| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Research Abstract |
It is a very important problem, when the cerebral ischemia advance to the irrevasible state. Concerning this degradation of cell membrane, and cytoskeletal proteins in the rat brain were inbestigated also for the clinical investigation, cerebral circulation and oxygen metabolism in moyamoya disease was studied.
1. Using the four-vessel occlusion model of adult wistar rats, we analyzed quantitatively the cerebral phospholipid moledcular species of diacyl phosplhatidylcholine and diacyl phosplhatidylcholine and released free fatty acids during ischemia. Total diacyl phosphatidylethanolamine molecular species decreased gradually but did not show any significant difference even at 60 minutes. By contrast, total diacyl phosphatidylethanolamine abrupltly decreased after 5 minutes and continued to decrease significantly thereafter. Polyunsaturated molecular species showed a higher ratio of degradation than saturated and monounsaturated molecular species of either phosphatidylcholine or phospha
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tidylethanolamine. Total Free fatty acid accumulated according to the time elaplsed, and statistical significance was obtained after 10 minutes. Free arachidonic and docosahexanoic acids were attributed to these significant accumulations at 10,15,and 30minutes. at 60 minutes, individual free fatty acids increased nonsplecifically. free fatty acids, which are hydrolyzed from plhosplholipid classes, are known to be further metabolized to bioactive substances such as prostaglandins and leukotrienes. Rapid degradation of phosplholipid molecular species, especially of diacyl polyunsaturated molecular species, could be an important finding to membrane perturbation. 2. Degradation of neurofilament (NF) triplet plroteins : NF200 (molecular weight (MW) 200,000), NF150(MW150,000), and NF68(MW 68,000) as well as of other cytoskeletal oroteins in the rat brain during ischemia was investigated. Sodium dodecyl sulfate-gel electropohoresis and immunoblot methods with anti-NF200 antibody were used for the study. Selective degradation of NF200 and NF150 was observed during the initial 10 to 50 minutes of ischemia. The degradation was demonstrated both in permanent ischemia caused by decapitation and in transient ischemia induced by four-vessel occlusion followed by reperfusion after 30 minutes of occlusion (modified pulsinelli method). The degradation suggests that the actibation of a protease occurs in the first 15 minutes of cerebral ischemia, which is the earliest irreversible neuronal change ever to be reported. 3. Cerebral rCBF, ROEF, rCMRO_2, and rCBV in moyamoya disease were studied by means of positron emmission tomography (PET). Though the value of rCBF was slightly higher in moyamoya disease, this difference was not statistically significant. On the other hand, in moyamoya disease rCBV increased significantly in gray matter, white matter, and basal ganglis. The ratio of CBF to CBV is considered to be the index of perfusion pressure and reciprocal of cerebral mean transit time under the normal autoregulation of CBF. This ratio was calculated and compared with the normal value for each tissue. The ratio was significantly decreased in each tissue in moyamoya disease, indicating the presence of a low perfusion pessure in the moyamoya brain. Less
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