1991 Fiscal Year Final Research Report Summary
Study on the Pathophysiology of Experimental Vascular Dementia in Gerbils using Magnetic Resonance Methods
| Project/Area Number |
02670375
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | National Cardiovascular Center |
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Principal Investigator |
NARITOMI Hiroaki National Cardiovascular Center Cerebral Circulation Laboratory Director, 循環動態機能部, 室長 (60132932)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Masahiro National Cardiovascular Center Radio-Isotope Experimental Institute Faculty, 生体工学部, 研究員 (50150800)
KANASHIRO Masaru National Cardiovascular Center Department of Biochemistry Faculty, 共通実験室, 研究員 (10132929)
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| Project Period (FY) |
1990 – 1991
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| Keywords | vascular dementia / chronic low perfusion / cerebral ischemia / 31P NMR spectroscopy / monogolian gerbils / arterial stenosis / behavioral abnormality / Cerebral blood flow |
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| Research Abstract |
In patients with vascular dementia, cerebral arteries are usually narrowed, and cerebral blood flow is reduced constantly. In order to clarlfy the role of arterial stenosis In the pathophysiology of vascular dementia, both common carotld arteries were narrowed in gerbils, and chronic effects of arterial stenosls were studied. In experiment 1, the common carotid arteries were narrowed by silver clips wlth 0.1 x 1.0 mm in diameter and 2.0 mm in length. The stenosis caused severe blood flow reduction of below 0.20 mi/g/min in 40% of animals and moderate flow reduction in the remaining 60% of animals. 40% of animals developed energy failure and died within 4 days after the stenosis. The remalning 60% of animals had no energy impairments as judged by in vivo 31P nuclear magnetic resonance spectroscopy (MRS) and remained free from ischemic symptoms. Histological examinations in these asymptomatic animals exhibited no ischemic change at 1 day after the stenosis. At 5 days, 4 weeks and 3 month
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s after stenosis, 40%, 53% and 60% of animals showed ischemic changes. Ischemic changes included large hemisphric cerebral infarction (type 1), multiple small infarction (type 2) and small patchy changes consisting of neuronal cell death (type 3). Type 3 ischemia was observed at 4 weeks and 3 months after the stenosls and most commonly seen in the cerebral cortex and strlatum. At 2 weeks and 3 months after the stenosls, these ischemic. animals exhibited remarkable depresslon of learning ability. In experiment 2, flve different grades of stenosis was produced at both common carotid arteries using polyethylene tubes with 0.28-0.58 mm in diameter and 2.0 mm in length. In the group with severe stenosis, secondary thrombus formation occurred at the carotid arteries leading to energy impairments and acute death. In the group with intermediate grade stenosis, carotid thrombus was seen in 30% of animals which developed type 1 or 2 ischemia. In the remaining animals, no carotid thrombus was observed, yet, type 3 ischemia was frequently observed. In the groups with moderate to mild grade stenosis, little ischemic changes resulted. Type 1 or 2 ischemia is probably caused by thrombotic arterial obstruction or artery-to-artery embolism. Type 3 ischemia is unlikely to result from such mechanism and is presumably attributable to chronic low perfusion. The results suggest that chronic low perfusion may produce small patchy ischemia in the brain and may play a role in the pathophysiology of vascular dementia. Less
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