Tomlinson D R, Townsend J, Fretten P
Diabetes. 1985 Oct;34(10):970-2. doi: 10.2337/diab.34.10.970.
This investigation examined the effect of treatment of streptozocin-diabetic rats with the aldose reductase inhibitor "Statil" (25 mg/kg/day p.o.) on axonal transport in cholinergic neurons of the sciatic and vagal nerves and on nerve polyol and sugar levels. Three weeks of experimental diabetes caused deficits in the accumulation of choline acetyltransferase activity proximal to 24-h constrictions in the left sciatic and vagus nerves. These deficits did not develop in age-matched, similarly diabetic rats that were treated with the aldose reductase inhibitor. The inhibitor prevented completely the build-up of sorbitol and markedly reduced the build-up of fructose in the sciatic nerves of the treated diabetic rats. The inhibitor also prevented the depletion of myo-inositol that was seen in the untreated diabetic animals. It is suggested that these findings indicate a possible approach to the elucidation of the pathogenesis of cardiac vagal dysfunction in diabetes mellitus.
本研究检测了用醛糖还原酶抑制剂“Statil”（25毫克/千克/天，口服）治疗链脲佐菌素诱导的糖尿病大鼠，对坐骨神经和迷走神经胆碱能神经元轴突运输以及神经多元醇和糖水平的影响。实验性糖尿病持续三周导致左坐骨神经和迷走神经在24小时缩窄近端胆碱乙酰转移酶活性积累出现缺陷。在年龄匹配、同样患糖尿病但用醛糖还原酶抑制剂治疗的大鼠中，这些缺陷并未出现。该抑制剂完全阻止了治疗组糖尿病大鼠坐骨神经中山梨醇的积累，并显著减少了果糖的积累。该抑制剂还阻止了未治疗糖尿病动物中所见的肌醇消耗。有人认为，这些发现提示了一种可能用于阐明糖尿病中心脏迷走神经功能障碍发病机制的方法。
