Jaramillo J, Simard-Duquesne N, Dvornik D
Can J Physiol Pharmacol. 1985 Jul;63(7):773-7. doi: 10.1139/y85-128.
The resistance of the action potential to ischemic inactivation observed in diabetic patients has been reproduced in vivo in rat rendered diabetic with streptozotocin and, acutely, in normal rats given p.o. a load of glucose. The resistance phenomenon was not detected in galactosemic rats. The preservation of the action potential was reversed by the administration of insulin, but not by treatment with an aldose reductase (AR) inhibitor. The ischemic resistance is attributed to the metabolic availability of excess glucose to the nerve. AR does not appear to be involved in the phenomenon.
在糖尿病患者中观察到的动作电位对缺血失活的抗性，已在体内通过链脲佐菌素诱导糖尿病的大鼠以及急性给予口服葡萄糖负荷的正常大鼠中再现。在半乳糖血症大鼠中未检测到抗性现象。给予胰岛素可逆转动作电位的保存，但使用醛糖还原酶（AR）抑制剂治疗则不能。缺血抗性归因于神经可利用过量的葡萄糖进行代谢。AR似乎不参与该现象。
