The ultrastructure of photochemically induced thrombi with embolization in a rat model.

Futrell, Nancy; Riddle, Jeanne M.

doi:10.1161/01.str.24.12.1983

Cited by 10 publications

(8 citation statements)

References 34 publications

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“…In the present work, spontaneous cerebral thrombosis was never seen in control mice. Similar results were reported in young Wistar and Fisher rats used as controls or in acute stroke experiments (Futrell and Riddle, 1993).…”

Section: Discussionsupporting

confidence: 88%

Hyperthermia induces ultrastructural changes in mouse pial microvessels

Fahim¹,

El‐Sabban²

1995

Anat. Rec.

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Section: Discussionsupporting

confidence: 88%

Hyperthermia induces ultrastructural changes in mouse pial microvessels

Fahim¹,

El‐Sabban²

1995

Anat. Rec.

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“…19 The embolic theory is supported by postmortem, 20 intraoperative, 21 and angiographic 22 studies showing emboli in cerebral arteries, by the observation of emboli in retinal arterioles during funduscopic examination, 23 ' 24 and by laboratory models. 25 The presence of TCD signals similar to the ones described in this report and distal to symptomatic ICA stenoses, 46 ' 9 their absence distal to asymptomatic ICA lesions, 6 - 13 and their response to anticoagulant treatment 11 had already suggested a relation between these signals and cerebral ischemia. Our finding of a significant association between HITS and cerebral or retinal ischemia provides in vivo evidence supporting the notion of cerebral embolism and furthers the findings of previous TCD studies.…”

Section: Discussionmentioning

confidence: 54%

Clinical correlates of high-intensity transient signals detected on transcranial Doppler sonography in patients with cerebrovascular disease.

Babikian

Hyde

Pochay

et al. 1994

Stroke

100

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Background and Purpose High-intensity transient signals detected by transcranial Doppler sonography have been associated with particulate cerebral emboli. Their clinical correlates are poorly understood. This study was undertaken to assess their relation to cerebral ischemia and to determine whether the severity of cerebral arterial stenosis has an impact on their occurrence.Methods We studied 96 arteries in 75 consecutive patients with extracranial or intracranial arterial lesions or potential cardiac sources of cerebral embolism. Sixty patients had histories of cerebral or retinal transient ischemic attacks or infarcts, and 15 were asymptomatic. The diagnosis of ischemia was based on the clinical presentation and was supported by extensive laboratory testing. A transcranial Doppler sonography unit equipped with special software for emboli detection was used. Signals were selected based on criteria established a priori.

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“…In addition, platelet accumulation occurs without endothelial damage within downstream microvascular beds or evidence for local platelet aggregation or adhesion. 12,13 This model is useful for the study of the pathogenesis and treatment of small cerebral infarcts caused by platelet embolization, but not for those caused by microthrombosis or small arterial wall damage.…”

Section: Toshima Et Al a New Model Of Cerebral Microthrombosis 2247mentioning

confidence: 99%

A New Model of Cerebral Microthrombosis in Rats and the Neuroprotective Effect of a Rho-Kinase Inhibitor

Toshima

Satoh

Ikegaki

et al. 2000

Stroke

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Background and Purpose-The aim of this study was to develop a new model of stroke based on endothelial damage and thrombotic occlusion in a perforating artery, leading to small cerebral infarcts and neurological deficits in rats. Moreover, the neuroprotective efficacy of fasudil, a rho-kinase inhibitor, was investigated in this model. Methods-Fifty-six male Sprague-Dawley rats were used in the present study. Rats were anesthetized with sodium pentobarbital, and 100 g of sodium laurate was injected into the left internal carotid artery on days 1 and 3. The thrombus induction and consequent of ischemic brain damage were examined by histopathological analyses and neurological deficit scoring in a posture reflex test. To investigate the neuroprotective effects of fasudil, 1 or 10 mg/kg was administered intraperitoneally 5 minutes after the first injection of sodium laurate and once daily thereafter on the following 2 days. Results-One hour after the injection of sodium laurate, microscopic examination of phosphotungstic acid hematoxylinstained sections (nϭ5) revealed that microthrombi containing fibrin strands obstructed the perforating arteries in the ipsilateral hemisphere. Under a transmission electron microscope (nϭ6), endothelial cells appeared exfoliated and the vascular lumen was obstructed by a thrombus composed of degranulated platelets, fibrin, leukocytes, and erythrocytes.No evidence of endothelial cell damage or thrombus could be found in the ipsilateral side of the pial artery (middle cerebral artery). Twenty-four hours after the second injection of sodium laurate (day 4), 13 of 15 rats (86.6%) showed mild to severe neurological deficits. Multiple small cerebral infarcts were observed in the hippocampus, cortex, and thalamus. Treatment with fasudil (1 and 10 mg/kg, nϭ15 each) resulted in a significant improvement in neurological deficits. Fasudil also significantly reduced the area of cerebral infarction. Conclusions-We present a new model of stroke in rats, in which the perforating arteries are selectively occluded by microthrombi. This model is useful to investigate the pathophysiology and treatment of small cerebral infarction, which is caused by perforating arterial occlusive diseases such as lacunar infarcts. Fasudil may be beneficial in the treatment of acute ischemic stroke. (Stroke. 2000;31:2245-2250.)

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The ultrastructure of photochemically induced thrombi with embolization in a rat model.

Cited by 10 publications

References 34 publications

Hyperthermia induces ultrastructural changes in mouse pial microvessels

Hyperthermia induces ultrastructural changes in mouse pial microvessels

Clinical correlates of high-intensity transient signals detected on transcranial Doppler sonography in patients with cerebrovascular disease.

A New Model of Cerebral Microthrombosis in Rats and the Neuroprotective Effect of a Rho-Kinase Inhibitor

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