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实验用Fluo-3负载细胞，在激光扫描共聚焦显微镜下直接监测缺氧后分散培养的大鼠海马CA1区神经元内游离Ca2+浓度（［Ca2+］i）的变化，观察腺苷对这种变化的影响并初步探讨其作用机制。结果发现，急性缺氧使海马神经元［Ca2+］i显著升高；腺苷（100μmol/L）明显抑制缺氧引起的［Ca2+］i增高，腺苷A1受体拮抗剂CPT以及K+通道阻断剂4-AP和ATP敏感性K+通道阻断glipizide均可拮抗腺苷的抑制作用。结果表明，腺苷通过其A1受体介导，可能激活4-AP和／或ATP敏感性K+通道，从而抑制缺氧引起的海马神经元胞内Ca2+升高。
The cells were loaded with Fluo-3 and the changes of intracellular free Ca2 + concentration ([Ca2 +] i) in hippocampal CA1 area of hypoxia rats were observed under laser scanning confocal microscopy. Influence and preliminary study of its mechanism of action. The results showed that acute hypoxia significantly increased [Ca2 +] i in hippocampal neurons; adenosine (100μmol / L) significantly inhibited the increase of [Ca2 +] i induced by hypoxia, blockade of adenosine A1 receptor antagonist CPT and K + channels Both 4-AP and ATP-sensitive K + channel block glipizide antagonized adenosine inhibition. The results indicate that adenosine, through its A1 receptor, may activate 4-AP and / or ATP-sensitive K + channels and thus inhibit intracellular Ca2 + elevation induced by hypoxia in hippocampal neurons.