentation, although primary arterial hypoperfusion may also be an etiology.

211 rior circulation and the associated cerebral hypoperfusion may be a factor in triggering hypertension

212 findings suggest that vasculopathy and focal hypoperfusion may be factors in the development of sickl

213 ut recent data instead suggest that cerebral hypoperfusion may be involved and that activation of cer

214 Fibrin emboli and focal hypoperfusion may explain the development of many sporad

215 Chronic hypoperfusion may put these people at risk for neuronal

216 ot investigation of whether chronic cerebral hypoperfusion might affect genomic distribution of these

217 is that concurrent early atherosclerosis and hypoperfusion might have greater early deleterious effec

218 effect of soluble thrombomodulin (sTM) in a hypoperfusion model of ischemic kidney injury.

219 from 69+/-8 to 41+/-7 mL/min (P:<0.05), with hypoperfusion most severe in the subendocardium.

220 value of tissue oximetry to detect systemic hypoperfusion, multisite NIRS such as a combination of c

221 ted against PAF-induced intestinal necrosis, hypoperfusion, neutrophil influx, and NOS suppression.

222 lue when it occurred on the same side as the hypoperfusion noted in IISPECT.

223 for detecting and quantifying the extent of hypoperfusion observed with SPECT perfusion imaging.

224 he viewer) was most strongly associated with hypoperfusion of right superior temporal gyrus (Fisher's

225 ion level-dependent (BOLD) data in detecting hypoperfusion of subacute stroke patients through compar

226 retinal artery occlusion demonstrate marked hypoperfusion of the deep capillary plexus.

227 e in MAG:PLP1 strongly suggests pathological hypoperfusion of the frontal cortex in Alzheimer's disea

228 It suggests hypoperfusion of the gut mucosa.

229 icular, potential barrier disruptors such as hypoperfusion of the gut, infections and toxins, but als

230 he viewer) was most strongly associated with hypoperfusion of the right angular gyrus (p < 0.0001).

231 Perioperative hypoperfusion of the spinal cord is a critical determina

232 This is likely due to hypoperfusion of the spinal cord, which is multifactoria

233 atistical parametric mapping (SPM) to detect hypoperfusion on (99m)Tc-hexamethylpropyleneamine oxime

234 In dementia, the pattern of hypoperfusion on ASL images closely matches the establis

235 Regional hypoperfusion on PWI and elevation of glutamate and glut

236 studies, demonstrating an effect of cerebral hypoperfusion on the expression of both isoforms of PGHS

237 nt of exercise-related left ventricular (LV) hypoperfusion or dysfunction.

238 occipital watershed area injury secondary to hypoperfusion or embolic factors.

239 was strongly associated with the presence of hypoperfusion or infarct in Wernicke's area, we tested t

240 les may become compromised because of either hypoperfusion or occlusion from aortic cross-clamping, o

241 patients with severe sepsis and evidence of hypoperfusion or septic shock who were admitted to the e

242 nsation in the setting of clinically evident hypoperfusion or shock, or as a bridge to more definitiv

243 aving refractory hypotension, signs of organ hypoperfusion, or both.

244 mic inflammatory response syndrome criteria, hypoperfusion/organ dysfunction) identified by a prospec

245 O SPECT studies of similar populations; this hypoperfusion persists after accounting for underlying c

246 mild therapeutic hypothermia in the delayed hypoperfusion phase.

247 damage and working memory impairments after hypoperfusion possibly via endothelial protection suppor

248 various cross-sectional studies, but whether hypoperfusion precedes neurodegeneration is unknown.

249 Factors other than tissue hypoperfusion probably account for much of the end-organ

250 r an intact coronary artery (model of stable hypoperfusion: Protocol 1) or a site of arterial injury

251 umstances and following resolution of tissue hypoperfusion, red blood cell transfusion should be targ

252 ith burn could be attributable to an initial hypoperfusion-related intestinal mucosal tissue injury.

253 1, the MCI group showed significant regional hypoperfusion relative to the CN group in the inferior r

254 sia was also suppressed, as were the typical hypoperfusion responses during cortical spreading depres

255 there has been a growing interest in tissue hypoperfusion resulting from inadequate fluid resuscitat

256 in the CNS leads to BBB breakdown and brain hypoperfusion resulting in secondary neurodegenerative c

257 ell-characterised mouse model has shown that hypoperfusion results in gliovascular and white matter d

258 Arterial hypoperfusion secondary to outflow obstruction from a ce

259 lation, especially with symptoms of cerebral hypoperfusion, should then be considered to be subject t

260 Patients without cortical hypoperfusion showed no hemispatial neglect.

261 rst 6 hrs of resuscitation of sepsis-induced hypoperfusion, specific levels of central venous pressur

262 e have previously demonstrated that cerebral hypoperfusion stimulates several physiological and molec

263 ce that were subjected to prolonged cerebral hypoperfusion stress developed white matter demyelinatio

264 lesion size over 12 weeks were the volume of hypoperfusion (strongest association), baseline NIHSS sc

265 a, and other conditions that can cause brain hypoperfusion such as obstructive sleep apnoea, congesti

266 ons for pathologies associated with cerebral hypoperfusion such as stroke, dementia and hypertension.

267 d hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisy

268 zheimer's disease and have reported areas of hypoperfusion that overlap considerably with hypometabol

269 response, widespread vascular collapse, and hypoperfusion that together serve as primary mechanisms

270 presence of a physiological stressor such as hypoperfusion, the brain is capable of dynamic functiona

271 ination of severe tissue damage and systemic hypoperfusion, this will progress rapidly to an endogeno

272 ction, in the form of either frank damage or hypoperfusion, to the left inferior parietal lobe, rathe

273 he interplay among hemorrhage-induced tissue hypoperfusion, trauma injuries, inflammatory response, a

274 animals acted as controls, and had cerebral hypoperfusion under baseline propofol anesthesia with an

275 has been used to study effects of oligemia (hypoperfusion) using neuropathological and neurochemical

276 ellent outcome was improved brain perfusion: hypoperfusion volume on mean transit time (MTT) map decr

277 evaluated the accuracy of ischemic core and hypoperfusion volumes for predicting infarct volume in p

278 Baseline ischemic core and hypoperfusion volumes were assessed prior to randomized

279 Ischemic core and hypoperfusion volumes, obtained primarily from CT perfus

280 all agreement for the presence of reversible hypoperfusion was 86%.

281 Transient global cerebral hypoperfusion was achieved with bilateral internal carot

282 e, peak hypoperfusion, and 5 and 10 min post hypoperfusion was analyzed by repeated measures ANOVA wi

283 We found that (a) interictal hypoperfusion was easier to demonstrate by SPECT but was

284 Risk of dementia with hypoperfusion was higher with increasing severity of whi

285 ingular and sustained treatment, the area of hypoperfusion was less in both hemodilution groups than

286 Further, the number of stroke lesions after hypoperfusion was reduced in the cilostazol-treated grou

287 atory-induced hypocapnia (and hence cerebral hypoperfusion) was prevented; and (2) that pharmacologic

288 To evaluate possible mechanisms of hypoperfusion, we also measured the levels of amyloid-be

289 ing the location of radiolabeled microsphere hypoperfusion were clearly seen, without need for image

290 Patients without tissue hypoperfusion were not coagulopathic, irrespective of th

291 ficant increases in the severity of cerebral hypoperfusion were observed after 60 min compared to 15

292 and increased anion gap, markers of systemic hypoperfusion, were also associated with twofold higher

293 esion molecules and gliosis, increased after hypoperfusion, were ameliorated with cilostazol treatmen

294 et-warm, n = 222); profile C, congestion and hypoperfusion (wet-cold, n = 91); and profile L, hypoper

295 ss agent for detecting reversible myocardial hypoperfusion when combined with single-photon emission

296 capture patients with hypovolemia and tissue hypoperfusion who are most likely to benefit from fluids

297 ial spin-labeling MR imaging showed regional hypoperfusion with AD, in brain regions similar to those

298 either sensitive nor specific for mesenteric hypoperfusion with regard to total gut blood flow reduct

299 perfusion (wet-cold, n = 91); and profile L, hypoperfusion without congestion (dry-cold, n = 16).

300 We hypothesized that reversing the hypoperfusion would normalize the motor activation patte