Effects of adenosine receptor antagonist on spinal neuronal injury after transient spinal cord ischemia.

为了探讨腺苷受体在短暂性脊髓缺血后脊髓神经元损伤中的作用，我们进行了以下实验。大鼠脊髓辅助缺血模型的估计：观察不同主动脉阻断时间的大鼠后肢运动功能，72小时后，主动脉阻断10 mm的大鼠有100%（8/8）出现完全截瘫。主动脉闭塞6 mm的大鼠虽有短暂性、轻度后肢运动无力，但均恢复正常行走（7/7）。腺苷受体激动剂和拮抗剂对短暂性脊髓缺血后脊髓神经元损伤的影响：脊髓缺血模型6 min后鞘内注射腺苷受体拮抗剂茶碱（100杯）未使运动功能恶化。（30马克杯或100马克杯）并没有改善脊髓缺血10分钟后的运动缺陷，鞘内注射选择性腺苷Al受体激动剂2-铬腺苷钠（10马克杯或30马克杯）并没有改善脊髓缺血10分钟后的运动缺陷。脊髓缺血10 min后对腰脑脊液谷氨酸浓度的影响：2-铬酶体在再灌注后3小时后才降低谷氨酸浓度，但在再灌注后4小时显著降低。我们的研究结果表明，腺苷受体的激活降低了脑脊液中谷氨酸的浓度，但在近端低血压减少脊髓侧支血流量的模型中，它在脊髓缺血性神经元损伤的机制中没有明显的作用。此外，先前报道的腺苷受体激活的保护作用可能是由于腺苷A2受体激活引起的血管扩张。

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.