Ronquist G, Frithz G
Eur Neurol. 1982;21(5):318-23. doi: 10.1159/000115498.
48 patients with cerebral arteriosclerosis were found to have a manifest release of adenylate kinase (AK) into cerebrospinal fluid (CSF). This release was most probably due to an increased leak in the brain cells subsequent to a lowered adenylate charge potential followed by a diminished electrochemical potential in these cells suffering from disturbed oxygen supply. A further increase of AK release into CSF was noted for the 22 patients receiving cardiac glycosides compared to the 26 patients not treated with these drugs. The mean AK value of the former group was 0.119 +/- 0.028 U/l compared to that of the latter group, being 0.089 +/- 0.025 U/l, and this difference was significant (p less than 0.001). The effect of cardiac glycosides is most probably explained by an additional lowering of the membrane electrochemical potential in brain cells of these patients due to the direct action of cardiac glycosides on the Na+- and K+-dependent ATPase system in these cells, resulting in an increased leak in the plasma membrane.
48例脑动脉硬化患者被发现其脑脊液(CSF)中腺苷酸激酶(AK)明显释放。这种释放很可能是由于这些供氧受干扰的细胞中腺苷酸电荷电位降低,随后电化学电位降低,导致脑细胞渗漏增加所致。与26例未接受这些药物治疗的患者相比,22例接受强心苷治疗的患者脑脊液中AK释放进一步增加。前一组的平均AK值为0.119±0.028U/l,而后一组为0.089±0.025U/l,这种差异具有统计学意义(p<0.001)。强心苷的作用很可能是由于强心苷直接作用于这些细胞中的钠钾依赖ATP酶系统,导致这些患者脑细胞的膜电化学电位进一步降低,从而使质膜渗漏增加。