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1  induced EEG silence during transient global cerebral hypoperfusion.
2 chieving EEG silence during transient global cerebral hypoperfusion.
3 ative low cardiac output are associated with cerebral hypoperfusion.
4 hat oestradiol augments the PGHS response to cerebral hypoperfusion.
5 ment or otherwise modify the Fos response to cerebral hypoperfusion.
6 us and that it modulates the Fos response to cerebral hypoperfusion.
7 ithout evidence of occlusive vasculopathy or cerebral hypoperfusion.
8 is lost and regained in the setting of acute cerebral hypoperfusion.
9 resulting from intracranial hypertension and cerebral hypoperfusion.
10 pressure target leads to potentially harmful cerebral hypoperfusion.
11 HD population and identify those at risk for cerebral hypoperfusion.
12 limited, spontaneously terminating period of cerebral hypoperfusion.
13  microvascular sensory web and contribute to cerebral hypoperfusion.
14 oxygen in face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% to 57%) to compensate for re
15 de deficit in cerebral endothelial cells and cerebral hypoperfusion(7).
16  cells, a rarefaction of brain microvessels, cerebral hypoperfusion, a disrupted blood-brain barrier
17            We hypothesized that estrogen and cerebral hypoperfusion alone would augment Fos abundance
18                     Recent data suggest that cerebral hypoperfusion and activation of cerebral ion tr
19 between biochemical markers and mediators of cerebral hypoperfusion and BBB leakiness, and Abeta and
20                                              Cerebral hypoperfusion and blood-brain barrier (BBB) lea
21 alters brain cytokine levels and exacerbates cerebral hypoperfusion and blood-brain barrier leakiness
22 n duration-dependent increase in severity of cerebral hypoperfusion and extension of ischaemic pathol
23 mechanism that causes repetitive episodes of cerebral hypoperfusion and neuroinflammation during migr
24 ion, focusing mainly on associations between cerebral hypoperfusion and neuronal degradation.
25 with anti-tau antibodies, despite persistent cerebral hypoperfusion and neurovascular dysfunction.
26 eatment--consistent with possible effects of cerebral hypoperfusion and reperfusion injury.
27 or for dementia since it may lead to chronic cerebral hypoperfusion and stroke.
28                                      Chronic cerebral hypoperfusion and VaD was induced by bilateral
29 egative neurological consequences of chronic cerebral hypoperfusion and VaD.
30 itive function in an animal model of chronic cerebral hypoperfusion and vascular dementia (VaD).
31 n the present study, we tested the effect of cerebral hypoperfusion and/or estradiol on the expressio
32 on with dabigatran prevented memory decline, cerebral hypoperfusion, and toxic fibrin deposition in t
33  present data provide evidence of widespread cerebral hypoperfusion associated with pathogenic angiog
34 anial pressure monitoring alone in detecting cerebral hypoperfusion at the bedside in patients with s
35 demonstrate that CE in DKA is accompanied by cerebral hypoperfusion before treatment and suggest that
36 mply that CSVD is primarily a consequence of cerebral hypoperfusion caused by AS.
37 ts of the posterior cerebral circulation and cerebral hypoperfusion could partially explain the patho
38 ng of intracranial pressure and treatment of cerebral hypoperfusion decrease secondary injury.
39 curacy of intracranial monitoring to predict cerebral hypoperfusion (defined as an oligemic regional
40 ed with hemodialysis (HD) may be at risk for cerebral hypoperfusion due to HD-induced BP decline in t
41                                  In summary, cerebral hypoperfusion either at rest or induced by hypo
42     Our study indicates that a single, mild, cerebral hypoperfusion event produces profound and long
43 mine the independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on cerebral oxyg
44                               Evidence links cerebral hypoperfusion from cardiac arrest, heart failur
45                                              Cerebral hypoperfusion has previously been associated wi
46 position of alpha-synuclein, (2) OH-mediated cerebral hypoperfusion impairs cognition and (3) the two
47 ell type specific dynamics following chronic cerebral hypoperfusion in mice.
48  question, we developed an oligemic model of cerebral hypoperfusion in the 3xTg-AD mouse model of AD.
49                                     Although cerebral hypoperfusion in the aged rats was not associat
50 otension (OH) is a common cause of transient cerebral hypoperfusion in the population.
51 ork in this laboratory has demonstrated that cerebral hypoperfusion increases the expression of prost
52                                              Cerebral hypoperfusion-indicated by decreased MAG:PLP1 a
53 ontributes to the pathophysiology of chronic cerebral hypoperfusion-induced brain injury and may ther
54 Comprehensive analyses revealed that chronic cerebral hypoperfusion induces a complex temporal expres
55 Comprehensive analyses revealed that chronic cerebral hypoperfusion induces a complex temporal expres
56 s cognitive impairment through hypertension, cerebral hypoperfusion, inflammation, arrhythmia, emboli
57 uggested mechanisms for the disorder include cerebral hypoperfusion, inflammation, gene polymorphisms
58                                      Chronic cerebral hypoperfusion is a major cause of age-related v
59                                              Cerebral hypoperfusion is among the mechanisms that may
60                                              Cerebral hypoperfusion is associated with accelerated co
61                                      Chronic cerebral hypoperfusion is associated with vascular demen
62                                     Regional cerebral hypoperfusion is characteristic of Alzheimer's
63 ypotension (OH) is common, and its resulting cerebral hypoperfusion is linked to adverse outcomes inc
64 irment and white matter damage after chronic cerebral hypoperfusion is unclear.
65                                              Cerebral hypoperfusion is widely implicated in cognitive
66 of the PGHS-2 gene expression in response to cerebral hypoperfusion/ischemia in neurons, we used a ce
67 ucible isoform of this enzyme, is induced by cerebral hypoperfusion/ischemia.
68                         However, despite the cerebral hypoperfusion, it is possible that the mild alk
69 ntrol and communication that are impacted by cerebral hypoperfusion leading to syncope.
70 ables were significant only in AHF (signs of cerebral hypoperfusion, low serum sodium, chronic obstru
71 the posterior circulation and the associated cerebral hypoperfusion may be a factor in triggering hyp
72 nsible, but recent data instead suggest that cerebral hypoperfusion may be involved and that activati
73                                              Cerebral hypoperfusion may initiate complex molecular an
74 preliminary findings suggest that a relative cerebral hypoperfusion may underlie depression in elderl
75 ted a pilot investigation of whether chronic cerebral hypoperfusion might affect genomic distribution
76 e aimed to investigate the effect of chronic cerebral hypoperfusion on cerebral hemodynamics and peri
77 ing and its association with tachycardia and cerebral hypoperfusion on standing in 28 patients with p
78 previous studies, demonstrating an effect of cerebral hypoperfusion on the expression of both isoform
79                  Passive hyperthermia causes cerebral hypoperfusion primarily from heat-induced respi
80 l syncope, including reduced cardiac output, cerebral hypoperfusion, pupil dilation and eye-roll.
81 ar fibrillation, especially with symptoms of cerebral hypoperfusion, should then be considered to be
82         We have previously demonstrated that cerebral hypoperfusion stimulates several physiological
83        Mice that were subjected to prolonged cerebral hypoperfusion stress developed white matter dem
84 implications for pathologies associated with cerebral hypoperfusion such as stroke, dementia and hype
85     This review focuses on the intradialytic cerebral hypoperfusion that can occur during routine hem
86 injury and the relationship of intradialytic cerebral hypoperfusion to cognitive outcomes will help i
87       All animals acted as controls, and had cerebral hypoperfusion under baseline propofol anesthesi
88                             Transient global cerebral hypoperfusion was achieved with bilateral inter
89 perventilatory-induced hypocapnia (and hence cerebral hypoperfusion) was prevented; and (2) that phar
90     Significant increases in the severity of cerebral hypoperfusion were observed after 60 min compar