Brismar T, Sima A A, Greene D A
Ann Neurol. 1987 May;21(5):504-7. doi: 10.1002/ana.410210515.
Acute reversible diabetic nerve dysfunction has been associated with a reversible myo-inositol-related (Na+ + K+)-ATPase defect, while poorly reversible chronic nerve dysfunction correlates with progressive axoglial dysjunction of peripheral nerve. The causal relationships between biochemical and neuroanatomical abnormalities and those of nodal membrane function are not known. Nodal clamp examinations were carried out in the sciatic nerve of diabetic BB-rats to elucidate the events underlying diabetic nerve dysfunctions and how these relate to metabolic and structural defects of diabetic nerve. With increasing duration of diabetes, there was a progressive decline in nodal action potentials attributable to decreased Na+ permeability and a decrease in the membranous Na+ gradient. Vigorous insulin therapy in short-term (6-week) diabetic BB-rats normalized the Na+-permeability defect and the membranous Na+ gradient. These defects did not reverse in long-term (24-week) diabetic animals subjected to the same treatment. This poorly reversible nodal dysfunction accounts for the not readily reversible conduction defect in chronic diabetes and is probably directly related to irreversible axoglial dysjunction.
急性可逆性糖尿病神经功能障碍与可逆性的肌醇相关的（钠+钾）-ATP酶缺陷有关，而可逆性较差的慢性神经功能障碍则与周围神经的渐进性轴突-神经胶质分离有关。生化和神经解剖学异常与结膜功能异常之间的因果关系尚不清楚。在糖尿病BB大鼠的坐骨神经中进行了结钳检查，以阐明糖尿病神经功能障碍的潜在机制，以及这些机制与糖尿病神经的代谢和结构缺陷之间的关系。随着糖尿病病程的延长，由于钠通透性降低和膜钠梯度降低，结动作电位逐渐下降。短期（6周）糖尿病BB大鼠的积极胰岛素治疗使钠通透性缺陷和膜钠梯度恢复正常。在接受相同治疗的长期（24周）糖尿病动物中，这些缺陷并未逆转。这种可逆性较差的结功能障碍导致了慢性糖尿病中不易逆转的传导缺陷，并且可能与不可逆的轴突-神经胶质分离直接相关。
