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Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats.

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Date
2016-10
Authors
Sasaki, Toshihiro
Hoffmann, Ulrike
Kobayashi, Motomu
Sheng, Huaxin
Ennaceur, Abdelkader
Lombard, Frederick W
Warner, David S
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Abstract
<h4>Background</h4>Cognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models.<h4>Methods</h4>Pilot work identified blood injectate volumes necessary to provide similar mortality rates (20-25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naïve rats were used as controls. Functional and cognitive outcome was assessed over 35 days.<h4>Results</h4>DB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB.<h4>Conclusion</h4>Both SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits.
Type
Journal article
Subject
Animals
Rats
Rats, Wistar
Subarachnoid Hemorrhage
Disease Models, Animal
Behavior, Animal
Maze Learning
Male
Cognitive Dysfunction
Permalink
https://hdl.handle.net/10161/23258
Published Version (Please cite this version)
10.1007/s12028-016-0250-1
Publication Info
Sasaki, Toshihiro; Hoffmann, Ulrike; Kobayashi, Motomu; Sheng, Huaxin; Ennaceur, Abdelkader; Lombard, Frederick W; & Warner, David S (2016). Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats. Neurocritical care, 25(2). pp. 293-305. 10.1007/s12028-016-0250-1. Retrieved from https://hdl.handle.net/10161/23258.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Ulrike Hoffmann

Assistant Professor of Anesthesiology

Frederick Wilhelm Lombard

Adjunct Associate Professor in the Department of Anesthesiology
1. Animal models of Subarachnoid Hemorrhage (SAH) induced Cerebral Vasospasm 2. Pathogenesis of Cerebral Vasospasm following SAH 3. Translational Research in SAH 4. Long-term Outcome following Endovascular Coiling of Unruptured Cerebral Aneurysms
Sheng

Huaxin Sheng

Associate Professor in Anesthesiology
We have successfully developed various rodent models of brain and spinal cord injuries in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma, subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression injury. We also established cardiac arrest and hemorrhagic shock models for studying multiple organ dysfunction.  Our current studies focus on two projects. One is to examine the efficacy of catalytic antioxidant in treating cerebral is
Warner

David Samuel Warner

Distinguished Distinguished Professor of Anesthesiology, in the School of Medicine
Humans may sustain a variety of forms of acute central nervous system injury including ischemia, trauma, vasospasm, and perinatal hypoxemia. The Multidisciplinary Neuroprotection Laboratories is dedicated to examining the pathophysiology of acute brain and spinal cord injury with particular reference to disease states managed in the perioperative or neurointensive care environments. Rodent recovery models of cerebral ischemia, traumatic brain injury, cardiopulmonary bypass, subarachnoid he
This author no longer has a Scholars@Duke profile, so the information shown here reflects their Duke status at the time this item was deposited.
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