Llewelyn J G, Patel N J, Wright D W, Thomas P K
Department of Neurological Science, Royal Free Hospital School of Medicine, London, England.
Metabolism. 1991 Oct;40(10):1079-83. doi: 10.1016/0026-0495(91)90133-h.
Streptozotocin (STZ)-induced diabetes in the rat causes a significant reduction in ouabain-sensitive Na,K-ATPase pumping activity measured by 86Rb+ influx, in sciatic endoneurium (by 54%) and dorsal root ganglia (by 22%). For endoneurium, the change is similar to that of ouabain-sensitive enzymatic Na,K-ATPase activity (42%), but in dorsal root ganglia, the decrease in enzymatic Na,K-ATPase activity was much greater. 86Rb+ efflux from dorsal root ganglia showed no difference between diabetic and control animals, confirming that the abnormal 86Rb+ influx reflects Na,K-ATPase function and not abnormal membrane permeability. The significance of these findings to pathogenetic mechanisms in diabetic neuropathy is discussed.
链脲佐菌素(STZ)诱导的大鼠糖尿病会导致坐骨神经内膜(降低54%)和背根神经节(降低22%)中通过86Rb+内流测量的哇巴因敏感的钠钾ATP酶泵活性显著降低。对于神经内膜,这种变化与哇巴因敏感的酶促钠钾ATP酶活性的变化(42%)相似,但在背根神经节中,酶促钠钾ATP酶活性的降低要大得多。糖尿病动物和对照动物的背根神经节86Rb+外流没有差异,这证实了异常的86Rb+内流反映的是钠钾ATP酶功能,而非异常的膜通透性。本文讨论了这些发现对糖尿病神经病变发病机制的意义。