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1 Ablation size was visualized by using 2% triphenyltetrazolium chloride.
2 measurement of formazan produced from 2,3,5-triphenyltetrazolium chloride.
3 troxyl reduction was confirmed using EPR and triphenyltetrazolium chloride.
4 dium was stained with thioflavin-S and 2,3,5-triphenyltetrazolium chloride.
5 reperfusion, infarct size was measured with triphenyltetrazolium chloride.
6 Postmortem infarct size was measured with triphenyltetrazolium chloride.
7 ea infarcted was determined by staining with triphenyltetrazolium chloride.
8 ), less decline in +/-dP/dt, and smaller MI (triphenyltetrazolium chloride, 21+/-11% versus 3+/-8%; P
9 )Na MRI correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced (1)H
10 farct size, determined by dual staining with triphenyltetrazolium chloride and phthalocyanine blue dy
11 farct size, determined by dual staining with triphenyltetrazolium chloride and phthalocyanine blue dy
12 ompared with postmortem myocardial staining (triphenyltetrazolium chloride) and microsphere blood flo
13 characterized by magnetic resonance imaging, triphenyltetrazolium chloride, and hemotoxylin and eosin
14 brains were sectioned and stained with 2,3,5-triphenyltetrazolium chloride, and the infarct area was
15 ricle, 2.2+/-0.5% versus 5.4+/-1.5%, P=0.04; triphenyltetrazolium chloride: anterior wall, 10.3+/-4.6
16 itially using the cell viability stain 2,3,5-triphenyltetrazolium chloride, but was determined in sub
17 abnormal time constants correlated well with triphenyltetrazolium chloride-determined infarct size (r
20 The brains were removed and stained with triphenyltetrazolium chloride for infarct volume determi
27 ined by quantitative image analysis of 2,3,5-triphenyltetrazolium chloride-stained brain sections.
28 tion of the pattern of dye staining on 2,3,5-triphenyltetrazolium chloride-stained heart slices agree
29 ined by threshold analysis and compared with triphenyltetrazolium chloride-stained sections of the ex
30 8.5% +/- 0.9 vs 11.3% +/- 0.9, P = .048) and triphenyltetrazolium chloride staining (9.4% +/- 1.5 vs
32 with infarct volumes as determined by 2,3,5-triphenyltetrazolium chloride staining (R(2) = 0.692, P
33 red by in vivo 23Na MRI correlated well with triphenyltetrazolium chloride staining (r=0.87, y=0.92x+
34 -dependent brain damage as revealed by 2,3,5-triphenyltetrazolium chloride staining (severe > moderat
36 s assessed by serial echocardiography, 2,3,5-triphenyltetrazolium chloride staining determined infarc
37 echo time 8 ms, 2-tesla system), followed by triphenyltetrazolium chloride staining for infarct detec
38 ion in infarct volumes (P < 0.001), based on triphenyltetrazolium chloride staining of serial cerebra
41 sessed by echocardiography couple with 2,3,5-Triphenyltetrazolium chloride staining to measure MI siz
42 was compared with pathological (exclusion of triphenyltetrazolium chloride staining) and ICE measurem
43 iated with a decreased infarct volume (2,3,5-triphenyltetrazolium chloride staining) in the striatum
47 y, magnetic resonance imaging, hemodynamics, triphenyltetrazolium chloride staining, and histological
49 Myocardial infarct size was measured through triphenyltetrazolium chloride staining, and polymorphonu
51 tion of cerebral infarct volumes measured by triphenyltetrazolium chloride staining, as well as impro
52 imaging results were confirmed by postmortem triphenyltetrazolium chloride staining, elastica van Gie
54 Infarcted, reperfused regions, identified by triphenyltetrazolium chloride staining, showed a signifi
68 (left ventricular pressure-volume curves; 1% triphenyltetrazolium chloride staining; creatine kinase
69 .9%) than true infarction as demonstrated by triphenyltetrazolium chloride (TTC) (24.6+/-1.4%, P<0.00
70 weeks), the lesion was assessed using 2,3,5-triphenyltetrazolium chloride (TTC) or hematoxylin and e
72 ) and to compare 99mTc-sestamibi imaging and triphenyltetrazolium chloride (TTC) staining for reliabi
73 ly to the rat, and often paired with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining for stroke
74 ed at 24 h after acute coronary occlusion by triphenyltetrazolium chloride (TTC) staining in wild-typ
76 e relationship of infarct size determined by triphenyltetrazolium chloride (TTC) staining versus (99m
84 Heart slices were imaged, then stained with triphenyltetrazolium chloride (TTC), and tissues were we
85 d with microsphere-determined blood flow and triphenyltetrazolium chloride (TTC)-stained tissue sampl
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