A model of selective experimental ischaemia in the primate thalamus.

Vajda, J.; Branston, Neil M.; Ladds, A.; Symon, Lindsay

doi:10.1161/01.str.16.3.493

Cited by 9 publications

(10 citation statements)

References 9 publications

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“…Although histopathological detection of infarcted tissue is reliable, it is an impractical method of calculating total infarct volume. Faced with these shortcomings, we modified a triple-vessel occlusion model developed by Zabramski and coworkers, 39 -42 on which the model presented here is based, while others have developed models of acute focal ischemia in territories other than the MCA: the anterior cerebral, [43][44][45] posterior choroidal, 46,47 or proximal basilar arteries. 48 While these other models have added much to the understanding of primate vascular anatomy, they have generally been considered inferior for a variety of reasons.…”

Section: Discussionmentioning

confidence: 99%

“…48 While these other models have added much to the understanding of primate vascular anatomy, they have generally been considered inferior for a variety of reasons. The use of electric coagulation to create occlusion of the lenticulostriate arteries 29 or the posterior choroidal artery 46 was associated with potential damage to adjacent cerebral tissue. The unpredictable localization of embolic material within MCA branches resulted in variable deep or cortical infarcts.…”

Section: Discussionmentioning

confidence: 99%

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A Modified Transorbital Baboon Model of Reperfused Stroke

Huang

Mocco

Choudhri

et al. 2000

Stroke

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Background and Purpose-Although pathophysiological studies of focal cerebral ischemia in nonhuman primates can provide important information not obtainable in rodent models, primate experimentation is limited by considerations of cost, availability, effort, and ethics. A reproducible and quantitative model that minimizes the number of animals necessary to detect differences between treatment groups is therefore crucial. Methods-Eight male baboons (weight, 22Ϯ2 kg) underwent left transorbital craniectomy followed by 1 hour of temporary ipsilateral internal carotid artery occlusion at the level of the anterior choroidal artery together with bilateral temporary occlusion of both anterior cerebral arteries (A1) proximal to the anterior communicating artery. A tightly controlled nitrous oxide-narcotic anesthetic allowed for intraoperative motor evoked potential confirmation of middle cerebral artery (MCA) territory ischemia. Animals survived to 72 hours or 10 days if successfully self-caring. Outcomes were assessed with a 100-point neurological grading system, and infarct volume was quantified by planimetric analysis of both MRI and triphenyltetrazolium chloride-stained sections. Results-Infarction volumes (on T2-weighted images) were 32Ϯ7% (meanϮSEM) of the ipsilateral hemisphere, and neurological scores averaged 29Ϯ9. All animals demonstrated evidence of hemispheric infarction, with damage evident in both cortical and subcortical regions in the MCA vascular territory. Histologically determined infarction volumes differed by Ͻ3% and correlated with absolute neurological scores (rϭ0.9, Pϭ0.003). Conclusions-Transorbital temporary occlusion of the entire anterior cerebral circulation with strict control of physiological parameters can reliably produce reperfused MCA territory infarction. The magnitude of the resultant infarct with little interanimal variability diminishes the potential number of animals required to distinguish between 2 treatment regimens. The anatomic distribution of the infarct and associated functional deficits offer comparability to human hemispheric strokes. (Stroke. 2000;31:3054-3063.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Modified Transorbital Baboon Model of Reperfused Stroke

Huang

Mocco

Choudhri

et al. 2000

Stroke

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“…First, their MCAO model effectively achieved ischemia and subsequent cerebral infarction. 35 Other NHP models only deliver isolated basal ganglia infarctions, 36,37 subcortical infarctions, [38][39][40][41][42] or brainstem infarctions. 43,44 Their model, however, demonstrated infarctions of both cortical and subcortical gray matter, including subcortical white matter, which is more representative of human ischemic stroke.…”

Section: Non-human Primate Stroke Modelsmentioning

confidence: 99%

Rodent models of ischemic stroke lack translational relevance… are baboon models the answer?

Kwiecien

Ding

2014

Neurological Research

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Rodent models of ischemic stroke are associated with many issues and limitations, which greatly diminish the translational potential of these studies. Recent studies demonstrate that significant differences exist between rodent and human ischemic stroke. These differences include the physical characteristics of the stroke, as well as changes in the subsequent inflammatory and molecular pathways following the acute ischemic insult. Non-human primate (NHP) models of ischemic stroke, however, are much more similar to humans. In addition to evident anatomical similarities, the physiological responses that NHPs experience during ischemic stroke are much more applicable to the human condition and thus make it an attractive model for future research. The baboon ischemic stroke model, in particular, has been studied extensively in comparison to other NHP models. Here we discuss the major shortcomings associated with rodent ischemic stroke models and provide a comparative overview of baboon ischemic stroke models. Studies have shown that baboons, although more difficult to obtain and handle, are more representative of ischemic events in humans and may have greater translational potential that can offset these deficiencies. There remain critical issues within these baboon stroke studies that need to be addressed in future investigations. The most critical issue revolves around the size and the variability of baboon ischemic stroke. Compared to rodent models, however, issues such as these can be addressed in future studies. Importantly, baboon models avoid many drawbacks associated with rodent models including vascular variability and inconsistent inflammatory responses - issues that are inherent to the species and cannot be avoided.

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“…Several investigators, however, have developed stroke models using occlusion in the ACA territory or that producing thalamic infarction (Hudgins and Garcia 1970;Vajda et al 1985).…”

Section: Location Of Arterial Occlusionmentioning

confidence: 99%

Models of Focal Cerebral Ischemia in the Nonhuman Primate

Fukuda¹,

Zoppo²

2003

ILAR Journal

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Ischemic stroke is a uniquely human disease syndrome. Models of focal cerebral ischemia developed in nonhuman primates provide clinically relevant platforms for investigating pathophysiological alterations associated with ischemic brain injury, microvascular responses, treatment responses, and clinically relevant outcomes that may be appropriate for ischemic stroke patients. A considerable number of advantages attend the use of nonhuman primate models in cerebral vascular research. Appropriate development of such models requires neurosurgical expertise to produce single or multiple vascular occlusions. A number of experimentally and clinically accessible outcomes can be measured, including neurological deficits, neuron injury, evidence of non-neuronal cell injury, infarction volume, real-time imaging of injury development, vascular responses, regional cerebral blood flow, microvascular events, the relation between neuron and vascular events, and behavioral outcomes. Nonhuman primate models of focal cerebral ischemia provide excellent opportunities for understanding the vascular and cellular pathophysiology of cerebral ischemic injury, which resembles human ischemic stroke, and the appropriate study of pharmacological interventions in a human relevant setting.

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A model of selective experimental ischaemia in the primate thalamus.

Cited by 9 publications

References 9 publications

A Modified Transorbital Baboon Model of Reperfused Stroke

A Modified Transorbital Baboon Model of Reperfused Stroke

Rodent models of ischemic stroke lack translational relevance… are baboon models the answer?

Models of Focal Cerebral Ischemia in the Nonhuman Primate

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