| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
We have investigated various metabolic changes occuring during brain ishemia by using NMR spectroscopy. A brain ischemic model adoped here was a 30 min ischemia caused by ligation of bilateral caroted arteries of gerbil mice. A coupled of NMR sudies were carried on this model,which included 1-H NMR,31-P NMR,23-Na NMR, and 19-F NMR.
Immedeately after acute brain ischemia high energy phosphate compounds like phosphocreatin, and ATP measured by 31-P NMR spectrometer decreased promptly, and inorganicphosphate built up. But these changes in high energy phosphate compounds returned to the initial state within 30 min after reperfusion of the circulation. The volume of NMR sensitive sodium was decreased just after initiation of the brain ischemia,which meant deterioration of Na pump of cell membran occured. Although the energic state returned to normal level after reperfusion of the blood,brain edema continuously progressed which could be detected by using Gd-DTPA enhanced H NMR imaging and T-1 relaxometry on the ischemic gebil brain.
The functional state of blood brain barrier could be monitored when we appleid some NMR sensitive substrate to the ischemic model animals. 5-fluorouracil is one of challengeable substrate because of its character of 19F NMR sensitivity and selective permiability of BBB. After 30 min brain ischemia we found that the 19-F NMR signal intensity of 5-FU from the ishemic brain was 2-3 times greater than that of normal control brain. We could detect the deterioration of selectivity of permiability of the BBB after acute brain ischemia by using 19-F NMR spectroscopy.
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