Gourine Alexander V, Llaudet Enrique, Thomas Teresa, Dale Nicholas, Spyer K Michael
Department of Physiology, Royal Free and University College London Medical School, Rowland Hill Street, UK.
J Physiol. 2002 Oct 1;544(Pt 1):161-70. doi: 10.1113/jphysiol.2002.024174.
The time course of adenosine release in the nucleus tractus solitarii (NTS) and ventrolateral medulla (VLM) during acute systemic hypoxia was investigated in the anaesthetised rat by means of amperometric enzymatic sensors. It was found that acute hypoxia induced a significant delayed increase in adenosine level (reaching levels as high as 5 microM) in the NTS and that hypoxia-induced release of adenosine was similar at various regions of the NTS along its rostro-caudal axis. Significantly smaller or no increases in adenosine levels at all in response to hypoxia were observed in the VLM. The increase in adenosine level in the NTS occurred during reoxygenation after the termination of the hypoxic challenge and was accompanied by a smaller increase in inosine concentration. At the dorsal surface of the brainstem, only release of inosine was detected following acute hypoxia. Addition of the ecto-5'-nucleotidase inhibitor alpha,beta-methylene ADP (200 microM) to the dorsal surface of the brainstem completely abolished the signal evoked by hypoxia, suggesting that the inosine arose from adenosine that was produced in the extracellular space by the prior release of ATP. This study indicates that following systemic hypoxia, adenosine levels in the NTS increase to a significantly greater extent than in the VLM. However, the increase in adenosine concentration in the NTS occurs too late to be responsible for the hypoxia-induced depression of the respiratory activity.
利用安培酶传感器在麻醉大鼠中研究了急性全身缺氧期间孤束核（NTS）和延髓腹外侧区（VLM）中腺苷释放的时间进程。结果发现，急性缺氧导致NTS中腺苷水平显著延迟升高（达到高达5微摩尔的水平），并且缺氧诱导的腺苷释放在NTS沿其头-尾轴的各个区域相似。在VLM中，对缺氧的反应中腺苷水平显著降低或根本没有升高。NTS中腺苷水平的升高发生在缺氧刺激终止后的复氧期间，并伴有肌苷浓度的较小升高。在脑干背表面，急性缺氧后仅检测到肌苷的释放。将胞外5'-核苷酸酶抑制剂α，β-亚甲基ADP（200微摩尔）添加到脑干背表面完全消除了缺氧诱发的信号，表明肌苷来源于先前释放的ATP在细胞外空间产生的腺苷。这项研究表明，全身缺氧后，NTS中的腺苷水平升高幅度明显大于VLM。然而，NTS中腺苷浓度的升高发生得太晚，无法解释缺氧诱导的呼吸活动抑制。
