Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 1: Angio-anatomy and description of an experimental model with selective embolization of the internal carotid artery bifurcation.

Watanabe, Osamu; Bremer, Alfonso M.; West, Charles R.

doi:10.1161/01.str.8.1.61

Cited by 43 publications

(21 citation statements)

References 25 publications

(13 reference statements)

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“…In other models in which in situ perfusion fixation was reportedly employed following MCA interruption or occlusion by several different methods, the effect of MCA occlusion on the dependent vascular bed was not examined. 26 - 21 The failure to observe occlusive material in perforating vessels in the regions of a lenticulostriate artery-dependent cerebral infarction in various primate models when specimens were prepared remotely after stroke induction may be explained by active endogenous fibrinolysis of occlusive thrombi within these small vessels within hours of thrombus formation as recently demonstrated for acute thrombotic occlusion during myocardial infarction. 34 Previous morphologic studies employing in situ perfusion fixation have been inconclusive.…”

Section: Discussionmentioning

confidence: 98%

Experimental acute thrombotic stroke in baboons.

Zoppo¹,

Copeland²,

Harker³

et al. 1986

Stroke

159

138

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SUMMARY To study the effects of antithrombotic therapy in experimental stroke, we have characterized a baboon model of acute cerebrovascular thrombosis. In this model an inflatable silastic balloon cuff has been implanted by transorbital approach around the right middle cerebral artery (MCA), proximal to the take-off of the lentlculostriate arteries (LSA). Inflation of the balloon for 3 hours in six animals produced a stereotypic sustained stroke syndrome characterized by contralateral hemiparesis. An Infarction volume of 3.2 ± 1 . 5 cm 3 in the ipsilateral corpus striatum was documented by computerized tomographic (CT) scanning at 10 days following stroke induction and 3.9 ± 1 . 9 cm 3 (n = 4) at 14 days by morphometric Deuropathotogic determinations of brain specimens fixed in situ by pressure-perfusion with 10% buffered formalin.Immediate pressure-perfusion fixation following deflation of the balloon was performed in 16 additional animals given Evans blue dye intravenously prior to the 3 hour MCA balloon occlusion. Light microscopy and transmission electron microscopy consistently confirmed the presence of thrombotic material occluding microcirculatory branches of the right LSA in the region of Evans blue stain, but not those of the contralateral corpus striatum.When autologous '"in-platelets were infused intravenously in four animals from the above group prior to the transient 3 hour occlusion of the right MCA, gamma scintillation camera imaging of each perfused-flxed whole brain demonstrated the presence of a single residual focus of '"in-platelet activity involving only the Evans blue-stained right corpus striatum. Focal right hemispheric activity was equivalent to 0.55 ± 0.49 ml of whole blood, and the occlusion score derived from histologic examination of the microcirculatton of the Evans blue-stained corpus striatum averaged 34.8 ± 2.8. Similar "'in-platelct imaging and histologic scoring experiments carried out hi four animals pretreated with the antithrombotic combination heparin and tidopidine showed marked reduction of both "'in-platelet activity (0.01 ± 0.03 ml vs. 0.55 ± 0.49 ml; p < 0.01) and thrombotic occlusion of the microcirculation (10.8 ± 7.4 units vs. 34.8 ± 2.8 units; p < 0.01) in the right corpus striatum following 3 hours of MCA occlusion. In separate control experiments "'inlabeled autologous platelets were infused after the 3 hour period of right MCA occlusion and subsequent balloon deflation hi two animals; no focus of '"in-platelet activity was demonstrated in fixed whole brain.We conclude that thrombi form in situ In the microcirculation of perforating branches of the LSA located in the ipsilateral corpus striatum following a 3 hour period of MCA occlusion and that these thrombi may be prevented when antithrombotic therapy is administered prior to MCA balloon occlusion. This model of acute thrombotic stroke may be useful to assess the safety and efficacy of thrombolytic therapies.

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Section: Discussionmentioning

confidence: 98%

Experimental acute thrombotic stroke in baboons.

Zoppo¹,

Copeland²,

Harker³

et al. 1986

Stroke

159

138

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“…7 -* The orbitofrontal artery is a prominent cortical vessel in the baboon and is often found within a few mm of the middle cerebral artery bifurcation. Watanabe 7 and Laurent et al* reported that the LLS arteries of the baboon most often arise as a cluster of vessels directly from the orbito-frontal artery. We have observed this occurrence in 6 of the 14 examined middle cerebral arteries (10 surgical observations and 4 postmortem following the injection of silicone rubber).…”

Section: Anatomical Considerationsmentioning

confidence: 99%

Selective lenticulostriate occlusion in the primate. A highly focal cerebral ischemia model.

Yonas¹,

Wolfson²,

Dujovny³

et al. 1981

Stroke

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SUMMARY A highly reliable model for the study of focal cerebral ischemia has been developed using a retro-orbital approach to occlude the lateral lenticulostriate arteries of the baboon. An infarction of the caudate, putamen and the anterior limb of the internal capsule has consistently been produced. Reliability has been attained because the anatomical variations of the lenticulostriate arteries of each animal can be fully appraised, permitting selective vessel occlusion. A well-defined clinical and radiographic lesion has also resulted from this procedure which was clinically well tolerated by all animals. Selective lenticulostriate occlusion provides a new approach to the study of focal cerebral ischemia in the sub-human primate, and serves for the evaluation of proposed therapies for treatment of focal cerebral ischemia.Stroke, Vol 12, No 5, 1981 AN IMPORTANT GOAL in the study of focal cerebral ischemia is a lower animal model with a lesion that resembles a stroke in man and permits its careful study. 1-2 If the model is to be used for the evaluation of a proposed therapy for focal cerebral ischemia, it must be highly reproducible. When subhuman primates are used, an even higher level of reproducibility is necessary to minimize the number of observations and, therefore, the number of valuable animals required to be studied, in order to draw a conclusion of significance. We report a technique for creating a highly reliable focal cerebral ischemic lesion in the baboon that fulfills these requirements as well as providing a unique opportunity to study the primate microcirculation. This technique depends upon selective occlusion of only the penetrating, lateral lenticulostriate (LLS) arteries. This is a fundamentally different approach from previous primate focal ischemia models which have all involved middle cerebral artery occlusion. ProcedureNine baboons (Papio cynocephalus/anubis) weighing between 8 and 10 kg were anesthetized with ketamine hydrochloride (Ketalar*) 5.0 mg/kg I.M. and pancuronium bromide (Pavulonf) .05 mg/kg. The animals were then intubated and ventilated on a respirator as guided by frequent blood gas determinations. Femoral arterial and venous catheters were inserted for monitoring arterial pressure and for the delivery of normal saline solution.• In order to expose the origins of the LLS arteries without brain retractions, we used a modified retroorbital approach. 8 The animals' heads were secured in a stereotaxic frame $ and the sagittal plane tilted 10°t oward the side of the surgery. After the skin about the right eye and temple was shaved and surgically prepared, a curvilinear incision was made around the lateral half of the orbit just cranial to the zygoma for approximately 1W inches. The temporalis and masseter muscles were incised and retracted away from the lateral orbital wall. Subperiosteal dissection was then extended into the lateral orbit. To provide additional space for exposure of the apex of the orbit, the posterior chamber of the eye was entered with a 22 gauge needle, ...

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“…We examined the temporal and regional pattern of neuronal apoptosis, as well as NFKB activation in this experimental transient focal ischemia in rats (1-hour ischemia with desired time interval for reperfusion) using the mono-filament model [48].…”

Section: Resultsmentioning

confidence: 99%

“…Exposiure to aE2 can activate the MAP kinase pathway (47), and this pathway is implicated in /3E2-mediated neuroprotection (14). In addition, aE2 has also been shown to have several other direct effects on nexu"ons, including modulation of the mitochondrial Na-f/K"^-ATPase activity (48), alteration of membrane fluidity (49), and inhibition of toxin-induced activation of NFKB (P. S. Green and J. W. Simpkins, xmpublished observations). It is unknown whether Ent-Ej can also interact with any of these cellular pathways.…”

Section: Ent-e2 ■Pe2mentioning

confidence: 99%

Neuroprotection from Brain Injury by Novel Estrogen

Simpkins¹

2003

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Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 1: Angio-anatomy and description of an experimental model with selective embolization of the internal carotid artery bifurcation.

Cited by 43 publications

References 25 publications

Experimental acute thrombotic stroke in baboons.

Experimental acute thrombotic stroke in baboons.

Selective lenticulostriate occlusion in the primate. A highly focal cerebral ischemia model.

Neuroprotection from Brain Injury by Novel Estrogen

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