1 The right kidneys were controls and remained
hypoperfused.
2 thalamic and midbrain structures which were
hypoperfused.
3 The volumes of critically
hypoperfused and hyperperfused brain (HypoBV and HyperBV
4 While signal intensity differences between
hypoperfused and normal myocardium were comparable for f
5 Autoregulation impairment was greatest in
hypoperfused and potentially viable tissue, suggesting t
6 These findings suggest that the brain is
hypoperfused and sympathetic outflow potentiated during
7 Automated quantification of
hypoperfused areas in patients with CTEPH can be perform
8 ker in the direction of baseline-perfused or
hypoperfused areas.
9 When flow is controlled, kidneys in
hypoperfused ARF can extract sufficient oxygen from ante
10 (UO) and glomerular filtration rate (GFR) in
hypoperfused ARF.
11 100% across the 24 h in acellular scaffolds
hypoperfused at a rate of 200 ml/min.
12 cular patency, and the rerouting of blood to
hypoperfused brain tissue through collateral anastomoses
13 G:PLP1) ratio, which declines in chronically
hypoperfused brain tissue.
14 irreversible tissue damage and of critically
hypoperfused but potentially salvageable tissue (i.e., t
15 he ischemic region, even when only dogs with
hypoperfused but transmurally viable myocardium were con
16 on of posterior brain territories in already
hypoperfused circulation.
17 In contrast, baseline-perfused and
hypoperfused contacts mainly demonstrated non-significan
18 positive oligodendroglial progenitors in the
hypoperfused corpus callosum.
19 our data show that neglect can be caused by
hypoperfused dysfunctional tissue not detectable by stru
20 in the hemisphere opposite to the previously
hypoperfused hemisphere (p < 0.001).
21 patients used the hand contralateral to the
hypoperfused hemisphere they would show unique activatio
22 his study was designed to study apoptosis in
hypoperfused hibernating myocardium subtending severe co
23 g myocyte death through myocyte apoptosis in
hypoperfused hibernating myocardium.
24 tivation of fibroblasts markedly exceeds the
hypoperfused infarct region and involves noninfarcted my
25 ors feature increased vessel density yet are
hypoperfused,
leading to tumor hypoxia.
26 lineate areas of hypoperfusion and calculate
hypoperfused lung volume (HLV).
27 ochemical evaluation of sham and chronically
hypoperfused mice a month after surgery revealed signifi
28 lderly which has been modeled in chronically
hypoperfused mice.
29 Reduced fatty acid oxidation in
hypoperfused myocardium is believed to result from impai
30 lycolytic production of lactate and alanine,
hypoperfused myocardium preferentially oxidized SCFA ove
31 Apoptosis was found not only in 24-h
hypoperfused myocardium, but also in 4-week hypoperfused
32 For quantification of PET signal in the
hypoperfused myocardium, K (1) (rate constant for transf
33 For quantification of PET signal in the
hypoperfused myocardium, K(1) (rate constant for transfe
34 hypoperfused myocardium, but also in 4-week
hypoperfused myocardium.
35 reduce the risk of ischemia in a critically
hypoperfused organ.
36 on of contrast enhancement into the formerly
hypoperfused perilesional zone.
37 ral blood flow distribution curve toward the
hypoperfused range, with a decrease in global cerebral b
38 The size of the
hypoperfused region was equivalent in both groups.
39 The
hypoperfused region was reduced by a median (IQR) 100% (
40 ent demonstrated focal radiotracer uptake in
hypoperfused regions where angiogenesis was stimulated.
41 .06), indicating metabolic adaptation of the
hypoperfused regions.
42 inning will functionally identify regionally
hypoperfused resting myocardium.
43 valuated visually before PEA for parenchymal
hypoperfused segments.
44 perfusion analysis, we are able to identify
hypoperfused territories and quantify the exact changes
45 fusion parameters improved and the extent of
hypoperfused territory declined (4.6% of LV mass +/- 1.4
46 action and the extents of microinfarction or
hypoperfused territory.
47 related to the extents of microinfarction or
hypoperfused territory.
48 ischemic core <70 mL, and volume of severely
hypoperfused tissue <100 mL).
49 EVT(pri) and demonstrated larger critically
hypoperfused tissue (Tmax > 6 seconds) volumes (median [
50 The algorithm identifies
hypoperfused tissue in mean transit time maps by simulta
51 ad a more severe intracellular acidosis than
hypoperfused tissue recruited to the final infarct (P <
52 .0001), which in turn was more acidotic than
hypoperfused tissue that survived (P < 0.0001).
53 numbral volume) was calculated as critically
hypoperfused tissue volume minus ischaemic core volume.
54 Critically
hypoperfused tissue was estimated as the volume of tissu
55 ventilation increases the volume of severely
hypoperfused tissue within the injured brain, despite im
56 th a colorized map which directly visualizes
hypoperfused tissue, combined with associated perfusion
57 Within
hypoperfused tissue, the lactate signal was higher in ar
58 d ischemic core and the volume of critically
hypoperfused tissue.
59 Exogenous Ang-1 enhances perfusion in
hypoperfused tissues only in the presence of increased l
60 actor (VEGF)/angiopoietin-1 (Ang-1) on adult
hypoperfused tissues.
61 ion in MIA-treated rats, all structures were
hypoperfused (
to 25+/-7% of baseline, 48+/-8% of vehicle
62 re perfusion increases due to the pruning of
hypoperfused vessels, rather than blood being rerouted.
63 iduals with schizophrenia were significantly
hypoperfused when compared to controls.
64 d positive correlation with MAG:PLP1, in the
hypoperfused white matter in Alzheimer's disease.
65 d well with radiolabeled microsphere-derived
hypoperfused zone (r = 0.89).
66 tween infarcted and viable tissue within the
hypoperfused zone after a single venous injection.
67 Regions within the
hypoperfused zone that had not undergone necrosis showed