Early changes in transient adenosine during cerebral ischemia and reperfusion injury.
Early changes in transient adenosine during cerebral ischemia and reperfusion injury.
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DOI：
10.1371/journal.pone.0196932
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发表时间：
2018
期刊：
影响因子：
3.7
通讯作者：
Venton BJ
中科院分区：
文献类型：
--
作者：
Ganesana M;Venton BJ
腺苷是中枢神经系统中重要的神经调节剂，在缺血事件中组织腺苷水平升高，从而减轻兴奋性毒性神经元损伤。最近，我们实验室开发了一种电化学快速扫描循环伏安法(FSCV)，它可以识别腺苷浓度的快速、自发变化，仅持续约3秒。在这里，我们研究了脑缺血和再灌流对尾壳核一过性腺苷释放浓度和频率的影响。麻醉大鼠分为常氧2小时、双侧颈总动脉结扎致脑缺血30分钟、再灌注90分钟三个时间点。一过性腺苷释放在脑缺血期增加，并在再灌流期间保持升高。与常氧相比，脑缺血和再灌流期间腺苷瞬变的总数增加了52%。每一事件的腺苷浓度没有增加，但由于事件发生的频率较高，在脑缺血和再灌流期间累积的腺苷浓度增加了53%。此外，我们评估了A2A拮抗剂SCH442416的作用，SCH442416是一种假定的神经保护剂，可以影响腺苷瞬变。SCH442416可显著降低脑缺血再灌流时的瞬时频率27%和累积浓度31%。我们的结果表明，在早期脑缺血-再灌注损伤中，这种腺苷快速释放模式增加。快速释放腺苷可在脑缺血时提供快速的局部神经调节和神经保护作用。
Adenosine is an important neuromodulator in the central nervous system, and tissue adenosine levels increase during ischemic events, attenuating excitotoxic neuronal injury. Recently, our lab developed an electrochemical fast-scan cyclic voltammetry (FSCV) method that identified rapid, spontaneous changes in adenosine concentrations that last only about 3 seconds. Here, we investigated the effects of cerebral ischemia and reperfusion on the concentration and frequency of transient adenosine release in the caudate-putamen. In anesthetized rats, data were collected for four hours: two hours of normoxia, 30 min of cerebral ischemia induced by bilateral common carotid artery occlusion, and 90 min of reperfusion. Transient adenosine release was increased during the cerebral ischemia period and remained elevated during reperfusion. The total number of adenosine transients increased by 52% during cerebral ischemia and reperfusion compared to normoxia. The concentration of adenosine per event did not increase but the cumulative adenosine concentration during cerebral ischemia and reperfusion increased by 53% because of the higher frequency of events. Further, we evaluated the role of A2A antagonist, SCH442416, a putative neuroprotective agent to affect adenosine transients. SCH442416 significantly decreased the transient frequency during cerebral ischemia-reperfusion by 27% and the cumulative concentration by 31%. Our results demonstrate that this mode of rapid adenosine release increases during early cerebral ischemia-reperfusion injury. Rapid adenosine release could provide fast, local neuromodulation and neuroprotection during cerebral ischemia.
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