ライフサイエンスコーパス: hypoperfusion

1 yperaemia) to pathological inverse coupling (hypoperfusion).

2 rysm can be one possible cause of pancreatic hypoperfusion.

3 d is driven by significant tissue injury and hypoperfusion.

4 no or nonexertional symptoms had myocardial hypoperfusion.

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

6 EEG silence during transient global cerebral hypoperfusion.

7 EEG silence during transient global cerebral hypoperfusion.

8 oid-beta are differentially impacted by mild hypoperfusion.

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

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

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

12 and assess its relationship with acute-stage hypoperfusion.

13 rtional to both injury severity and systemic hypoperfusion.

14 pendently with severity of injury and tissue hypoperfusion.

15 correlation between FMZ binding and initial hypoperfusion.

16 L; p < 0.0001), possibly indicating systemic hypoperfusion.

17 products, reductions in microcirculation and hypoperfusion.

18 d failed to show a relationship with initial hypoperfusion.

19 ith intracranial stenosis to protect against hypoperfusion.

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

21 with normal vital signs but ongoing, occult hypoperfusion.

22 vascular lumen, resulting in prolonged renal hypoperfusion.

23 part, to tissue hypoxia due to local spinal hypoperfusion.

24 racellular potassium, and in part because of hypoperfusion.

25 when organ dysfunction occurs as a result of hypoperfusion.

26 l velocities did not identify subendocardial hypoperfusion.

27 eventually causing organ dysfunction due to hypoperfusion.

28 cardiac output are associated with cerebral hypoperfusion.

29 zation, heparin-induced thrombocytopenia, or hypoperfusion.

30 associated with different sites of cortical hypoperfusion.

31 to increase oxygen extraction in response to hypoperfusion.

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

33 e oxygen unloading during hypocapnia-induced hypoperfusion.

34 lt of experimental atherosclerosis and renal hypoperfusion.

35 adiol augments the PGHS response to cerebral hypoperfusion.

36 therwise modify the Fos response to cerebral hypoperfusion.

37 at it modulates the Fos response to cerebral hypoperfusion.

38 phasia or neglect showed concurrent cortical hypoperfusion.

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

40 strongly predicts cortical ischaemia and/or hypoperfusion.

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

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

43 rking memory and white matter function after hypoperfusion.

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

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

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

47 significantly greater in areas with critical hypoperfusion (40-60%: 0.42% per mmHg and 60-80%: 0.46%

48 t in cerebral endothelial cells and cerebral hypoperfusion(7).

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

50 Hypoperfusion abnormalities evidenced by SPECT are more

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

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

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

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

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

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

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

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

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

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

61 Although interictal hypoperfusion and ictal hyperperfusion are established l

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

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

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

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

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

67 sing mainly on associations between cerebral hypoperfusion and neuronal degradation.

68 -tau antibodies, despite persistent cerebral hypoperfusion and neurovascular dysfunction.

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

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

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

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

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

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

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

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

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

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

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

80 As a reflection of both hypoperfusion and tissue damage, the assay of arterial L

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

82 eurological consequences of chronic cerebral hypoperfusion and VaD.

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

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

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

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

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

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

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

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

91 erine spiral artery remodeling and placental hypoperfusion, and thus the development of PE.

92 abigatran prevented memory decline, cerebral hypoperfusion, and toxic fibrin deposition in the AD mou

93 s between fine motor impairment, grey matter hypoperfusion, and white matter volume loss.

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

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

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

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

98 ated in patients with CLD due to both tissue hypoperfusion as well as decreased LA clearance.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 siopathology unfolds in eyes with panretinal hypoperfusion courtesy of the transparent ocular media a

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

119 tributions of normalized radiotracer counts, hypoperfusion defects, and hypoperfusion severities and

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

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

122 the presence of hypotension or tachycardia, hypoperfusion, deterioration, and refractory shock.

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

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

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

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

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

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

129 nferior posttransplant outcomes due to organ hypoperfusion during cardiac arrest and mechanical traum

130 Kidney hypoperfusion during episodes of systemic hypotension or

131 f a coronary artery had inducible myocardial hypoperfusion during noninvasive provocative testing.

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

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

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

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

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

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

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

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

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

141 Cerebral hypoperfusion has previously been associated with mild c

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

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

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

145 These results support a key role for hypoperfusion/hypoxia in postictal memory impairments an

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

147 portantly, the induction of severe postictal hypoperfusion/hypoxia was prevented in animals treated b

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

149 hat long-lasting periods of severe postictal hypoperfusion/hypoxia, not seizures per se, are associat

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

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

156 specific dynamics following chronic cerebral hypoperfusion in mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 s to the pathophysiology of chronic cerebral hypoperfusion-induced brain injury and may therefore rep

178 ptosis in mediating neurovascular damage and hypoperfusion-induced TAK1 loss, which subsequently prom

179 sive analyses revealed that chronic cerebral hypoperfusion induces a complex temporal expression and

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

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

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

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

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

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

186 Inducible hypoperfusion is a common finding in hypertrophic cardio

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

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

189 , this work suggests hyperoxia-induced brain hypoperfusion is accompanied by enhanced cognitive proce

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 Chronic cerebral hypoperfusion is associated with vascular dementia (VaD)

195 Regional cerebral hypoperfusion is characteristic of Alzheimer's disease (

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

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

198 The significance of ictal hypoperfusion is not well understood.

199 Cerebral hypoperfusion is widely implicated in cognitive impairme

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

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

202 n identified eight of 17 patients (47%) with hypoperfusion (ischemic burden of 17% +/- 5).

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

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

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

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

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

208 owerful predictor than baseline diffusion or hypoperfusion lesion volumes.

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

210 The spectrum of acute oxygenation-based hypoperfusion maculopathy (OHM) is consistent with that

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

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

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

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

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

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

217 Cerebral hypoperfusion may initiate complex molecular and cellula

218 Chronic hypoperfusion may put these people at risk for neuronal

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

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

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

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

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

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

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

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

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

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

229 It suggests hypoperfusion of the gut mucosa.

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

231 hypoxia in EAE is associated with a profound hypoperfusion of the inflamed spinal cord.

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

233 Perioperative hypoperfusion of the spinal cord is a critical determina

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

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

236 o investigate the effect of chronic cerebral hypoperfusion on cerebral hemodynamics and perivascular

237 ve was performed in patients with myocardial hypoperfusion on noninvasive testing.

238 Regional hypoperfusion on PWI and elevation of glutamate and glut

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

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

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

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

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

244 of CE in patients suffering from prefrontal hypoperfusion or white matter diseases.

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

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

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

248 mild therapeutic hypothermia in the delayed hypoperfusion phase.

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

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

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

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

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

254 1, the MCI group showed significant regional hypoperfusion relative to the CN group in the inferior r

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

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

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

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

259 Arterial hypoperfusion secondary to outflow obstruction from a ce

260 diotracer counts, hypoperfusion defects, and hypoperfusion severities and was evaluated for predictio

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

262 Patients without cortical hypoperfusion showed no hemispatial neglect.

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

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

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

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

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

268 review focuses on the intradialytic cerebral hypoperfusion that can occur during routine hemodialysis

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

270 Severe cases have pulmonary hypoperfusion that is likely due to abnormal alveolar ve

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

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

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

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

275 d the relationship of intradialytic cerebral hypoperfusion to cognitive outcomes will help inform the

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

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

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

279 embolic events, bleeding, and rhythm-related hypoperfusion underlie many of these models.

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

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

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

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

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

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

286 Transient global cerebral hypoperfusion was achieved with bilateral internal carot

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

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

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

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

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

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

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

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

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

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

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

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

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

300 over 30 min) for management of shock and/or hypoperfusion within 12h of cardiac surgery.

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

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