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EXPERIMENTAL FOCAL CEREBRAL ISCHEMIA PRO-DUCED BY EMBOLIZATION WITH SILICONE CYLINDER IN NORMOTENSIVE (NTR) AND SPONTANEOUSLY HYPERTENSIVE RATS (SHR): COMPARISON OF NEUROLOGICAL AND PATHOLOGICAL FINDINGS Tetsuji Takeda 1 , Takeshi Shima 2 , Yoshikazu Okada 2 , Kanji Yamane 2 , Keiji Ohta 3 , Tohru Uozumi 4 1Department of Neurosurgery, Ehime Prefectural Hospital 2Department of Neurosurgery, Chugoku Rousai Hospital 3Department of Neurosurgery, Matsue Red Cross Hospital 4Department of Neurosurgery, Hiroshima University pp.1119-1125
Published Date 1989/11/1
DOI https://doi.org/10.11477/mf.1406206426
  • Abstract
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A focal cerebral ischemic model was produced by occlusion of the intracranial main cerebral artery with a silicone cylinder in normotensive (NTR) and spontaneously hypertensive rats (SHR). Main cerebral artery could be successfully occlu-ded in approximately 90%. The most frequent embolized site was the distal part of the internal cerebral artery (ICb) and less frequently the ho-rizontal segment of the anterior cerebral artery (Al). Mortality rate of NTR with ICb occlusion (NTR-ICb) was 43% at 72 hours after emboliza-tion and that of SHR with ICb occlusion (SHR-ICb) was 67% at 24 hours after embolization. NTR-ICb showed neurological signs (i. e. circling movement, hemiparesis, poor response to pain sti-muli) and histologically, showed infarction in the deep cerebral structures (i. e. thalamus, hypothala-mus, hippocampus, and internal capsule) accompa-nied with mild disruption of blood-brain barrier (BBB). SHR-ICb showed more serious neurological signs and more severe cerebral infarction in the deep cerebral structures with severe disruption of BBB.

In SHR-ICb, ischemic cerebral edema was more prominent which may deteriorated symptoms and pathological findings compared to NTR-ICb. This embolization model is proposed to be useful for studying the pathophysiology of focal cerebral ischemia, especially, early ischemic edema.


Copyright © 1989, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 2185-405X 印刷版ISSN 0006-8969 医学書院

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