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1 diet and modeled VCID via unilateral common carotid artery occlusion.
2 before and after ischemia induced by middle carotid artery occlusion.
3 ding condition that occurs in the setting of carotid artery occlusion.
4 agonists and pepducins was effective against carotid artery occlusion.
5 perfusion deficits even after release of the carotid artery occlusion.
6 pler probe, combined with ipsilateral common carotid artery occlusion.
7 bal ischemia was induced by bilateral common carotid artery occlusion.
8 anaesthetized rats with a unilateral common carotid artery occlusion.
9 e of stroke risk in patients with unilateral carotid artery occlusion.
10 middle cerebral artery and bilateral common carotid artery occlusion.
11 littermates after 3 min of bilateral common carotid artery occlusion.
12 zone 1-2 weeks after 10 min bilateral common carotid artery occlusions.
14 similar in HRG-deficient and wild-type mice, carotid artery occlusion after FeCl3 injury was accelera
15 cFvSCE5-scuPA (75 U/g body weight) prevented carotid artery occlusion after ferric chloride injury in
16 into Mrp14(-)/(-) mice decreased the time to carotid artery occlusion after injury, indicating that p
17 ts with symptomatic atherosclerotic internal carotid artery occlusion (AICAO) and hemodynamic cerebra
18 e present pooled analysis (120 with internal carotid artery occlusion and 360 with isolated middle ce
20 obtained in a patient with a right internal carotid artery occlusion and an infarct in the middle ce
21 mg was given i.v. and 3 min later bilateral carotid artery occlusion and blood withdrawal-induced hy
22 natinib induced severe responses, leading to carotid artery occlusion and extensive vessel wall damag
23 l of surgical revascularisation for complete carotid artery occlusion and haemodynamic ischaemia, wer
25 dult mice that consists of unilateral common carotid artery occlusion and hypoxia with tightly regula
26 gina, previous ipsilateral CE, contralateral carotid artery occlusion and other severe comorbid illne
27 rfusion was achieved with bilateral internal carotid artery occlusion and pharmacologically induced s
28 asted Wistar rats underwent bilateral common carotid artery occlusion and severe hypotension (50 mmHg
29 neuronal integrity in a model of unilateral carotid artery occlusion and systemic hypobaric hypotens
31 ) by hypoxia (FiO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arteria
32 ed in the AQP4(-/-) vs. AQP4(+/+) mice after carotid artery occlusion, as were blood-brain barrier (B
37 ebral ischaemia in mouse is bilateral common carotid artery occlusion (BCCAo) and the neuropathologic
39 sion and VaD was induced by bilateral common carotid artery occlusion (BCCAO) in adult male Sprague D
43 level of blood flow reduction was induced by carotid artery occlusion (CAO) over a similar 3 week tim
44 rmore, PKCdY311F mice exhibit longer time to carotid artery occlusion compared with WT control using
45 aroreceptor afferent inactivation, caused by carotid artery occlusion, elicit similar patterns of c-F
46 ongolian gerbils were subjected to bilateral carotid artery occlusion, exposed to nesting material an
47 n ovariectomized rats after transient middle carotid artery occlusion followed by a 24-h reperfusion.
48 erbils by a 5-min period of bilateral common carotid artery occlusion followed by reperfusion for 6 d
49 2/3(-/-)) were subjected to bilateral common carotid artery occlusion, followed by reperfusion and tr
50 displayed a significantly prolonged time to carotid artery occlusion following Rose Bengal administr
57 uent stroke risk in patients with unilateral carotid artery occlusion, in order to define better the
58 method to monitor retinopathy in a bilateral carotid artery occlusion-induced ocular ischemia, we obs
59 od to demonstrate that 14 days of unilateral carotid artery occlusion induces increases in the calibe
61 ation and brain infarct injury in the middle carotid artery occlusion ischemia/reperfusion model.
62 l ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulat
63 tective properties in vivo (gerbil bilateral carotid artery occlusion model: BCAO) and in vitro (isch
66 focal ischemia in a filament model of middle carotid artery occlusion nor caused postthrombotic hemor
67 le cerebral artery +/- intracranial internal carotid artery occlusions on baseline computed tomograph
69 in of global forebrain ischemia by bilateral carotid artery occlusions plus systemic hypotension.
71 sham operation (n=6) or 15 min of bilateral carotid artery occlusion resulting in global cerebral is
72 ediated cerebrovascular adaptation to common carotid artery occlusion resulting in hypoperfusion.
73 induced a dose-dependent prolongation of the carotid artery occlusion time in HCII(+/+) mice that was
78 ected to global ischemia by bilateral common carotid artery occlusion under controlled ventilation fo
79 middle cerebral artery or terminal internal carotid artery occlusion using computed tomographic angi
81 scle contraction) or baroreceptor unloading (carotid artery occlusion) were sensitive to SP knockdown
82 hemic injury was induced by bilateral common carotid artery occlusion, whereas severe focal stroke in
84 raphically proven asymptomatic left internal carotid artery occlusion with normal CT after a gunshot