| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1990: ¥1,300,000 (Direct Cost: ¥1,300,000)
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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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