| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
To examine the role of adenosine receptor on spinal neuronal injury after transient spinal cord ischemia, following expeniments were performed.
1. Estimation of the rat spinal aid ischemia modeL : Motor function of hind limbs of the rats, which suffered different duration of aortic occlusion, were observed for 72 hours 100% (8/8) of the rats, of which aorta were occluded for 10 mm, showed complete paraplegia. Though the rats, of which aorta were occluded for 6 mm, showed transient and slight motor weakness of hind limb, all of them (7/7) recovered to normal walk.
2. Effects of adenosine receptor agonist and antagonist on spinal neuronal injury after transient spinal aid iachemia :
Intrathecal injection of theophylline, an adenosine receptor antagonist, (100 mug) did not worsen the motor function after 6 min spinal cord ischemia model Intrathecal injection of propentofylline, an adenosine re-uptake inhibitor, (30 mug or 100 mug) did not improve the motor deficit after 10 min spinal cord ischenia Intrathecal injection of 2-chroloadenosina a selective adenosine Al receptor agonist, (10 mug of 30 mug) did not improve the motor deficit after 10 min spinal cord ischemia.
3. Effect of on glutamate concentration in lumbar cerebral spinal fluid after 10 min spinal cord ischemia : Though 2-chroloadenosme did not reduce the concentration of glutamate till 3 hours after reperfusion, reduced significantly at 4 hours alter reperfusion.
Our results indicated that adenosine receptor activation reduced the glutamate concentration in CSF, but, it would not have significant role in the mechanism of spinal ischemic neuronal injury in the model in which spinal collateral blood flow was reduced by proximal hypotension. Also it was suggested that protective effect of adenosine receptor activation reported previously may be due to vasodilation by adenosine A2 receptor activation.
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